Fundamental Critical Care Support:

Surgical
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 Fundamental Critical Care Support: Surgical

Editors

Antonio Joao Gandra d’Almeida, MD, MDM, FACS, FCCM, OF-3

Head of Education and Simulation of Coimbra

Armed Forces Medical Services Teaching and Research Center
Portugal
No disclosures

Keith Killu, MD, FACP, FCCM

Assistant Professor of Clinical Medicine
Keck School of Medicine
University of Southern California
Division of Pulmonary, Critical Care and
Sleep Medicine
Los Angeles, California, USA
No disclosures

Mary Jane Reed, MD, FACS, FCCM

Geisinger Medical Center
Director Biocontainment Unit
Associate, Departments of Critical Care
Medicine and General Surgery
Danville, Pennsylvania, USA
No disclosures

Contributors

Kwame Asante Akuamoah-Boateng, DNP, ACNP-BC, MSN, RN,

FCCM
Lead Advance Practice Provider – Division of Acute Care Surgery
Virginia Commonwealth University Health
Department of Surgery
Richmond, Virginia, USA
No disclosures

Darrell E.R. Alley, MBA, MD, FACS, FCCP, FCCM

Surgical Intensivist
Houston Methodist Sugar Land Hospital
Sugar Land, Texas, USA
No disclosures

Promise Ariyo, MD
Johns Hopkins Hospital
Baltimore, Maryland, USA
No disclosures

Marie R. Baldisseri, MD, MPH, FCCM

Professor of Critical Care Medicine and Neurocritical Care
University of Pittsburgh Medical Center
Pittsburgh, Pennsylvania, USA
No disclosures

Michael C. Banks, MD, MEHP

Assistant Professor
Anesthesiology and Critical Care Medicine
Johns Hopkins University School of Medicine
Baltimore, Maryland, USA
No disclosures

Dionne J. Blyden, MD
Senior Staff Physician
Henry Ford Hospital
Detroit, Michigan, USA
No disclosures

Bryan Boling, DNP, ACNP

Assistant Program Director, APP Critical Care
Fellowship Program
University of Kentucky, Anesthesia Critical Care
Lexington, Kentucky, USA
Adjunct Assistant Professor, Acute Care
Nurse Practitioner Program
Georgetown University
Washington, DC, USA
No disclosures

Leandro Braz de Carvalho, MD

Intensive Care and Anesthesiology Physician
Belo Horizonte, Minas Gerais, Brazil
No disclosures

Melissa E. Brunsvold, MD, FACS, FCCM

Associate Professor of Surgery
University of Minnesota
Minneapolis, Minnesota, USA
No disclosures

Marilyn N. Bulloch, PharmD, BCPS, FCCM

Associate Clinical Professor and Director of Strategic Operations
Auburn University Harrison School of Pharmacy
Kimberly, Alabama, USA
No disclosures

Victor E. Coba, MD
Cardiac Surgery ICU Medical Director
Henry Ford Hospital
Detroit, Michigan, USA
No disclosures

Bryan Collier, DO, FACS, FCCM

Professor of Surgery, Virginia Tech Carilion
School of Medicine
Section Chief of Acute Care Surgery,
Trauma and Surgical Critical Care Medical
Director, Carilion Roanoke Memorial Hospital
Surgical Critical Care Fellowship
Program Director
Director of Surgical Nutrition
Roanoke, Virginia, USA
No disclosures

Gary R. Collin, MD, FACS, FCCM

Chief of Surgery & Director, Surgical Critical Care
Salem Veterans Affairs Medical Center
Salem, Virginia, USA
No disclosures

Craig Coopersmith, MD, FACS, MCCM

Emory Critical Care Center
Emory University School of Medicine
Atlanta, Georgia, USA
No disclosures

Michaelia Cucci, PharmD, BCCCP, BCPS

Pharmacy Clinical Specialist — Trauma/Surgical ICU
Cleveland Clinic Akron General
Akron, Ohio, USA
No disclosures

Patrick T. Delaplain, MD
Resident
University of California, Irvine
Orange, California, USA
No disclosures

Lauren Donatelli-Seyler, DO, FACOS, FACS

Director of Education, Division of Trauma,
Critical Care and Acute Care Surgery
University Hospitals Cleveland Medical Center
Cleveland, Ohio, USA
No disclosures

Todd Dorman, MD, FSACME, MCCM

Senior Associate Dean for Education Coordination
Associate Dean Continuing Medical Education
Professor and Vice Chair for Critical Care
Department of Anesthesiology &
Critical Care Medicine
Johns Hopkins University School of Medicine
Baltimore, Maryland, USA
No disclosures

David J. Dries, MD, MSE, MCCM

HealthPartners Institute
Professor of Surgery
University of Minnesota
Saint Paul, Minnesota, USA
No disclosures

Vanessa Goldenberg, MD
Critical Care Medicine
Mount Sinai School of Medicine
New York, New York, USA
No disclosures

J. Peter Gruen, MD
Director of Critical Care
Los Angeles County & University of Southern California Medical Center
Los Angeles, California, USA
No disclosures

Merhnaz Hadian, MD, MS, JD, FCCM

Assistant Clinical Professor of Medicine
David Geffen School of Medicine at UCLA
Founder
INSPIRE CCM
Hollywood, California, USA
No disclosures

Mark E. Hamill, MD, FCCM

Associate Professor
Trauma Surgeon, Surgical Intensivist, and Acute Care Surgeon
University of Nebraska Medical Center
Omaha, Nebraska, USA
No disclosures

Kristie A. Hertel, ACNP, CCRN, MSN, RN, FCCM

Advanced Practice Provider
Vidant Medical Center
Greenville, North Carolina, USA
No disclosures

Jorge Luis Hidalgo, MD, MACP, FCCP, MCCM

Professor of Critical Care
Karl Heusner Memorial Hospital/Belize
Healthcare Partners
Belize City, Belize
No disclosures

Stuart D. Hurst, MD
Assistant Professor
Trauma and Surgical Critical Care
Department of Surgery
Emory University School of Medicine
Atlanta, Georgia, USA
No disclosures

Ella A. Illuzzi, ANP-BC

Mount Sinai Hospital
New York, New York, USA
No disclosures

Kaori Ito, MD, PhD, FACS

Assistant Professor
Division of Acute Care Surgery,
Department of Emergency Medicine
Teikyo University School of Medicine
Tokyo, Japan
No disclosures

Shabbar HK Joad, MD, FNB, FCCP, FICCM, FICM, FCCM

Director of Critical Care
Fortis Hospital, Jaipur, Rajasthan
India
No disclosures

Victor C. Joe, MD, FACS

Clinical Professor of Surgery
Medical Director, UC Irvine Health
Regional Burn Center
UC Irvine Health Medical Center
Orange, California, USA
No disclosures

Stefan W. Leichtle, MD, FACS

Associate Professor of Surgery
Virginia Commonwealth University
Medical Center
Richmond, Virginia, USA
No disclosures

Francis Theodore Lytle, MD

Medical Director Adult Cardiothoracic
Intensive Care
Section Chief, Intensive Care, Harrington
Heart & Vascular Institute
Associate Chief Medical Office, University
Hospitals Cleveland Medical Center
Assistant Professor, Department of Anesthesiology, Case Western Reserve
University
Cleveland, Ohio, USA
No disclosures

Anthony R. Manasia, MD, FCCP

Professor of Medicine and Surgery
Icahn School of Medicine at Mount Sinai
New York, New York, USA
No disclosures

Bushra Mina, MD, FCCP, FACP, FCCM

Assistant Professor, Zucker Medical School at Hofstra Northwell
Director, Pulmonary Critical Care Fellowship
Chief, Pulmonary Medicine
Lenox Hill Hospital,
New York, New York, USA
No disclosures

Douglas F. Naylor, Jr, MD, FACS, MCCM

Department of Surgery
Department of Trauma, Critical Care and Acute Care Surgery
University Hospitals, Cleveland Medical Center
Cleveland, Ohio, USA
No disclosures

Mark A. Newell, MD, MMM, FACS

Associate Professor of Surgery
Brody School of Medicine
East Carolina University
Greenville, North Carolina, USA
No disclosures

Frank M. O’Connell, MD, FACP, FCCP

Staff Anesthesiologist
AtlantiCare Regional Medical Center
Ponoma, New Jersey, USA
No disclosures

John M. Oropello, MD, FCCM

Program Director, Critical Care Medicine
Director, Transplant ICU
Mount Sinai School of Medicine
New York, New York, USA
No disclosures

Richard K. Patch, III, MD

Assistant Professor of Anesthesiology and Medicine
Mayo Clinic
Rochester, Minnesota, USA
No disclosures

Michael A. Pisa, ACNP, ACNP-BC

Hospital of the University of Pennsylvania
Philadelphia, Pennsylvania, USA
No disclosures

Sujanthy S. Rajaram, MD, MPH, FACCP, FAASM, FCCM

Professor of Medicine
Sidney Kimmel Medical College of Thomas Jefferson University
Critical Care Medicine, Gagnon
Cardiovascular Institute
Morristown Medical Center
Morristown, New Jersey, USA
No disclosures

Sophia Chu Rodgers, DNP, ACNR, MSN, FNP, FAANP, FCCM

Critical Care Nurse Practitioner
Lovelace Medical Group
Lovelace Health Systems
Albuquerque, New Mexico, USA
No disclosures

Mark B. Safford, MD, FACP, FCCP

Director Step-Down Unit
Medical Director Cardiac Critical Care Unit
Critical Care Surgery and Medicine
Saint Barnabas Medical Center
Livingston, New Jersey, USA
No disclosures
Raul M. Sanchez-Leon, MD, FACP, FCCP, CNSC
Critical Care Attending, Houston Methodist Hospital
Assistant Professor of Clinical Medicine,
Weill Cornell Medical College
Adjunct Assistant Professor of Medicine,
Texas A&M University College of Medicine
Houston, Texas, USA
No disclosures

Greg P. Schaefer, DO
Medical Director, Surgical Critical Care
West Virginia University School of Medicine
Morgantown, West Virginia, USA
No disclosures

Varothayan Sriskantharaja, MBBS

University of Colombo
Colombo, Sri Lanka
No disclosures

Daniel N. Storzer, DNP, ACNP, FCCP, FCCM

Intensivist
ThedaCare Regional Medical Center
Appleton, Wisconsin, USA
No disclosures

Denise Torres, MD, FACS

Interim Chair Surgical Institute
Geisinger Health System
Interim Chair Geisinger Department of Surgery
Division Chief, Acute Care Surgery
Geisinger
Danville, Pennsylvania, USA
No disclosures

Daniel Wu, DO, FACOS. FACS, FCCM

Associate Trauma Program Medical Director
Trauma Intensivist, Acute Care Surgeon
Penn Medicine Lancaster General Hospital
Lancaster, Pennsylvania, USA
No disclosures
 Acknowledgments

The following individuals contributed to the development of Fundamental

Critical Care Support: Seventh Edition, a portion of which is included in
Fundamental Critical Care Support: Surgical.

Fundamental Critical Care Support, Seventh Edition

Editors

Mark E. Hamill, MD, FACS, FCCM

Associate Professor
Trauma Surgeon, Surgical Intensivist, and Acute Care Surgeon
University of Nebraska Medical Center
Omaha, Nebraska USA
No disclosures

Kristie A. Hertel, RN, MSN, CCRN, ACNP-BC, FCCM

Advanced Practice Provider
Vidant Medical Center
Greenville, North Carolina, USA
No disclosures

Javier Perez-Fernandez, MD, FCCM, FCCP

General Manager
Intensive Care Solutions
Medical Director, Critical Care Services
Baptist Hospital of Miami
Miami, Florida, USA
No disclosures

Contributors

Mohamed Abou El Fadl, MD

Critical Care and Neurocritical Care Medicine
Intensive Care Solutions
Baptist Health South Florida
Miami, Florida, USA
No disclosures

Albert Abreu, MBA, MIS, RRT

Director, Cardiopulmonary
West Kendall Baptist Hospital
Miami, Florida, USA
No disclosures

Kazuaki Atagi, MD, PhD, FCCM

Director of Critical Care Medicine
Nara Prefecture General Medical Center
Nara, Japan
No disclosures

Jennifer Axelband, DO, FCCM, FACOEP

Director Neurocritical Care
Network Critical Care Education Director
St. Luke’s University Health Network
Bethlehem, Pennsylvania, USA
No disclosures

Abdullah Bakhsh, MSSS, FAAEM

Assistant Professor of Emergency Medicine
King Abdulaziz University
Jeddah, Saudia Arabia
No disclosures

Marie Baldisseri, MD, MPH, FCCM

Professor of Critical Care Medicine and Neurocritical Care
University of Pittsburgh Medical Center
Pittsburgh, Pennsylvania, USA
No disclosures

Jennifer Bath, MSN, RN, ACNS-BC, CEN, TCRN

Clinical Nurse Specialist for Trauma Services
Carilion Roanoke Memorial Hospital
Roanoke, Virginia, USA
No disclosures

Javier O. Belmo, RRT

Manager, Cardiopulmonary
West Kendall Baptist Hospital
Miami, Florida, USA
No disclosures

Ana Berbel Caban, MD

Intensivist and Infectious Diseases Physician
Intensive Care Solutions
Miami, Florida, USA
No disclosures

Sherry Boone, MSN, ACNP-C, RN, CCRN

Assistant Professor of Nursing
Carilion Roanoke Memorial Hospital
Radford University Carilion
Roanoke, Virginia, USA
No disclosures

Gregory H. Botz, MD, FCCM

Professor of Anesthesiology and Critical Care
University of Texas MD Anderson Cancer Center
Houston, Texas, USA
No disclosures

Matthew T. Carr, MD
Attending Physician
Department of Emergency Medicine
The Brookdale Hospital Medical Center
Brooklyn, New York, USA
No disclosures

Kimberley Chavez, MD
Cooper University Hospital
Camden, New Jersey, USA
No disclosures

Heidi M. Clarke, PharmD, BCCCP

Clinical Manager
Director PGY2 Critical Care Residency
Baptist Hospital of Miami
Miami, Florida, USA
No disclosures

Ivan Co, MD
University of Michigan
Ann Arbor, Michigan, USA
No disclosures

Bryan R. Collier, DO, FACS, FCCM

Professor of Surgery
Chief of Acute Care Surgery
Carilion Roanoke Memorial Hospital
Roanoke, Virginia, USA
No disclosures

Gary R. Collin, MD, FACS, FCCM

Chief of Surgery & Director of Surgical
Critical Care
Salem Veterans Affairs Medical Center
Salem, Virginia, USA
No disclosures

Ian Del Conde, MD, FACC

Associate Director of Cardiology
Miami Cardiac & Vascular Institute
Baptist Hospital
Miami, Florida, USA
No disclosures
David Dries, MD, MSE, MCCM
HealthPartners Institute
Professor of Surgery
University of Minnesota
Minneapolis, Minnesota, USA
No disclosures

Christina Dunbar Matos, DO

University of Louisville
Advanced Heart Failure/VAD/
Transplant Department
Louisville, Kentucky, USA
No disclosures

Emily Faulks, MD
Assistant Professor of Surgery
Trauma and Critical Care Surgeon
Carilion Roanoke Memorial Hospital
Roanoke, Virginia, USA
No disclosures

Karel Fuentes, MD
Intensive Care Solutions
Medical Director of Neurocritical Care
Baptist Health Neuroscience Center
Miami, Florida USA
No disclosures

Nicole M. Garcia, MD, FACS

Clinical Assistant Professor
Department of Surgery
East Carolina University,
Brody School of Medicine
Greenville, North Carolina, USA
No disclosures

Robert C. Gibson, RN, MS, ACNP-BC

Critical Care Education Coordinator
Mercy Hospital of Buffalo
Buffalo, New York, USA
No disclosures

Carrie L. Griffiths, PharmD, BCCCP, FCCM

Associate Professor and Clinical Pharmacy
Specialist: Virtual Critical Care
Wingate University School of Pharmacy
Wingate, North Carolina, USA
No disclosures

Jorge L. Hidalgo, MD, MACP, MCCM

Professor of Critical Care
Karl Heusner Memorial Hospital
Belize Healthcare Partners
Belize City, Belize
No disclosures

Steven M. Hollenberg, MD, FACC, FAHA, FCCP

Professor of Medicine
Hackensack Meridian School of Medicine
Program Director, Cardiology
Hackensack University Medical Center
Hackensack, New Jersey, USA
No disclosures

John C. Hunninghake, MD
Pulmonary/Critical Care Physician
Assistant Professor of Medicine (USU)
San Antonio Military Medical Center (BAMC)
San Antonio, Texas, USA
No disclosures

Robert C. Hyzy, MD, MCCM, ATS-F, FCCP

Professor of Internal Medicine
Medical Director, Critical Care Medicine Unit
University of Michigan Health System
Ann Arbor, Michigan, USA
No disclosures

Kaori Ito, MD, PhD, FACS

Assistant Professor
Teikyo University
Tokyo, Japan
No disclosures

Richard Iuorio, MD
Mount Sinai Hospital
New York, New York, USA
No disclosures

Muhammad Jaffar, MD, FCCM

Anesthesiology Residency Program Director
Detroit Medical Center
Wayne State School of Medicine
Detroit, Michigan, USA
No disclosures

David Jury, MD, MS

Staff Intensivist and Anesthesiologist
Department of Intensive Care and Resuscitation
Cleveland Clinic Foundation
Cleveland, Ohio, USA
No disclosures

Keith Killu, MD, FCCM

Assistant Professor of Clinical Medicine
Keck School of Medicine
University of Southern California
Los Angeles, California, USA
No disclosures

Anand Kumar, MD, FCCM

Professor
University of Manitoba
Winnipeg, Canada
No disclosures

James J. Lamberg, DO
Penn Medicine Lancaster General Health
Lancaster, Pennsylvania, USA
No disclosures

Amy Lucas, MSN, RN, CCNS, CCRN-K

Clinical Nurse Specialist
Carilion Roanoke Memorial Hospital
Roanoke, Virginia, USA
No disclosures

Michael Malian, MD, MA, FACS

Trauma/Critical Care Surgeon
Beaumont Dearborn Hospital
Dearborn, Michigan, USA
No disclosures

Miguel A. Matos, DO, MBA, MHA, MS

Carilion Clinic
Roanoke, Virginia, USA
No disclosures

Andrew G. Miller, MS, RRT-ACCS, RRT-NPS

Respiratory Care Practitioner, ECMO Specialist
Duke University Medical Center
Durham, North Carolina, USA
No disclosures

Frank M. O’Connell, MD, FACP, FCCP

Staff Anesthesiologist
AtlantiCare Regional Medical Center
Pomona, New Jersey, USA
No disclosures

John M. Oropello, MD, FCCM

Program Director, Critical Care Medicine
Director, Transplant ICU
Mount Sinai School of Medicine
New York, New York, USA
No disclosures

Lauren A. Plante, MD, MPH, FACOG

Professor
New York Medical College
Valhalla, NY, USA
No disclosures

Kehllee Popovich, MSN, ACNP-BC

System Lead, APP Education
Clinical APP, Structural Heart
University Hospitals Cleveland Medical Center
Cleveland, Ohio, USA
No disclosures

Don C. Postema, PhD

HealthPartners
Minneapolis, Minnesota, USA
No disclosures

Ignacio Previgliano, MD
Professor of Neurology
Maimónides University
Director
Hospital Fernández
Buenos Aires, Argentina
No disclosures

Jose Javier Provencio, MD, FCCM

Louise Nerancy Professor in Neurology and Neuroscience
University of Virginia
Charlottesville, Virginia, USA
No disclosures

Nitin Puri, MD, FCCP

Co-Director Center for Critical Care
Cooper University Hospital
Camden, New Jersey, USA
No disclosures

April Miller Quidley, PharmD, BCCCP, BCPS, FCCM, FCCP

Supervisor, Critical Care and Emergency Medicine
Vidant Medical Center
Greenville, North Carolina, USA
No disclosures

Ahmed Reda Taha, MD, FRCP, FCCP, FCCM

Clinical Assistant Professor of Medicine
Cleveland Clinic Lerner College of Medicine
Case Western Reserve University
Critical Care Institute
Abu Dhabi, United Arab Emirates
No disclosures

Michael Ritchie, MD
Clinical Assistant Professor of Medicine
University of Louisville School of Medicine
Louisville, Kentucky, USA
No disclosures

Sophia Chu Rodgers, DNP, ACNP, FNP, FAANP, FCCM

Critical Care Nurse Practitioner
Lovelace Medical Group
Lovelace Health Systems
Albuquerque, New Mexico, USA
No disclosures
William Rodriguez-Cintron, MD, FCCM
Chief, Pulmonary/Critical Care Medicine
San Juan VA Medical Center
San Juan, Puerto Rico
No disclosures

Gloria M. Rodríguez-Vega, MD, MCCM

Chief, Department of Critical Care
HIMA San Pablo Caguas
Caguas, Puerto Rico
Speaker bureau: Chiesi, clevedipine

Gregory P. Schaefer, DO, FACS

Medical Director, Surgical Critical Care
West Virginia University School of Medicine
Morgantown, West Virginia, USA
No disclosures

Alberto Sirven, MD, FACOG

West Kendall OBGYN
Miami, Florida, USA
No disclosures

David J. Skarupa, MD, FACS

Associate Professor of Surgery
University of Florida College of Medicine – Jacksonville
Jacksonville, Florida, USA
Principal Investigator at UF Health Jacksonville for a multi-center funded
phase 2 study on vascular conduits.

Whitney Sprinkel, BSN, CCRN

Registered Nurse
Carilion Roanoke Memorial Hospital
Roanoke, Virginia, USA
No disclosures

Christine C. Toevs, MD, MA, FCCM

Trauma/Critical Care Surgeon
Terre Haute Regional Hospital
Terre Haute, Indiana, USA
No disclosures

Shari A. Toomey, MBA, RRT, NPS

Clinical Team Leader
Carilion Clinic Children’s Hospital
Roanoke, Virginia, USA
No disclosures

Arlene Torres, DNP, ARNP, CCRN, ACNP-BC

Allied Health Care Professionals Manager
Intensive Care Solutions
Baptist Hospital of Miami
Miami, Florida, USA
No disclosures

Jonathan Trager, DO, FAAEM, FCCP

Saint Luke’s University Hospital
Clinical Assistant Professor (Adjunct)
Lewis Katz School of Medicine
Temple University
Philadelphia, Pennsylvania, USA
No disclosures

Robert J. Walter, MD, DHCE, FACP, FCCP

Chief, Pulmonary/Critical Care Medicine
Brooke Army Medical Center
Fort Sam Houston, Texas, USA
No disclosures

Daniel Wu, DO, FACOS, FACS, FCCM

Acute Care Surgeon
Trinity Health–St. Mary Medical Center
Langhorne, Pennsylvania, USA
No disclosures
Sergio Zanotti-Cavazzoni, MD, FCCM
Chief Medical Officer
Memorial Hermann Memorial City
Medical Center
Bellaire, Texas, USA
No disclosures
Contents

Chapter Title

Copyright
Preface
1. Recognition and Assessment of the Seriously Ill Patient

Approach to the Surgical Patient, Part 1: Overview of the Care

2.
for the Critically Ill Patient
3. Approach to the Surgical Patient, Part 2: Surgical Emergencies

4. Diagnosis and Management of Acute Respiratory Failure

5. Surgical Airway Emergencies

6. Mechanical Ventilation

7. Monitoring Oxygen Balance and Acid-Base Status

8. Diagnosis and Management of Shock

9. Neurologic Support

10. Neurosurgical ICU

Life-Threatening Infections: Diagnosis and Antimicrobial Therapy

11.
Selection
12. Basic Trauma and Burn Support

13. Abdominal Surgical Emergencies: Part 1

14. Abdominal Surgical Emergencies: Part 2

15. Acute Coronary Syndromes

16. Cardiovascular Surgical Emergencies

Management of Life-Threatening Electrolyte and Metabolic
17.
Disturbances
18. Management of Special Populations
19. Surgical Soft Tissue Complications and Urgencies

Appendix Title

1 Rapid Response System

2 Arterial Blood Gas Analysis and Treatment

3 Brain Death

4 Organ Donation
 PREFACE

Through the years, the Fundamental Critical Care Support (FCCS) family of
educational programs has been an essential resource for frontline critical care
learners and educators, teaching basic concepts to assess and manage the
patient until an intensivist arrives, or the patient can be safely transferred to a
higher level of care. Now, the FCCS family of products has been expanded to
include Fundamental Critical Care Support: Surgical.

Until now, no standardized course has covered the most common urgent
surgical conditions that can lead to critical illness. FCCS: Surgical augments
and expands on FCCS essentials. Its primary purpose is to provide an in-
depth and broad understanding of the initial care of the seriously ill surgical
patient by providing a deeper understanding of the pathophysiology of this
population. The increasing complexity of surgical procedures on sicker
patients leads to a knowledge gap between surgical and nonsurgical providers
in the initial care, stabilization, and disposition of seriously ill surgical
patients, making this course necessary. This tool can help frontline providers
better assess and address the needs of critically ill surgical patients,
facilitating better utilization of surgical specialties or stabilizing patients when
immediate surgical or critical care expertise is not available.

The course follows the standardized format of FCCS products. The chapters
in this first edition have been carefully written, reviewed, and organized to
reflect the most current guidelines and practices and are based on current
evidence where applicable. Chapters begin with learning objectives and case
studies that provide real-life examples and focus on key clinical findings and
patient presentation. Using the case study as a jumping-off point maximizes
learning and the flow of information.

To develop this course, the participation of a distinguished volunteer group of

national and international multidisciplinary critical care experts was
invaluable. Our thanks to the authors, support staff, and leadership of the
Society for bringing this course to completion. And a heartfelt thanks to our
audience members who commit to improving patient care.

We hope FCCS: Surgical will help establish a tradition of offering educational

content to those faced with critically ill surgical patients, thus promoting the
mission of SCCM: Right Care, Right Now.

António Gandra d’Almeida MD, MDM, FACS, FCCM, OF-3

Editor
Keith Killu, MD, FACP, FCCM
Editor

Mary Jane Reed, MD, FACS, FCCM

Editor
 Chapter 1
RECOGNITION AND ASSESSMENT
OF THE SERIOUSLY ILL PATIENT

Objectives
Recognize the early signs and symptoms of critical illness.
Describe a framework for the initial assessment of the seriously ill
patient.
Explain the DIRECT methodology as a framework to approach the
initial management of critically ill patients.

Case Study
A 58-year-old man with a history of hypertension presents to the emergency
department with a 3-day history of fever, cough, and increasing shortness of
breath. On arrival to the hospital, the patient has a temperature of 38.5°C
(101.3°F), heart rate of 118 beats/min, respiratory rate of 26 breaths/min, a
blood pressure of 100/72 mm Hg, and a pulse oximetry reading of 90% on
room air.
– What findings are potential clues to a seriously ill patient?
– Which aspects of the physical examination would you concentrate on
initially?
 – Which laboratory and radiographic investigations would you order for
this patient?

I. INTRODUCTION
Clinicians often think that patients with a critical illness present with sudden
acute clinical deterioration. However, in retrospect these patients usually have
shown early signs and symptoms that could have clued clinicians to the
potential of serious illness. Early identification of patients at risk for life-
threatening illness makes it easier to manage them and is associated with
improved patient outcomes. Time-sensitive interventions and early
stabilization usually require less aggressive treatments and prevent further
deterioration. Many clinical problems, if recognized early, can be managed
with simple measures such as supplemental oxygen, respiratory therapy
interventions, intravenous fluids, dextrose administration, or effective
analgesia. The early identification of patients in trouble allows clinicians to
identify the main physiologic problem, determine its underlying cause, and
begin specific treatments. The longer the interval between the onset of an
acute illness and the appropriate intervention, the more likely it is that the
patient’s condition will deteriorate, even to cardiopulmonary arrest. Several
studies have demonstrated that physiologic deterioration precedes many
cardiopulmonary arrests by hours, suggesting that early intervention could
prevent the need for resuscitation, admission to the ICU, and other sentinel
events. Many hospitals are using rapid response systems to identify patients at
risk and begin early treatment. (See Appendix 1 for further information on
the organization and implementation of a rapid response system.) The
purpose of this chapter is to describe the general principles involved in
recognizing and assessing seriously or critically ill patients.

II. RECOGNIZING THE PATIENT AT RISK

Recognizing that a patient is seriously or critically ill is usually not difficult
when there are clear signs and symptoms present. However, in early stages,
some signs may be subtle and clinicians may not fully appreciate the severity
of the clinical picture. Young and otherwise healthy patients are usually much
slower to exhibit the typical signs and symptoms of acute illness than elderly
patients or those with comorbidities and/or impaired cardiopulmonary
function. Thus, recognition of serious illness in young and healthy patients
may be more challenging. Individuals who are immunosuppressed or
debilitated may not demonstrate a vigorous and clinically obvious
inflammatory response. Some conditions, such as cardiac arrhythmias, do not
evolve with progressively worsening and easily detectable changes in
physiology but rather present as an abrupt change of state. In most
circumstances, a balance exists between the patient’s physiologic reserve and
the acute disease. Patients with limited reserve are more likely to be
susceptible to severe illness and to experience greater degrees of organ-
system impairment. The goal for the clinician is to recognize the potential for
serious illness as early as possible. Early recognition can facilitate time-
sensitive interventions and offer patients the best chance of a good outcome.
Identifying patients at risk for deterioration requires assessment of the current
physiologic changes caused by their acute disease process as well as their
potential physiologic reserve based on their chronic health issues and
comorbid factors.

Patients seldom deteriorate abruptly, even

though clinicians may recognize the deterioration
suddenly.

A. Assessing Severity

Tachycardia in response to physiologic

abnormalities (ie, fever, low cardiac output) may
be increased with pain and anxiety or suppressed
 in patients who have conduction abnormalities or
are receiving ß-blocker medications.

“How sick is this patient?” is one of the most important questions clinicians
must answer because it will dictate the urgency needed to stabilize, treat, and
ultimately triage a patient to the appropriate level of care. Evaluation of
severity of illness in any given clinical situation starts with proper
measurement of vital signs and other specific physiologic variables
(Appendix 1). Obtaining a heart rate, respiratory rate, a well-measured blood
pressure, temperature, and pulse oximetry can be completed efficiently and
will set the basis for an accurate patient assessment. Acute illness typically
causes predictable physiologic changes associated with both disease-specific
and general clinical signs. For example, a patient’s physiologic response to a
bacterial infection may result in fever, delirium, shaking chills, and
tachypnea. The most important step is to recognize these signs and initiate
physiologic monitoring to quantify the severity of disease and take appropriate
action. Sick patients may present with confusion, irritability, impaired
consciousness, or a sense of impending doom. They may appear short of
breath and demonstrate signs of a sympathetic response, such as pallor,
sweating, or cool extremities. Symptoms may be nonspecific, such as nausea
and weakness, or they may identify the involvement of a particular organ
system (for example, chest pain). Therefore, a high index of suspicion is
required when measuring vital signs: heart rate, blood pressure, respiratory
rate, oxygenation, temperature, and urine output. Clinical monitoring helps to
quantify the severity of the disease process, tracks trends and rates of
deterioration, and directs attention to those aspects of physiology that most
urgently need treatment. Studies have identified several clinical findings that
independently predict a higher risk of mortality. Some of these findings
include low blood pressure, oliguria, prolonged capillary refill time, and skin
mottling. A recent prospective cohort study found that the presence of a
higher respiratory rate, higher systolic blood pressure, lower central
temperature, altered consciousness, and decreased urine output were
independently associated with mortality when documented on day 1 of an
ICU stay. When these findings were all present, they offered similar or
improved prognostic abilities compared with validated severity of disease
scores. The goals at this stage of assessment are to recognize that a problem
exists and to maintain physiologic stability while pursuing the cause and
refining treatment with the implementation of disease-specific interventions.

Even normal vital signs may be early indicators

of impending deterioration if they differ from
prior measurements.

B. Immediate Therapeutic Interventions

Making an accurate diagnosis in the acutely ill patient often must take second
place to treating life-threatening physiologic abnormalities. In the early phases
of evaluation, the clinician must identify any physiologic derangement that
requires immediate attention with supportive therapeutic measures. Correcting
the problem may be as simple as providing oxygen or intravenous fluids.

There may not be sufficient time for a lengthy pursuit of a differential

diagnosis initially if the patient is seriously ill and needs to be stabilized.
However, an accurate diagnosis is essential for refining treatment options
once physiologic stability is achieved. The general principles of taking an
accurate history, performing a brief, directed clinical examination followed by
a secondary survey, and organizing laboratory and radiographic investigations
are fundamentally important. Good clinical skills and a disciplined approach
are required to accomplish these tasks.

III. INITIAL ASSESSMENT OF THE CRITICALLY ILL

PATIENT
A framework for assessing the acutely ill patient is provided in Table 1-1 and
discussed below. Further information on specific issues and treatments can be
found in later chapters of this text.

A. History

A primary and secondary survey approach is

recommended in the assessment of a seriously ill
patient.

The patient’s history usually provides the most valuable information for
diagnosis. Many seriously ill patients may have altered levels of consciousness
or confusion and are incapable of providing a reliable history. Often the
current history, past medical history, and medication list must be obtained
from family members, caregivers, friends, neighbors, medical records, or
other healthcare providers. The risk of critical illness is increased in patients
with the following characteristics:

Emergency admission (limited information)

Advanced age (limited reserve)
Severe coexisting chronic illness (limited reserve, limited options
for management)
Severe physiologic abnormalities (limited reserve, refractory to
therapy)
Need for, or recent history of, major surgery, especially an
emergency procedure
Severe hemorrhage or need for a massive blood transfusion
Deterioration or lack of improvement
 Immunodeficiency
Combination of these factors

Table 1-1 Framework for Assessing the Acutely Ill or Injured Patient

A complete history includes the present complaint, treatment history, hospital

course to the present (if applicable), past illnesses, past surgical procedures,
current medications, and any medication allergies. A social history, including
alcohol, tobacco, or illicit drug use, and a family history, including the degree
of physical, emotional, and psychosocial independence, are essential and
often overlooked. The history of the present complaint must include a brief
review of systems that should be replicated in the examination that follows.

Critical illness is often associated with inadequate cardiac output, respiratory

compromise, and a depressed level of consciousness. Specific symptoms will
typically be associated with the underlying condition. Patients may report
nonspecific symptoms such as malaise, fever, lethargy, anorexia, or thirst.
Organ-specific symptoms may direct attention to the respiratory,
cardiovascular, or gastrointestinal systems. Distinguishing acute from chronic
disease is important at this point because chronic conditions may be difficult
to reverse and may act as rate-limiting factors during the recovery phase of
critical illness.

B. Examination

Ongoing deterioration or development of new

symptoms warrants repetition of the primary
survey followed by a detailed secondary survey.

Look, listen, and feel. The patient must be fully exposed for a complete
examination. The initial examination must be brief, directed, and
concentrated on the basic elements of airway, breathing, circulation, and level
of consciousness. As the treatment proceeds, a more detailed secondary
survey should be conducted to refine the preliminary diagnosis and assess the
response to the initial treatment. A full examination must be performed at
some point and will be guided by the history and other findings.

Tachypnea is the single most important indicator

of critical illness.
 Paradoxical breathing is a sign of severe
respiratory compromise.

Remember the ABCs of resuscitation: airway, breathing, and circulation. The

airway and respiratory system should be assessed first, as summarized in
Table 1-2. Observe the patient’s mouth, chest, and abdomen. There may be
obvious signs suggesting airway obstruction, such as vomitus, blood, or a
foreign body. The patient’s respiratory rate, pattern of breathing, and use of
accessory respiratory muscles will help to confirm and assess the severity of
respiratory distress or airway obstruction. The respiratory rate should be
assessed visually by counting the number of breaths because respiratory rates
displayed on cardiac monitors are subject to different degrees of artifact and
thus can be inaccurate. Tachypnea is the single most important indicator of
critical illness. Therefore, the respiratory rate must be accurately measured
and documented. Although tachypnea may result from pain or anxiety, it may
also indicate pulmonary disease, severe metabolic abnormalities, or infection.
Look for cyanosis, paradoxical breathing, equality and depth of respiration,
use of accessory muscles, and tracheal tug. An increase in the depth of
respiration (Kussmaul breathing) may indicate severe metabolic acidosis.
Periodic breathing with apnea or hypopnea (Cheyne-Stokes respiration)
usually indicates severe brainstem injury or cardiac dysfunction. Ataxic
breathing (Biot respiration) indicates severe neuronal damage, which is
associated with a poor prognosis. Agitation and confusion may result from
hypoxemia, whereas hypercapnia will usually depress the level of
consciousness. Low oxygen saturation can be detected with pulse oximetry,
but this assessment may be unreliable if the patient is hypovolemic,
hypotensive, or hypothermic. End-tidal CO2 monitoring is available on
specific nasal cannulas as well as via ventilator tubing and is an appropriate
adjunct monitoring device for patients at high risk for hypercapnic respiratory
failure. Noisy breathing (eg, grunting, stridor, wheezing, gurgling) may
indicate partial airway obstruction, whereas complete airway obstruction will
result in silence.

Table 1-2 Assessment of Airway and Breathing

A decrease in the blood pressure may be a late

sign of cardiovascular disturbance signaling
failure of the compensatory mechanisms.

Inadequate circulation may result from primary abnormalities of the

cardiovascular system or secondary abnormalities caused by metabolic
disturbances, sepsis, hypoxia, or drugs (Table 1-3). Clinicians are primed to
recognize low blood pressure as a worrisome sign. However, a normal blood
pressure does not rule out severe underlying circulatory problems. Studies
have shown that even transient drops in blood pressure are associated with
worse outcomes. Central and peripheral pulses should be assessed for rate,
regularity, volume, and symmetry. Capillary or nail-bed refill examination
may aid in detecting hypovolemia if delayed. A combination of clinical
findings (skin color, diminished distal pulses, decreased urine output, cool
temperature of extremities, prolonged capillary refill) have been found to be
useful in predicting low cardiac output states.

Evaluation of the patient’s pulse can provide some clues to ongoing

circulatory issues. Patients with hypovolemia or low cardiac output will have a
weak and thready peripheral pulse. A bounding pulse suggests hyperdynamic
circulation, and an irregular rhythm usually signifies atrial fibrillation or some
other arrhythmia. A ventricular premature beat is often immediately followed
by a compensatory pause, and the subsequent beat often has a larger pulse
volume. Pulsus paradoxus is defined as a greater than 10 mm Hg decrease in
the systolic blood pressure with deep inspiration; it can occur with profound
hypovolemia, constrictive pericarditis, cardiac tamponade, asthma, and
chronic obstructive pulmonary disease. Change in location and character of
the left ventricular impulse (usually located in the fifth intercostal space in the
left parasternal area) may suggest left ventricular hypertrophy, congestive
heart failure, cardiac enlargement, severe mitral regurgitation, or severe
aortic regurgitation. The turbulent flow of blood through a stenotic heart valve
or a septal defect may produce a palpable thrill at the site of the left
ventricular impulse.

Table 1-3 Assessment of Circulation

In addition to the ABCs, a quick external examination should look for pallor,
cyanosis, diaphoresis, jaundice, erythema, or flushing. The skin may be moist
or dry; appear thin, edematous, or bruised; or demonstrate a rash (ie,
petechiae, hives). Fingernails may be clubbed or show splinter hemorrhages.
The eyes might reveal abnormal pupils or jaundice. The conjunctiva may be
pale, indicating an anemia. The patient may be alert, agitated, somnolent,
asleep, or obtunded. These physical findings can help to guide decisions
regarding differential diagnoses and the need for further testing.

Palpation of the abdomen is an essential part of the examination of the

critically ill patient. Areas of abdominal tenderness and palpable masses must
be identified. The size of the liver and spleen must be noted as well as any
associated tenderness. It is important to assess the abdomen for rigidity,
distension, fluid wave, guarding, or rebound tenderness indicating possible
viscous perforation, infection, or peritonitis. Auscultation may reveal a
vascular bruit concerning for an aneurysm or the absence of bowel sounds
indicating a change in normal bowel patterns. A high suspicion for
intrauterine or ectopic pregnancy must be considered in all women of
childbearing age who present with lower quadrant pain. The flanks and back
should be examined, if possible.

A neurologic evaluation in a potentially critically ill patient is focused on

establishing changes in mentation/level of consciousness and quickly
identifying focal deficits that could represent an underlying neurologic
emergency. In young patients, slight changes in level of consciousness and
mental status may represent serious underlying disease. In older patients with
cognitive impairment at baseline, changes in mental status are commonly
associated with serious illness and may be the first and only presenting sign.
The Glasgow Coma Scale score should be recorded during the initial
assessment of central nervous system function and limb movement. Pupillary
size and reaction should be documented, and a more detailed assessment of
central and peripheral sensory and motor functions should be undertaken
when time permits.

C. Chart Review and Documentation

Difficulty in obtaining a pulsatile waveform by

pulse oximetry may be indicative of a
vasoconstricted state.

Critically ill patients have abnormal physiology that must be documented and
tracked. Physiologic monitoring provides parameters that are useful only
when they are accurate and interpreted by trained personnel. The values and
trends of these data provide key information for the assessment of the
patient’s status and guidance for treatment. Data must be charted frequently
and correctly to ensure good patient care. Particular attention must be paid to
the accuracy and reliability of the data. For example, a true and reproducible
arterial line pressure measurement depends on patient position, equipment
calibration, and proper zeroing of the instruments. The source of the data also
should be noted. Is the recorded temperature from an esophageal or Foley
temperature probe? Was the blood pressure measured with a manual cuff or
with a pressure transducer in an arterial line? Was the appropriate size of
blood pressure cuff used? The medication record is an invaluable source of
information about prescribed and administered drugs.
 An accurate measure of urine output, usually
with an indwelling catheter, is essential in
critically ill patients.

Routine monitoring and charting should include heart rate, heart rhythm,
respiratory rate, blood pressure, core temperature, fluid balance, and
Glasgow Coma Scale score. The fluid balance should include loss from all
tubes and drains as well as any fluids used to flush drains. The inspired
oxygen concentration should be recorded for any patient receiving oxygen,
and the oxygen saturation level should be charted if measured with pulse
oximetry. Patients in the ICU setting may have central venous catheters or
continuous cardiac output catheters in place. These catheters can measure
central venous pressure, various cardiac pressures, stroke volume variations,
cardiac output, and mixed venous saturation. These complex monitoring
devices require specific operational expertise. Likewise, the data must be
interpreted by someone with clinical experience and expertise in critical care.
Finally, proper documentation of current continuous medication infusions
along with the drip rate is especially important to provide an accurate picture
of clinical condition.

D. Investigations

The presence of a metabolic acidosis is one of the

most important indicators of critical illness.

Additional investigative tests should be based on information obtained from

the patient’s history and physical examination as well as on previous test
results. Standard biochemistry, hematology, microbiology, and radiology tests
should be performed as indicated. In the evaluation of electrolyte results,
decreasing total serum carbon dioxide and/or an increased anion gap are
evidence of metabolic acidosis. An arterial blood gas analysis is one of the
most useful tests in an acutely ill patient, providing information about blood
pH, arterial oxygen tension, and arterial carbon dioxide tension. Additional
tests, such as lactate, blood glucose, serum electrolytes, and renal function,
can often be obtained from the same blood sample. Increased levels of lactic
acidosis have been associated with increased mortality in various critical
conditions. Elevated lactic acid can be an ominous sign and should be closely
monitored.

IV. TRANSLATING INFORMATION INTO EFFECTIVE

ACTION
This chapter discussed a simple framework based on a primary and
secondary survey as a basis for systematically approaching critically ill
patients (Table 1-1). The primary goals of this framework are to first ensure
physiologic stability and then proceed to treatment of the underlying cause.
The basic principles are summarized as the ABCs of resuscitating the severely
ill patient: airway— ensuring a patent airway; breathing—providing
supplemental oxygen and adequate ventilation; and circulation—restoring
circulating volume. These early interventions should proceed regardless of the
situation, whereas the context of the clinical presentation (ie, trauma,
postsurgical situation, presence of chronic illness, advanced age) directs
attention to the differential diagnosis and potential treatments. The clinical
history, physical examination, and laboratory tests should aid in clarifying the
diagnosis and determining the patient’s degree of physiologic reserve.
Because the typical features of critical illness may be more effectively
disguised in young and previously healthy patients than in elderly or
chronically ill patients, an acute deterioration may seem to occur more
abruptly in younger patients. Thus, it is particularly important to assess trends
in vital signs and physiologic parameters as the patient undergoes treatment.
These trends can help determine a patient’s response and clarify the
diagnosis.
More experienced help must be obtained if a patient’s condition is
deteriorating and there is uncertainty about the diagnosis or treatment.
Transfer to the most appropriate site for care is influenced by local resources,
but transfer to a high-dependency unit or ICU must be considered. Transfer
to a tertiary care facility within the region may be necessary if resources at the
current facility are not capable of caring for the patient.

Key Points
Recognition and Assessment of the Seriously Ill Patient
Early identification of a patient at risk for critical illness is essential
to improving patient outcomes.
The clinical manifestations of impending critical illness are often
nonspecific. Tachypnea and metabolic acidosis are two of the most
important predictors of risk; they signal the need for more detailed
monitoring and investigation.
Resuscitation and physiologic stabilization often precede a
definitive diagnosis and treatment of the underlying cause.
A detailed history is essential for making an accurate diagnosis,
determining a patient’s physiologic reserve, and establishing a
patient’s treatment preferences.
Frequent clinical and laboratory monitoring of a patient’s response
to treatment is essential.

Suggested Readings
1. Cretikkos MA, Bellomo R, Hillman K, et al. Respiratory rate: the
neglected vital sign. Med J Aust. 2008;188:657-659.
2. Elder A, Japp A, Verghese A. How valuable is physical
examination of the cardiovascular system? BMJ.
2016;354:i3309.
3. Hiemstra B, Eck RJ, Keus F, et al. Clinical examination for
diagnosing circulatory shock. Curr Opin Crit Care.
2017;23(4):293-301.
4. Hiemstra B, Eck RJ, Wiersema R, et al. Clinical examination for
the prediction of mortality in the critically ill: The Simple
Intensive Care Studies-I. Crit Care Med. 2019;47(10):1301-
1309.
5. National Institute for Health and Care Excellence (NICE)
Guidelines. Acutely ill adults in hospital: recognising and
responding to deterioration. Published July 2007.
https://www.nice.org.uk/guidance/cg50. Accessed February 20,
2020.
 Chapter 2
APPROACH TO THE SURGICAL
PATIENT, PART 1: OVERVIEW OF
THE CARE FOR THE CRITICALLY
ILL PATIENT

Objectives
Describe the physiologic disorders that occur with surgery.
Identify common complications that occur in critically ill surgical patients
and their treatment.
List the effects of anesthesia in the perioperative period.
List and distinguish the different types of adverse drug interactions caused
by anesthetics in the postoperative period.
Describe the components in a successful handoff of a critically ill surgical
patient to the ICU team.

Case Study
A 67-year-old man with a history of chronic obstructive pulmonary disease (COPD)
and coronary artery disease presents with abdominal pain and distension
accompanied by fevers, tachycardia, and hypotension, which is responsive to a fluid
challenge. A workup reveals evidence of perforated sigmoid diverticulitis with free
air and fluid throughout the pelvis. On examination, he has generalized peritonitis,
and he is taken to the operating room and undergoes a sigmoid colectomy with
creation of an end colostomy. At the time of the surgery, he has a large amount of
feculent fluid throughout his pelvis with a significant inflammatory response.
Intraoperatively he had significant bleeding requiring a blood transfusion and
developed progressive hypotension requiring the initiation of a norepinephrine drip
to maintain adequate blood pressure. His abdomen is irrigated, a colostomy
created, and his fascia is closed primarily. He remains intubated and is admitted to
the ICU postoperatively for further resuscitation and management. Several hours
later, his abdomen is becoming progressively distended, his hemodynamics are
worsening, and he is developing hypoxia with high peak airway pressures.
– What are the immediate interventions needed?
– What is the probable differential diagnosis?
– Is there any role for repeat surgical consultation or intervention?

I. INTRODUCTION

Effective management of the postoperative patient

involves attention both to basic critical care
principles as well as specific issues related to
anesthesia and the surgical procedure performed.

Critical care management involves well-defined principles that cross multiple

medical specialties. However, there are numerous challenges in patient care that
can affect the presentation and outcomes of patients who have undergone surgical
procedures. Outside the specialties of surgery and anesthesia, there may not be a
complete understanding of these situations and the immediate management
considerations. Although the medical management of these patients is often very
similar to the nonsurgical patient, lack of knowledge of some of the changes related
to anesthesia and surgical care could significantly worsen the outcomes in this
patient population. The goal of this text is to introduce the nonsurgical provider to
the specific anesthesia and surgical changes that can influence the critical care
management of this population. This chapter will concentrate on the changes in the
physiology of the surgical patient, specific considerations regarding anesthesia care,
considerations for care of the unstable patient in the postoperative period, as well as
adequate transfer and handoff of information from the operating room to the critical
care unit.

II. PHYSIOLOGIC CONSIDERATIONS IN THE SURGICAL

PATIENT
The way the body responds to major systemic injuries depends on multiple factors.
The physiologic reserve of a patient’s organ systems, the nature of the injury, the
time when the insult happens, the virulence of the damage, and the timeliness in
recognition and resuscitation affect the body’s response.
In the surgical patient, the primary cellular injury during the perioperative period is
caused by direct surgical trauma, heating, vaporization, traction, or indirect damage
from changes in global or local perfusion, which impairs oxygen and nutrient
delivery. Some surgical patients can present as catastrophes in which the
physiologic insult makes massive demands on the body’s ability to respond, sustain
life, and restore homeostasis. A secondary injury may be caused by the effect of
locally released inflammatory mediators or hormones as a result of the stress related
to the surgical procedure. The initial assessment also needs to consider many
special populations, including pediatric, obstetric, geriatric, and obese patients.

A. Stress Response
In general, the stress response to surgery is proportional to the type of injury and
the duration of the insult. The injury results in localized tissue trauma, which leads
to release of cytokines and inflammatory mediators. These events drive a complex
bundle of metabolic, hormonal, and immunologic responses in the body.

Surgical procedures activate a stress response similar

to other types of severe disease or injury.

The goal is always to recognize problems early before the patient’s physiology
becomes significantly deranged. When successful, this usually allows for minimal
intervention and will positively impact patient recovery. Performing regular
assessments and promptly correcting abnormal physiology averts deterioration and
prevents compensatory mechanisms from becoming overwhelmed.
Indirect cellular injury during surgery is caused by changes in the blood supply or
oxygen and nutrient delivery. Early diagnosis requires continuous monitoring and
repeated evaluation of organ function to detect early signs of organ dysfunction.

B. Volume Status
A fall in intravascular volume is often a crucial factor in the initiation of the systemic
response. Perioperative hypovolemia has multiple potential causes, including:

Blood loss as a result of trauma or surgery

Plasma loss as a result of loss of integumentary system barrier function
because of burns
Abnormally high insensible losses from fevers, excess sweating, surgical
exposure of abdominal contents, or hyperventilation
Interstitial sequestration caused by epithelial dysfunction from injury or
toxins
Inflammatory exudate into the peritoneal cavity from multiple causes,
including acute pancreatitis or generalized peritonitis secondary to intra-
abdominal infection
Sepsis syndrome with both relative and absolute hypovolemia as a result
of peripheral vasodilatation and third-space losses from increased
capillary permeability

Falling intravascular volume has several wide-ranging effects on normal physiology.

Hypovolemia stimulates sympathetic activity by removing baroreceptor inhibition in
an attempt to maintain blood pressure by increasing cardiac output and peripheral
resistance. This explains the mild tachycardia commonly seen in postoperative
patients. This compensatory mechanism is most effective in young fit individuals,
and when it fails, decompensation is often sudden and rapid. This catecholamine
response also has profound metabolic effects, increasing the turnover of
carbohydrates, proteins, and lipids, resulting in a state of catabolism. Failing renal
perfusion activates the renin-angiotensin-aldosterone system, increasing renal
reabsorption of sodium and water. A centrally mediated increase in antidiuretic
hormone (ADH) secretion promotes further conservation of intravascular volume.

C. Cardiac Output
Many factors can influence cardiac output and peripheral perfusion in the
perioperative period. Circulatory efficiency may be impaired by hypovolemia, and
myocardial contractility may be depressed by anesthetic agents and other drugs.
Anesthetic drugs can cause peripheral dilatation, and positive-pressure ventilation
diminishes venous return. Trendelenburg positioning and induced
pneumoperitoneum for laparoscopic surgery can further stress cardiovascular
physiology. Significant events such as sepsis, pulmonary embolism, or myocardial
infarction may precipitate cardiovascular collapse. Uncontrolled pain in the peri- or
postoperative period can lead to increased catecholamine and adrenocorticotrophic
hormone secretion with similar effects.

D. Hypothermia
Hypothermia imposes enormous metabolic demands on the patient. Pediatric and
geriatric patients are especially at risk. The causes are multifactorial, including
excess heat loss during a prolonged surgical procedure or through skin with burn
damage, as well as direct cooling caused by massive resuscitation. As the body core
temperature falls, physiologic functions like perfusion and blood clotting are
impaired. These changes place the patient at risk. In the adult patient, significant
hypothermia can lead to multiple complications, including:

Inhibition of tissue oxygen delivery

Predisposition to dysrhythmias
Coagulopathies (with difficulty in maintaining homeostasis and increased
risk of bleeding-related complications)
Electrolyte abnormalities
Oliguria
Shivering which increases oxygen requirements and potentially
predisposes patients to cardiac ischemia and delay in wound healing
E. Coagulopathy
Response to injury is associated with blood coagulation changes. The general
metabolic responses to injury activate thrombotic mechanisms and initially depress
intrinsic intravascular thrombolysis. Thus, the postoperative patient is in a
prothrombotic state and may sustain intravenous thrombosis and consequent
thromboembolism. If substantial hemorrhage occurs, clotting factors eventually
become exhausted, causing failure of clotting. Both processes can activate this
inflammatory response and may initiate widespread intravascular thrombosis,
depleting clotting factors and precipitating disseminated intravascular coagulation
with failure of normal clotting.

F. Malnutrition

Changes in intravascular volume status, cardiac

output, coagulopathy, as well as malnutrition are
common findings in the postoperative patient.

Response to injury and surgical procedures are also associated with starvation and
stress-induced catabolism. Patients with major surgical conditions are often
malnourished before the surgery. Also, most patients are allowed nothing by mouth
for 6–12 hours preoperatively, and many do not start eating for an extended period
postoperatively.

G. Metabolic Responses to Pathophysiologic Stress

Glucose production is increased by catecholamine-induced gluconeogenesis. In
addition, secretion of adrenocorticotropic hormone (ACTH) is enhanced. Multiple
hormones contribute to the general catabolic response, including glucocorticoids
(cortisol), glucagon, and growth hormone. Insulin acts as an antagonist of most of
these substances and is secreted in increased amounts from the second and third
day after injury.

In severe trauma or extensive surgeries, in particular, if they are complicated by

sepsis, critical factors in the systemic response are increased because of
sympathetic activity together with increased circulating catecholamines and insulin.
Cytokine responses signal other cells to prepare for action to compensate for
starvation, provide additional energy and building blocks for tissue repair, and
conserve sodium and water.

In general, the activation of these multiple pathways is associated with a wide range
of physiologic effects, including:

Increased secretion of growth hormone and thyroid hormones, both of

which inhibit the effects of insulin and promote catabolism
Enhanced hepatic glycogenolysis and gluconeogenesis
Lipolysis in response to catecholamines and glucagon, which releases
fatty acids from adipose tissue; these provide the primary energy source
for peripheral tissues
Increased pituitary ACTH release induces a massive rise in circulating
glucocorticoids; cortisol levels can increase tenfold immediately after
surgery, remaining elevated for days or weeks
Glucocorticoids also enhance gluconeogenesis and promote catabolism of
muscle protein and liberation of amino acids
Reduced insulin secretion and inhibition of its tissue effects which block
cellular use of glucose
Stimulation of glucagon secretion further enhances glycogenolysis and
gluconeogenesis
In normal healthy adults, nitrogen balance is consistently maintained. Protein
turnover results in daily excretion of 12–20 g of urinary nitrogen, which is replaced
by dietary intake. In the hypermetabolic state, such as in the postoperative or
trauma patient, nitrogen losses can increase substantially. Most importantly, the
increased metabolic environment prevents proper use of enteric or parenteral
nutrition. This process results in significant destruction of skeletal muscle. This state
of negative nitrogen balance contrasts markedly with simple starvation in which
body protein is preserved.
The effects of significant body insults on lipid metabolism are similar to simple
starvation in that most of the energy requirements are met from fat stores. Surgical
catabolism reverses only as the patient recovers from the illness, and therefore,
early parenteral nutrition has little effect, although administration of carbohydrates
may spare some protein loss. When the patient has been severely ill, carbohydrate
metabolism is minimal, and most energy comes from the catabolism of protein and
fat.

Multiple factors influence local perfusion to organs. Retraction of tissue, clamping

or coagulation of blood vessels, and mobilization of the bowel can alter regional
perfusion and compromise the delivery of oxygen and nutrients, leading to cellular
dysfunction. Local perfusion may also be affected during pneumoperitoneum
because of direct pressure effects and changes in oxygen delivery and impact on
vital organs. Even after surgery, there is evidence that microcirculatory blood flow
around surgical sites, such as anastomosis, can be impaired for a significant period
postoperatively even in the face of normal global oxygen delivery.
Fluid, electrolyte, and acid-base derangements can be identified by conducting a
careful assessment, particularly in those high-risk patients preoperatively. Those
with abnormalities need to be closely monitored in the preoperative, perioperative,
and postoperative periods. If abnormalities are detected, aggressive management
can then proceed promptly. Plasma urea and electrolytes should be checked daily.
Severely ill patients with abdominal infection, sepsis, fistulas, and extensive burns
are more likely to sustain significant problems of fluid balance and malnutrition.
Therefore, in these patients, maintenance of intravascular volume needs to consider
the multiple areas for volume loss, including:
Replacement perioperative fluids
Providing maintenance fluids
Replacement of any ongoing blood losses
Replacement of insensible losses
Replacement of third-space losses

The metabolic responses to anesthesia and surgical

stress can have profound implications for the patient
in the perioperative and postoperative periods.
In this context, third-space losses refer to the sequestration of fluids in a
nonfunctional extracellular space or fluid shifts into a body cavity (transcellular
space), such as ascites and pleural effusion. Quantifying perioperative third-space
fluid loss is difficult, and estimation tools are inexact. Reestablishing normal
perfusion is more critical than replacing a calculated fluid loss.

To reduce the stress and the metabolic effects of surgery, the following must be
considered:

Surgical Aspects
Reduce primary surgical injury and blood loss.

Reestablishing normal perfusion is more critical than

replacing an arbitrary estimation of third-space fluid
loss.

Anesthetic Aspects
Attention to individualized control of a patient’s physiology during
surgery optimizes outcomes. Care in the administration of analgesia
needs to be considered with the aim of reducing total opioid use to avoid
the risk of decreased respiratory drive and ileus. The management of
fluids needs to be individualized to maintain cellular perfusion, reduce
extracellular fluids flux, and prevent salt and water overload, which can
lead to cardiac dysfunction, pulmonary edema, and tissue fluid
accumulation.
Postoperative Goals
By encouraging early gut function and enteral feeding, the patient
achieves these benefits: hormonal effects of duodenal feeding,
maintenance of gut perfusion, reduced surgical insult, avoidance of
nasogastric tubes, and regular quantities of nutrition. Early mobilization
to minimize complications, such as chest infection and deep vein
thrombosis/pulmonary embolism, stimulates muscle function to maintain
strength and reduce insulin resistance.
III. PERIOPERATIVE CHANGES IN THE POSTOPERATIVE
SURGICAL PATIENT
A. Postoperative Surgical Patient

Patients in the immediate postoperative period are

subject to disorders in normal respiratory, cardiac,
homeostatic, and autonomic function.

The postoperative surgical patient emerging from anesthesia is subject to

derangements in respiratory and cardiac physiology, temperature regulation,
coagulation, and autonomic function. It is imperative on receiving the patient from
the operating room to rapidly assess the patient’s hemodynamic stability, ongoing
fluid losses (urine output, surgical drains, nasogastric tube, evidence for bleeding,
etc.), mental status, respiratory status, and neuromuscular function. Hypotension
may have several causes, including residual cardiovascular depression from
inhalational anesthetics (these agents cause vasodilation and myocardial depression
in a dose-dependent fashion), hypovolemia, hemorrhage, and autonomic
dysfunction after reversal of neuromuscular blockade. Spinal and epidural
anesthesia can also cause hypotension. The patient’s medical history, details of the
surgical procedure, and anesthesia record of the medications and fluids
administered can point the clinician toward the cause for hemodynamic
derangements. Physical examination of the patient is often helpful. Important
considerations regarding the postoperative surgical patient are listed in Table 2-1.

Table 2-1 Considerations When Examining a Postoperative Surgical Patient

B. Blood and Blood Product Transfusion
Several reasons exist for a restrictive transfusion practice. One reason is the low risk
of viral infectious disease transmission. Other significant complications of
transfusion include volume overload, acute hemolytic transfusion reaction (rare),
transfusion-related acute lung injury (TRALI), and very importantly, suppression of
the immune system.
The storage of red blood cells results in decreased levels of 2,3-diphosphoglycerate
(2,3-DPG), which results in a leftward shift in the oxygen-hemoglobin dissociation
curve. This results in the transfused red blood cells more avidly binding oxygen
with diminished oxygen transport to potentially ischemic tissues.
Patients may be coagulopathic following surgery, especially if the surgery was
prolonged, there was significant blood loss or volume shifts, the patient sustained
massive trauma, or the patient is septic or has systemic inflammatory response
syndrome (SIRS). It may be prudent to check a platelet count, prothrombin time
(PT), international normalized ratio (INR), partial thromboplastin time (PTT),
fibrinogen level, and titer of fibrin split products (FSP). Some institutions use
viscoelastic testing technology (such as thromboelastography or rotational
thromboelastometry), which gives a broad overview of the coagulation cascade and
allows specific deficiencies to be identified and corrected. The pH and temperature
of the patient should also be aggressively monitored because severe derangements
in these parameters may profoundly affect the coagulation cascade in the absence of
any abnormalities in laboratory measurements of hemostasis. In response to recent
evidence regarding transfusion practices in massive blood loss, the use of crystalloid
solutions has diminished.
In contrast, the use of a 1:1:1 ratio for the transfusion of packed red blood cells,
fresh frozen plasma, and platelets in patients requiring massive transfusion has been
associated with better outcomes. This has resulted in less third spacing of fluids, a
more rapid return of intestinal function, and better overall clinical outcomes.
Transfusion of large volumes of crystalloid solutions, especially normal saline, in
patients who sustained significant hemorrhagic shock results in a dilutional
coagulopathy, hyperchloremic metabolic acidosis, an increased risk of acute kidney
injury, and poorer outcomes.

C. Respiratory Status
A respiratory status of a patient in the perioperative period is also of concern. If the
patient is extubated, look for evidence of fatigue, a rapid shallow respiratory rate,
use of accessory respiratory muscles, and the patient’s level of consciousness. An
agitated patient gasping for air or a somnolent patient who is difficult to arouse may
both require reintubation. This a clinical decision that does not require an arterial
blood gas. Assess the patient’s skin color:

Is there evidence of cyanosis?

Is the patient intubated?
If so, what are the ventilator settings?

Specific complications related to the effects of

anesthesia, as well as the interaction with the
patient’s routine medication regimen and disease
processes, must be considered in the perioperative
period.

Difficulties with oxygenation or hypoxemic respiratory failure may arise as a result

of fluid overload, acute respiratory distress syndrome, or congestive heart failure.
Acute respiratory distress syndrome may have many etiologies in the perioperative
period, including aspiration of gastric contents (often on induction), soiling of the
peritoneum with enteric contents resulting in sepsis, transfusion-related lung injury,
or systemic inflammatory response syndrome resulting from severe traumatic injury.
Bedside thoracic echocardiography may help distinguish cardiogenic from
noncardiogenic causes of increased lung water. Hypercapnic respiratory failure may
result from splinting from pain following a thoracic or high abdominal incision, from
exacerbation of underlying chronic obstructive pulmonary disease or asthma, or
from the residual effects of opioids or inhalational anesthetics. It has been shown in
healthy volunteers that even subanesthetic concentrations of inhalational anesthetic
gas alter the ventilatory response to hypercarbia and hypoxemia.

D. Effects of Anesthesia and Drug Interactions

1. Drug Interactions
The potential for drug interactions and idiosyncratic reactions is a genuine
possibility, given the number of medications administered to a surgical patient in
the perioperative period and medications that the patient may be taking for
preexisting medical conditions before the surgical procedure. A surgical patient may
typically receive an antibiotic (perhaps two or three), an anxiolytic (benzodiazepine),
opioids, non-opioid analgesics, muscle relaxants, antiemetic agents, possibly
vasoactive agents (either vasopressors, anticholinergics, vasodilators, beta-blockers,
etc.) as well as a reversal for muscle relaxation if extubation is planned. An elevated
temperature in the postoperative period may have many causes, including malignant
hyperthermia, malignant neuroleptic syndrome, central anticholinergic syndrome,
and the serotonin syndrome. Drug interactions with anesthetic agents cause many of
the toxidromes mentioned previously.

2. Serotonin Syndrome

This is a clinical entity usually caused by the interaction of two or more

medications, which increase the levels of serotonin in the body. Many
antidepressants are serotonin reuptake inhibitors, and these may interact with other
drugs typically given in the perioperative period (which also increases serotonin
levels), including meperidine, ondansetron, metoclopramide, and tramadol. A range
of symptoms from mild to severe may occur, including agitation, elevated
temperature, diaphoresis, dilated pupils, and tremor. Complications of severe
temperature elevation can occur, including seizures and rhabdomyolysis. A patient
may be using recreational substances such as ecstasy (MDMA), cocaine, or
amphetamines, which will also cause serotonin levels to be elevated. Management of
these patients involves discontinuation of the responsible drugs, treating agitation
with benzodiazepines as appropriate, and using active cooling measures to bring the
patient’s body temperature to a normal range. Some clinicians have advocated for
the use of serotonin antagonists, such as cyproheptadine, which must be
administered enterally. Depending on the type of surgical procedure that the patient
underwent, this may or may not be feasible.

3. Malignant Hyperthermia

This is a very rare but feared complication of general anesthesia. It is known to

have a genetic component, with familial expression, but spontaneous cases have also
been reported. Exposure of a susceptible patient to triggering agents known to
cause this clinical entity can result in muscle rigidity, hypercarbia, tachycardia,
hypertension, severe temperature elevation, hyperkalemia, mottling of the skin, and
cyanosis. The most commonly known triggering agents are succinylcholine and
inhalational anesthetics (halothane, isoflurane, desflurane, etc.). Because of
abnormalities caused by these triggering agents, increased intracellular calcium
builds up in the muscle of these patients, causing prolonged contraction and
consumption of adenosine triphosphate. Treatment consists of stopping exposure to
the triggering agents (inhalational anesthetics), actively cooling the patient, and
administration of dantrolene. If a patient manifests an episode of malignant
hyperthermia, family members should be tested for this condition because
inheritance is often in an autosomal-dominant fashion.

4. Malignant Neuroleptic Syndrome

This is a manifestation of antipsychotic drug toxicity, which may mimic malignant
hyperthermia. Malignant neuroleptic syndrome presents with altered mental status,
muscular rigidity, hyperthermia, and autonomic dysfunction. Generally, younger
males who have recently begun treatment with tranquilizers, such as the
butyrophenones (haloperidol) or the phenothiazines (chlorpromazine, fluphenazine),
are the population at risk for this condition, especially with high doses of these
drugs or dehydration. Treatment in the postoperative period with the antiemetic
metoclopramide may exacerbate this condition. Most antipsychotic drugs require
dopamine antagonism for their clinical effect, and this is the mechanism thought to
produce this syndrome. Treatment is supportive with the termination of the
precipitating drug, active cooling with ice water immersion for severe hyperthermia
(temperature > 41°C [106°F]), rehydration, administration of benzodiazepines
and/or muscle relaxants to control muscle rigidity, and administration of
bromocriptine in doses of 2.5 to 10 mg three times a day.

5. Central Anticholinergic Syndrome

This is another clinical entity that can be seen in the postoperative period as a result
of drug interactions. Tricyclic antidepressants, antihistamines, antiparkinsonian
drugs, and pharmacologic agents used to treat schizophrenia may interact with
medications such as scopolamine, atropine, or glycopyrrolate to produce a
syndrome with agitated delirium, hyperthermia, and seizures. Physostigmine
administered intravenously may cause rapid resolution of mental status changes and
be diagnostic at the same time. This agent is a tertiary amine and is therefore
uncharged, which allows it to cross the blood-brain barrier. Thereafter, it reversibly
binds to acetylcholinesterase and prevents the degradation of acetylcholine in the
central nervous system. This enables the neurotransmitters to accumulate and
competitively reverse muscarinic receptor inhibition. Active cooling measures for
hyperthermia and benzodiazepines for agitated delirium may also be helpful.

6. Medication Reversal

If a patient has been given muscle relaxants (vecuronium or rocuronium) to

facilitate surgery, it is imperative to ensure that their effects are reversed or are no
longer present at the end of the procedure if tracheal extubation is planned.
Patients should be assessed for the ability to follow commands, a strong hand grip,
the ability to hold their head up for 5 seconds, and being able to generate a forced
vital capacity of 10 to 12 mL/kg. It is advisable to reverse short- or intermediate-
acting muscle relaxants. Incomplete reversal of neuromuscular paralysis manifests
as uncoordinated muscle movements (“fish out of water”), agitation and weak
handgrip. Hypercarbia, hypocalcemia, and hypermagnesemia appear to exacerbate
the situation as does the presence of an underlying neuromuscular disorder
(multiple sclerosis, myasthenia gravis). Any doubt about a patient’s muscle strength
should preclude tracheal extubation until baseline muscular function has returned.

Occasionally, a patient may present with an altered mental status and prolonged
emergence from anesthesia. A careful review of the medications administered
during surgery, the patient’s medical history, baseline vital signs, baseline
electrolytes, and concomitant medications may offer clues regarding the etiology of
a significant delay to consciousness. Overmedication with benzodiazepines and/or
opioids are common and can usually be addressed with their respective reversal
agents (flumazenil and naloxone).
7. Medication History
If a patient was known to have hypertension, what was the baseline blood pressure
before the start of surgery? A patient with a baseline blood pressure of 140/90 mm
Hg who had blood pressures of 90/60 mm Hg intraoperatively may be at risk for
cerebral ischemia and infarction. Was the patient hypothyroid and taking a
supplement? When was the last time the patient received his or her thyroid
medication? A history of illicit substance use may contribute to the clinical picture.
Finally, consultation with a neurologist, especially if there is concern about an
underlying seizure disorder, may be helpful.

8. Regional Anesthesia
For patients undergoing surgical procedures on the lower abdomen or the lower
extremities, regional anesthesia with either a spinal or epidural technique is often
chosen. When neuraxial anesthesia is employed, the clinician should be aware of
the cardiorespiratory changes that usually take place. Three sets of nerves, the
autonomic, sensory, and motor, are affected with the autonomic being the most
sensitive to blockade with local anesthetic and the motor being the least sensitive.
Hypotension and bradycardia mimicking shock caused by spinal cord trauma may
occur if the level of the spinal blockade spreads in a cephalad direction to include
the cardioaccelerator fibers, which are located in thoracic dermatomes T2 to T4.
This may require the use of intravenous sympathomimetic agents, such as
ephedrine, and volume loading with crystalloid solutions to counteract the
vasodilation seen with blockade of the sympathetic nervous system. These
hemodynamic changes are temporary and resolve as the agent injected into the
cerebral spinal fluid or epidural space dissipates (usually in the case of bupivacaine,
this is 2 or 3 hours). If there is significant cephalad spread of local anesthetic into
the thoracic dermatomes, the intercostal muscles may be affected. Most patients
tolerate this well; however, those with diaphragmatic dysfunction (hyperinflated
lungs seen in emphysema and chronic bronchitis) may have respiratory
embarrassment. If the level of the neuraxial blockade inadvertently rises to the
cervical dermatome, the patient may not be able to breathe because diaphragmatic
function is now affected. This is commonly referred to as a high spinal and requires
the clinician to either take over respiration with mask ventilation or to secure the
airway with an endotracheal tube.
IV. SURGICAL IMPLICATIONS FOR THE IMMEDIATE
POSTOPERATIVE PERIOD
Patients who have undergone surgical procedures have many commonalities, but
also significant differences based on the specific procedure performed. In general,
once the effects of anesthetic agents have subsided, patients should have a
reasonably quick return to normal cardiovascular physiology. When this is delayed,
or when there are new abnormalities that develop, the immediate concern should be
for a complication related to the surgical procedure. However, exacerbation of a
comorbid condition or the development of a new perioperative complication may
also be taking place. Rapid differentiation between these issues is essential to allow
for appropriate and timely intervention.

In general, immediate postoperative complications can be broken down into one of

several relevant categories. We will examine each category independently to identify
the immediate surgical and nonsurgical interventions.

A. Postoperative Respiratory Failure

In general, the development of new postoperative respiratory failure can have a
wide variety of causes and may be multifactorial. Once immediate issues, such as
respiratory depression caused by narcotic analgesia or persistent neuromuscular
blockade, have been ruled out, it is crucial to search for other causes of
postoperative respiratory decline. One important consideration is the patient’s
comorbidities before the surgical procedure. Does the patient have preexisting
chronic obstructive pulmonary disease or congestive heart failure? If so, workup
and treatment can commence as usual. Was the patient immobile or otherwise at
high risk for venous thromboembolism or pulmonary embolism?

Postoperative respiratory failure has many causes, from simple atelectasis to

aspiration to massive pulmonary embolism, and any workup must consider the
broad differential involved as well as the specific surgical procedure involved. One
important consideration is inadequate postoperative pain control leading to
splinting. Although patients with chest or upper abdominal surgery are at the
highest risk, it is essential to assess the patient’s respiratory effort and, if significant
splinting as a result of pain is occurring, reevaluate the postoperative pain regimen.
The increasing use of neuraxial anesthesia for high-risk procedures can significantly
decrease the likelihood of suboptimal pain control in the immediate postoperative
period, with a decrease in the potential respiratory complications.
One important consideration is postoperative respiratory failure in the patient who
has undergone a bowel resection and anastomosis. In addition to other causes, it is
important to include intraabdominal sepsis secondary to a bowel leak or
anastomotic breakdown in the overall differential. Although these complications are
typically delayed for several days, to miss one of these complications results in
devastating implications for the patient.

B. Postoperative Hypotension
There are many root causes of postoperative hypotension. However, in the
postoperative patient, the obvious risk above and beyond the other reasons is severe
postoperative anemia or acute bleeding. Understanding the basics of the
intraoperative course is essential in early diagnosis and management. Important
immediate considerations include:
Did the patient have excessive intraoperative blood loss?
If a bowel anastomosis was performed, could the patient be bleeding
from the anastomosis within the gastrointestinal tract?
Was the procedure exceptionally long, possibly placing the patient at risk
for hypovolemia because of increased insensible losses?
What was used to correct the patient’s volume status?
If excessive crystalloid or exclusively packed red blood cells were used,
could the patient be at risk for coagulopathy? Significant coagulopathy
may place the patient at risk for postoperative bleeding.
If the patient has drains in the surgical field, what is the amount and
character of the drainage, and has it changed significantly in the
postoperative period?
If a significant risk for hypovolemia exists, a gentle fluid challenge may
be indicated. If there is concern for coagulopathy, traditional coagulation
laboratory tests (PT/PTT/INR/fibrinogen) or viscoelastic testing should be
obtained and any abnormalities aggressively corrected. If critical and
symptomatic anemia exists, transfusion of packed red blood cells should
 be initiated. An immediate severe and progressive anemia may not
accompany acute hemorrhage until volume resuscitation is begun.

Postoperative hypotension should raise the concern

for possible bleeding as well as the consideration for
other sources, such as sepsis or effects of neuraxial
anesthesia.

1. Cardiogenic Source

Postoperative hypotension of a cardiogenic origin can be more ominous.

Perioperative myocardial ischemia and infarction can present with a wide variety of
symptoms, from classic crushing substernal chest pain to cardiac arrhythmia,
asymptomatic hypotension, and sudden cardiovascular collapse, or they may be
completely asymptomatic. Surgical patients are also prone to silent myocardial
ischemia given their potential altered mental status, comorbidities including
diabetes mellitus, and distracting pain from surgical incisions. Maintaining a high
index of suspicion is essential to allow for early diagnosis and management. In the
early postoperative period, the management of cardiac ischemia is complicated by
the potential risk of bleeding if aggressive anticoagulation and antiplatelet therapy
are warranted. Close communication with the surgical team is essential to weigh the
risks of bleeding versus the benefits of early reperfusion and salvage of at-risk
myocardium. Although in some patients, such as those who underwent a neurologic
or spinal procedure, any postoperative bleeding may be problematic; in others, the
true potential risk from postoperative hemorrhage may be somewhat minimal.
Another rare consideration is Takotsubo or catecholamine/stress-induced
cardiomyopathy. Although the presentation may mimic that of acute myocardial
ischemia and infarction, including symptoms such as heart failure and arrhythmias,
no occlusive lesion is seen on coronary angiography. Care is typically supportive in
nature, with the judicious use of vasopressors and inotropic agents. Early
recognition and aggressive management are important because perioperative
myocardial infarction carries a greater risk for mortality than a similar event in a
medical patient.

2. Neuraxial Analgesia
A critical consideration regarding postoperative hypotension is the use of neuraxial
analgesia. Patients with spinal or epidural anesthesia may experience vasodilation
with relative hypovolemia because of the anesthetic effects. The hypotension will
generally respond well to a decrease or discontinuation of the anesthetic agent;
however, volume resuscitation or occasionally short-term use of vasopressors is
sometimes needed to maintain tissue perfusion until the anesthetic is fully
metabolized.

3. Vasopressor Use

It is crucial to consider the implications of vasopressor use in the immediate

postoperative patient. Although vasodilatory shock secondary to sepsis is
undoubtedly on the differential for hypotension, especially in surgical cases
involving massive contamination or when preoperative sepsis/systemic inflammatory
response syndrome already existed, caution should be used in assuming that it is
the only cause of hypotension that exists. In the postoperative patient, any
significant increase in vasopressor requirements should prompt an evaluation for
hypovolemia or acute hemorrhage. Using vasopressors when the underlying cause
of hypotension is hypovolemia is undesirable. The vasoconstriction may increase
blood pressure, worsen tissue perfusion, and lead to a higher risk of organ failure
and worse outcomes. Vasopressors may potentially place any bowel anastomosis at
an increased risk of breakdown. Restoring intravascular volume should be the
primary goal in the resuscitation of the hypovolemic patient with the judicious use of
vasopressors if necessary.

C. Abdominal Compartment Syndrome

For patients undergoing abdominal surgery, especially in cases complicated by
perforation or requiring significant resuscitation, a concern in the patient with
progressive respiratory and hemodynamic instability is abdominal compartment
syndrome (Chapter 14). Patients at risk include those with severe injuries, complex
abdominal surgical procedures, and the need for large-volume resuscitation. The
use of appropriate damage control techniques can significantly decrease the risk of
postoperative abdominal compartment syndrome. These techniques are further
described in Chapter 3. Early involvement of the surgical team is essential if
developing compartment syndrome is suspected.

D. Wound Infections
 Surgical wound infections, while typically presenting
in a delayed fashion, can appear hours after a
surgical procedure and be rapidly progressive.

One of the most common nosocomial infections involves surgical wound infections
and resulting complications. The specific risk is highly dependent on the specifics of
the surgical procedure involved, including the presence of significant contamination
at the time of the initial surgical intervention, the particulars of the surgical
procedure performed, as well as the surgical wound classification (Table 2-2).
Although infection rates of 1% to 3% occur in clean wounds, the rate may be as
high as 40% in cases involving gross contamination. Surgical wound infections
usually present in a somewhat delayed fashion, starting 5–6 days after the surgical
procedure and persisting up to 30 or more days, and are not typically a concern in
the immediate postoperative period. However, rarely a surgical wound will develop
an infection of an invasive and aggressive pathogen such as clostridia species and
certain streptococcal species. In these cases, significant symptoms can develop
within hours of the index surgery or injury. These infections are characterized by
rapid progression and require early and aggressive surgical management, including
early wound opening with aggressive debridement as well as antibiotic therapy. Any
significant delay in the identification and intervention of these rare infections will
place the patient at substantial risk.

Table 2-2 Surgical Wound Classifications

Data taken from the American College of Surgeons and CDC criteria on Surgical Wound Classifications
E. Venous Thromboembolism
Although guidelines for some high-risk procedures recommend initiation of
chemical prophylaxis for venous thromboembolism (VTE) in the preoperative
setting, most elective surgical patients have deep vein thrombosis (DVT) prophylaxis
initiated postoperatively, which might leave them at risk for the development of
interoperative VTE or pulmonary embolism. For patients hospitalized before their
surgical procedure, guidelines regarding chemical prophylaxis for VTE should be
followed. When performing urgent or emergent surgical procedures in this
population, the decision to continue or withhold chemical prophylaxis for DVT
before the surgical procedure depends on multiple factors, including the bleeding
risk of the specific procedure performed as well as the type of anesthesia being
used. For patients undergoing high-risk procedures, especially intracranial or spine
procedures, in which even a small postoperative bleed might have devastating
complications, it is generally advisable to withhold preoperative chemical
prophylaxis for DVT. However, for many other surgical procedures, the current
trend is to continue chemical prophylaxis for DVT throughout the procedure. It is
essential to discuss with the surgical team the timing and safety for the initiation of
postoperative chemical prophylaxis for DVT. However, if neuraxial anesthesia
(spinal, epidural) is used, it may be necessary to withhold chemical prophylaxis or
use a different form, such as unfractionated heparin, which may be somewhat less
effective, albeit with a lower risk of bleeding.

V. OPERATING ROOM SUMMARY AND CRITICAL HANDOFF

INFORMATION
A. Handoff Process
Modern surgical procedures offer improvements in quality and duration of life.
Through that process, surgical patients experience multiple transitions in care. This
is especially true of surgical patients who will be cared for by numerous providers in
a variety of physical locations as they progress from preoperative areas, through the
operating room, and then to the intensive care unit.

Studies of the transition of care within hospitals, and specifically, the transition from
the operating room to the intensive care unit, had demonstrated an association with
adverse events. These changes in location, environment, and caregivers have
parallels to processes in commercial aviation, nuclear power, and professional
racing. Application of successful communication and teamwork processes from
these industries have been integrated into anesthesia and surgery with resultant
reductions in complications.

The handoff process, also known as the handover process, typically involves
multiple providers, information of high complexity and volume, and patients with
rapidly evolving physiology. Effective communication and teamwork are essential
elements of a successful transition from the operating room to the intensive care unit
for the critically ill or injured patient. Patients are especially vulnerable when they
cannot participate in the handoff process because of sedation or anesthesia.
Numerous studies have demonstrated the negative impact that ineffective or absent
patient handoffs have on outcomes. Both qualitative and quantitative investigations
of the handoff process have identified omissions in the transfer of key information,
concerns regarding the volume of data (either too comprehensive or too brief), and
general dissatisfaction with the handoff process. Investigators are exploring the
communication and teamwork dynamics that contribute to both errors and
successes with this process. Several authors have described efforts to quantify the
quality of the handoff process as well as the communication methods which transmit
the information. Providers giving and receiving handoffs are generally more
satisfied with the process when a checklist or script is used, also reporting fewer
errors. Observational trials of handoffs using a checklist or script consistently
demonstrated fewer errors in the handoff, both in the number of critical items
omitted as well as the accuracy of information being conveyed.

Effective communication during handoffs in the

postoperative period is essential for providing safe
care by all team members involved.

Even established and effective handoff processes can benefit from introspection and
self-evaluation. Having providers familiar with team dynamics, crisis management
communication, and perioperative care, and observing established processes during
real-time handoffs using validated assessment tools can provide beneficial
information and feedback. Providers participating in the handoff process should
also be queried as to their perceptions of handoff effectiveness and quality.
Outcomes of these investigations should be used to develop and refine handoff
processes with a plan for ongoing reevaluation to ensure sustained positive change.

B. Communication Process
Providers involved in the handoff process often have multiple responsibilities
competing for their attention. Interruptions are a frequent occurrence in all aspects
of medical care. Prominent patient safety organizations have advocated for using a
‘Time-Out’ process before invasive procedures and surgeries. At that moment,
providers cease activity unrelated to the time-out process. The room is silent, like
the sterile cockpit concept observed by airline pilots during the takeoff process.
Information is confirmed and read back by other providers analogous to the
methods used in nuclear submarines. Other providers in the immediate area should
demonstrate respect for the importance of information being transferred and avoid
interruptions during the handoff. Because the innate attention span of adults
engaged in intensive activity is typically limited, the handoff should remain focused
to allow maximum attention from both senders and recipients. Figure 2-1 illustrates
the communication flow and elements that degrade the handoff (distractions) and
improve handoff (feedback).
 Figure 2-1. Elements of Effective Communication Flow

To facilitate an effective handoff process, it is vital to identify the major players

involved, including the messengers, the recipients, and the information to be
conveyed. Each messenger and recipient have essential elements that must be
accurately conveyed to allow for the continuation of safe postoperative care in the
intensive care unit (Table 2-3).

Table 2-3 Major Players and Considerations in the Handoff Process

Providers have unique perspectives and biases based on their role in patient care,
which can impact the effectiveness of communication and accuracy of information
being conveyed. The use of a standardized and scripted format for postoperative
handoffs (Figure 2-2, Figure 2-3) has been shown to reduce errors. Within the
script, each provider understands the information that must be conveyed to achieve
effective handoff. Beyond the transfer of information, the method of communication
is of equal or greater importance. Assigning specific responsibilities for which
providers communicate information will be unique to each institution.
 Figure 2-2. SBAR Handoff (Situation, Background, Assessment,
Recommendation)

One study compared the handoff process to a pit-stop for a Formula-1 racing team.
Although each team member has specific responsibilities, it is necessary for the
entire team to be aware of other members’ responsibilities so that processes can be
refined with the greatest efficiency. Further, each member learns to communicate
verbally and nonverbally to share essential information in a timely fashion. Essential
equipment, tires, and fuel must be handled properly to avoid injury or malfunction.
Finally, the process must be accomplished quickly, 7 seconds on average, to
minimize interruption of road racing. Many parallels exist between the pit-stop and
the handoff, including team integration of skill sets, effective communication,
brevity to allow ongoing workflow, and safe handling of the patient and equipment.
A mature, organized, and sustainably implemented handoff process will yield
positive results for patients, providers, and institutions.

Figure 2-3. Handoff/Handover Template

VI. CONCLUSION
As stated previously, the critically ill postoperative patient requires attention to
multiple potential areas of concern. Although a surgical complication requiring
emergent reoperation may be occurring, other aspects of patient care, including
anesthetic complications, medical complications, or exacerbation of existing
comorbidities, might also require immediate attention. Immediate evaluation and
aggressive intervention are critically important to rapidly diagnosis and intervene as
necessary. Care providers from multiple disciplines need to work together, ensuring
that the entire team is aware of critical information to ensure good patient outcomes.

Case Study
Over the next 60 minutes, the patient has a progressive decline with worsening
hypoxia, increasing peak airway pressures, decreasing urine output, and worsening
hypotension. The crystalloid resuscitation that was started in the operating room
continues, and he receives an additional 4 liters of normal saline without any
improvement in his hemodynamics or urine output. His vasopressor requirements
continue to increase, requiring 20 µg/min of norepinephrine and 0.03 units/min of
vasopressin to maintain a mean arterial pressure (MAP) of 55 mm Hg. Dynamic
monitoring is initiated with a high pulse pressure variation, and an abdominal
ultrasound demonstrates free fluid as well as a collapsible inferior vena cava (IVC).
Laboratory tests demonstrate a hemoglobin of 5.5 g/dL and a hematocrit of 15%.
Blood transfusion is initiated, and the critical care team requests an urgent surgical
reevaluation. The patient’s abdomen is becoming more distended.

As the surgical team comes to the bedside, bladder pressure is obtained,

demonstrating a pressure of 35 mm Hg. The patient is emergently brought back to
the operating room for a diagnosis of abdominal compartment syndrome and likely
postoperative hemorrhage. At re-exploration, the patient’s ventilatory status
improves significantly after his abdomen is reopened. Intraoperatively, he is found
to have 2.5 liters of intra-abdominal blood with bleeding from a mesenteric vessel
as well as a significantly edematous bowel. The bleeding is controlled, the patient is
transfused a total of 6 units of packed red blood cells, 5 units of fresh frozen
plasma, and 1 unit of pooled platelets. Following the transfusion, his hemodynamics
improve significantly, and his vasopressors are weaned. Because of the increased
abdominal pressures and significant bowel edema, temporary abdominal closure is
performed. On return to the ICU, his hemodynamics are significantly improved.
Over the next several days, the patient develops an acute kidney injury, which
eventually resolves, and his vasopressors are weaned off. His acute postoperative
hypoxic respiratory failure slowly improves. He returns to the operating room
several times but eventually undergoes abdominal closure and is extubated.

Key Points
Approach to the Surgical Patient, Part 1
Multiple physiologic changes occur during surgical procedures affecting
the perioperative and postoperative periods.
Surgical procedures can induce a profound physiologic stress response
with a wide range of metabolic responses.
Attending to specific surgical, anesthesia, and postoperative aspects of
care can help limit the surgical stress encountered.
Cardiovascular instability in the postoperative period could have several
causes including the residual effects of anesthesia, hypovolemia,
autonomic dysfunction as a result of the reversal of neuromuscular
blockade, residual effects of regional anesthesia, or profound
hypocalcemia if large amounts of blood products were transfused.
Profound acidosis may cause a patient to be less responsive to inotropes
and vasopressors.
Significant complications can arise from transfusion of packed red blood
cells, including infectious complications, volume overload, acute lung
injury, and coagulopathy.
Because of the multiple classes of drugs administered perioperatively,
life-threatening drug interactions can occur, including malignant
hyperthermia, malignant neuroleptic syndrome, serotonin syndrome,
central anticholinergic syndrome, and incomplete reversal of
neuromuscular blockade.
Respiratory failure in the postoperative period is often multifactorial,
including aspects of preoperative comorbidities, anesthesia technique,
surgical procedures, and pain control.
 Postoperative hypotension should always prompt an investigation of
possible bleeding. As acute hemorrhage is being ruled out, other causes,
including perioperative myocardial infarction, must be considered.
New or increasing postoperative vasopressor needs should prompt an
investigation for possible hemorrhage. Adequate volume resuscitation
must be ensured.
Surgical patients are at high risk for VTE, and appropriate prophylaxis
using chemical and mechanical techniques should be used for
prevention.
Multiple handoffs during patient care are associated with adverse events
and worse outcomes.
The use of a checklist or script during the handoff process can help
ensure adequate transfer of critical information and improve provider
satisfaction.
Each specific provider involved in the care of a patient may have
significant and unique information to convey during the handoff process.

Suggested Readings
1. Catchpole KR, de Leval MR, McEwan A, et al. Patient handoff from
surgery to intensive care: using Formula 1 pit-stop and aviation models
to improve safety and quality. Paediatr Anaesth. 2007;17:470-478.
2. Gubler KD, Gentilello LM, Hassantash SA, Maier RV. The impact of
hypothermia on dilutional coagulopathy. J Trauma. 1994;36:847.
3. Kulaylat MN, Dayton MT. Surgical Complications. In: Sabston Textbook
of Surgery, 20th ed. Townsend C, Beauchamp RD, Evers BM, Mattox
K (eds). Elsevier; 2016.
4. Lane-Fall MB, Beidas RS, Pascual JL, et al. Handoffs and transitions in
critical care (HATRICC): protocol for a mixed methods study of
operating room to intensive care unit handoffs. BMC Surg.
2014;14:96.
 5. Mayo NE, Feldman L, Scott S, et al. Impact of preoperative change in
physical function on postoperative recovery: argument supporting
rehabilitation for colonic surgery. Surgery. 2011;150(3):505-514.
6. Scott MJ, Miller TE. Pathophysiology of major surgery and the role of
enhanced recovery pathways and the anesthesiologist to improve
outcomes. Anesthesiol Clin. 2015;33(1):79-91.
7. Moon TS, Gonzales MX, Woods AP, Fox PE. Improving the quality of
the operating room to intensive care unit handoff at an urban teaching
hospital through a bundled intervention. J Clin Anesth. 2016;31:5-12.
8. Nagpal K, Abboudi M, Manchanda C, et al. Improving postoperative
handoff: a prospective observational study. Am J Surg.
2013;206(4):494-501.
9. Rose DK, Cohen MM, Wigglesworth DF, DeBoer DP. Critical
respiratory events in the postanesthesia care unit. Patient, surgical and
anesthetic factors. Anesthesiology. 1994;81(2):410-418.
10. Veenhof AA, Vlug MS, van der pass MH, et al. Surgical stress response
and postoperative immune function after laparoscopy or open surgery
with fast track or standardized perioperative care: a randomized trial.
Ann Surg. 2012;255(2):216-221.

Suggested Websites
1. American Society of Anesthesiologists Standards and Guidelines.
www.asahq.org/standards-and-guidelines
2. Ausmed. www.ausmed.com/articles/postoperative-complications
3. World Health Organization.
www.who.int/surgery/publications/Postoperativecare.pdf
 Chapter 3
APPROACH TO THE SURGICAL
PATIENT, PART 2: SURGICAL
EMERGENCIES

Objectives
Recognize the signs and symptoms of a surgical emergency based on
the patient’s history and clinical presentation.
Prioritize appropriate treatment and management of a surgical
emergency.
Optimize the use of damage control techniques.
Employ frailty assessment to stratify perioperative risk.

Case Study
A 70-year-old woman with a history of hypertension, diverticular disease, and
atrial fibrillation treated with warfarin presented with abdominal pain, nausea,
vomiting, and fever. The patient’s computerized tomography (CT) scan
revealed perforated diverticulitis, and she subsequently underwent a left
sigmoidectomy. On postoperative day one, the patient reports increasing
abdominal pain and bloating. Her vital signs are as follows: temperature
38.6°C (101.4°F), blood pressure 99/59 mm Hg, heart rate 110 beats/min,
respiratory rate 26 breaths/min, and pulse oximetry 93% on room air. On
examination, the patient is confused, tachypneic, and the abdomen is tense,
distended, and inappropriately tender to palpation with murky output from
the Jackson-Pratt (JP) drain.
– What information is needed to determine whether the patient has a
surgical emergency?
– What immediate interventions should be performed?

I. INTRODUCTION
A stratified approach is appropriate for the patient presenting with distress
after a surgical procedure. Initial priorities include knowledge of the
procedure performed and a high index of suspicion which may be triggered
by changes in physical examination. Deterioration in vital signs, altered
mental status, oliguria, direct or indirect evidence of bleeding and change in
drainage from surgical sites should trigger focused evaluation relevant to
patient complaints with imaging and collection of laboratory data. The older
patient and individuals with significant comorbidities should receive particular
attention as they are at risk for rapid decompensation.
Patients at greater risk for perioperative deterioration can be identified by
measures intended to detect reduced physiologic reserve resulting in limited
resistance to adverse postoperative events. A variety of interventions reduce
perioperative risk such as optimization of nutrition, control of alcohol and
tobacco use, appropriate preparation of organs to be treated in the operating
room, conditioning as possible, use of minimally invasive surgical techniques
which reduce operative trauma and avoidance of opioids where practical in
postoperative pain management.
Identification of patients at risk and rapid intervention to support these
individuals based on threatened organ systems is essential to restore a
favorable hospital course in the postoperative patient.

II. RAPID RESPONSE

A variety of complications can occur after surgery. Postsurgical complications
can be general (eg, hemorrhage) or more specific to the type of procedure
performed (eg, anastomotic leak after small bowel resection). Complications
can manifest immediately or several days after surgery. Close monitoring of
patients who have undergone any surgical intervention, whether it be minor or
major, is essential for the identification, management, and prevention of these
complications. Specific surgical emergencies and management, including
airway, neurologic, cardiovascular, abdominal, and musculoskeletal, will be
discussed in depth in the following chapters.

Early recognition and intervention in a surgical emergency can improve a

patient’s outcome and prevent further complications. Patients who have
surgery are at higher risk for rapid deterioration, and in certain
circumstances, immediate surgical intervention is indicated for survival. If a
patient has undergone surgery and is exhibiting abnormal signs and
symptoms in the postoperative period, what is your approach?

A. Approach to the Surgical Patient

1. Diagnosis
Often you are called to the bedside for an acute change in a patient’s clinical
condition. Table 3-1 provides examples of vital signs and clinical changes in a
patient’s condition that require immediate attention. These changes in a
postoperative patient can potentially indicate a surgical emergency.

Table 3-1 Acute Changes in Patient’s Condition

A thorough and timely physical examination is essential to an accurate
diagnosis. The patient’s clinical status will often prioritize the examination.
The emphasis is on a quick, focused examination centered on acute
symptoms. Keeping in mind the patient’s recent surgery, an overall
assessment includes history, vital signs, visual and physical examination, and
data collection (medications, laboratory and diagnostic tests).

2. Visual Examination

Subtle changes in vital signs (eg, mild

tachycardia and increased respiratory rate) can
occur as an inflammatory response to surgery.
However, severe changes (hypotension and
significant tachycardia) can suggest something
more severe, such as shock.
Observe the patient’s overall appearance and condition (eg, level of distress).
Assess vital signs, which should include the following: heart rate, blood
pressure reading (arterial blood pressure and waveform or noninvasive cuff),
respiratory rate, and pulse oximetry reading. This is a quick assessment that
should take no more than a few minutes. If the patient is unstable, focus on
optimizing the patient’s hemodynamics and follow the ABC mnemonic:
airway, breathing, and circulation.

3. Physical Examination

Prioritize the examination based on the chief complaint and other associated
symptoms. As you perform your physical examination, simultaneously assess
whether the patient is alert and oriented. If the patient is lethargic or
unresponsive, and there is no contraindication, with gentle pressure, rub the
patient’s sternum with a closed fist to assess whether he or she is awake and
can move all extremities. Acutely ill patients may be agitated, obtunded, or
delirious. Altered mental status is often secondary to a metabolic disturbance
or medications administered in the postoperative period, such as analgesics.
Neurosurgical patients should undergo a detailed neurologic examination
quickly.

Continue to assess the level of consciousness and

distress throughout the examination.

Assess whether there are signs of intracranial pathology such as a seizure,

stroke, or herniation. Observe for seizure activity (abnormal movements or
shaking), check pupil response, or any spontaneous eye movement. If the
patient can cooperate with a neurologic examination, assess for signs of a
stroke such as facial drooping, arm drift, and slurred speech. Reassess the
patient’s vital signs and ensure the patient is protecting his or her airway. The
patient may require immediate intervention at this time (benzodiazepine for
seizure or intubation for respiratory distress).
One of the most common problems after surgery is pain. A thorough
assessment of pain is vital for reaching a differential diagnosis in surgical
emergencies. If the patient cannot cooperate with your examination, look for
signs of pain such as facial cues, agitation, or physiologic changes (elevated
heart rate and blood pressure) throughout the examination. If the patient can
participate in the review, a useful method to assess pain is the OLDCARTS
mnemonic: Onset, Location, Duration, Characteristics, Alleviating/Aggravating
factors, Radiation, Treatment, and Severity. Pain can be accompanied by
other symptoms such as diaphoresis, nausea, or vomiting.
Respiratory distress after surgery can be a primary or a secondary variable.
Apply supplemental oxygen as needed. Assess the patient’s overall
appearance, mental status, skin color (cyanosis), work of breathing, and use
of accessory muscles. Tachypnea is often the first sign of serious illness.
Auscultate breath sounds and assess whether the chest is symmetrically
rising. Perhaps the recent surgical intervention put the patient at risk for
pneumothorax or hemothorax. Be mindful of patients at high risk for
pulmonary embolism and look for associated symptoms (rapid breathing,
chest pain, and tachycardia). If the patient has a chest tube, assess for a leak,
obstruction, and output color and volume.

A change in the patient’s hemodynamics after surgery, such as hypotension

and tachycardia, can be a sign of shock (hypovolemic, neurogenic,
anaphylactic, cardiogenic, or septic). If time permits, review previous vital
signs to detect changes or trends in the patient’s condition. Note the mean
arterial pressure (MAP) and check for signs of inadequate organ perfusion
(eg, altered mental status, slow capillary refill, the skin is cool to touch).
Postoperative patients are at risk for hypovolemic shock as a result of severe
blood loss or under-resuscitation during or after surgery. The patient’s recent
surgery will give you clues for the type of shock. Look for signs of bleeding
from the surgical site and drains. If a patient underwent abdominal surgery
with large-volume resuscitation, or there is a concern for intra-abdominal
bleeding, look for signs of elevated intra-abdominal pressure (IAP). High
IAPs can cause intra-abdominal hypertension and lead to abdominal
compartment syndrome, which is a surgical emergency. Elevated IAP
decreases blood flow to abdominal organs and the inferior vena cava (IVC),
causing increased intracranial pressure (altered mental status), decreased
cardiac output (hypotension), and decreased urine output. The patient can
also be in septic shock from an intra-abdominal source (anastomotic leak,
perforation, or mesenteric ischemia) after abdominal surgery. The abdomen
can mask infection; therefore, a thorough abdominal examination to rule out
acute abdominal pathology should be performed with close attention to
peritoneal signs (guarding, tenderness to percussion, rebound tenderness),
surgical incisional site, and drains.
Observe for any arrhythmias associated with hypotension. Obtain an
electrocardiogram (ECG) to analyze the rate and rhythm. Note any recent
medications administered that can cause hypotension or an arrhythmia.

Patients who are elderly, have a history of

diabetes mellitus, or have chronic corticosteroid
use may not present with typical signs of acute
abdominal pathology.

Inspect the surgical incision for dehiscence (opening of the surgical incision),
evisceration (abdominal organs protrude from incision), signs of infection
(erythema or purulent drainage), or bleeding. Make a note of any drains, the
output color, and volume. Serosanguinous drainage is normal; purulent
drainage is often a sign of infection, bilious or enteric drainage may indicate
an anastomotic leak, and bright red drainage is concerning for acute
hemorrhage. It is essential to know the surgical procedure performed and the
specific location of surgical drains or catheters to anticipate potential
complications. A review of the surgical notes and a discussion with the
operating surgeon often reveals pertinent information that can help guide your
diagnosis and management.

Assess the patient’s skin for pallor or cyanosis, temperature, rash, or

increased capillary refill. Remove opaque dressings to evaluate wounds or
incisions carefully. If the patient had recent surgery or trauma to a limb,
assess carefully for pulses or worsening edema.

B. Patient Management

Delegate specific tasks to staff members to

facilitate timely management.

Surgical emergencies require early intervention given the patient’s high risk of
rapid deterioration. Once the likely diagnosis is reached, time is of the
essence. Therefore, a prompt consult with the appropriate surgical team is
prudent. The patient may have undergone spinal surgery, but if the diagnosis
is a pneumothorax, the cardiothoracic surgical team should be informed.

The focus should always remain on the patient’s clinical condition. The
clinical presentation should prioritize your management decisions; for
example, the patient may need to be intubated and mechanically ventilated
before the surgical intervention. The presentation will also drive specific
laboratory or diagnostic tests that may be useful for diagnosis and treatment.
Such tests may include the following: an arterial blood gas (ABG), lactate,
complete cell count with differential (CBC), fibrinogen, basic metabolic panel
(BMP), creatine phosphokinase (CPK), amylase, lipase, liver function tests,
PT/PTT, and cardiac enzymes. Also, ensure the patient has an active blood
type and screen and activate the massive transfusion protocol if indicated.
Obtain pertinent imaging that can be done quickly and efficiently at the
bedside; for example, ultrasonography of the abdomen for abdominal
pathology concerns, a portable chest radiograph to evaluate the lungs or rule
out abdominal free air, or an abdominal radiograph to evaluate for free air,
ileus, or obstruction. Further imaging (eg, CT scan) may help confirm a
diagnosis, but given the patient’s instability, it may be too risky for
transportation at this critical time. Integrate all the objective and subjective
information you have obtained to form a principal diagnosis.
The ultimate goal is to optimize and stabilize the patient. Continue to monitor
the patient’s mental status, vital signs, repeat the focused assessment, and
frequently recheck your interventions. At this time, patients may need to be
triaged to a higher level of care while waiting for surgical management. It is
also essential to keep the patient and family apprised of the situation and
plan.

C. Case Resolution
Consider the patient from the case study described previously.

How does the patient appear?

Is she in distress?
What are her complaints?

She has increasing abdominal pain and bloating. Review her recent vital
signs, which are as follows: temperature 38.6°C (101.4°F), blood pressure
99/59 mm Hg, heart rate 110 beats/min, respiratory rate 26 breaths/min,
and pulse oximetry 93% on room air. On examination, the patient is
confused, tachypneic, and the abdomen is tense, distended, and
inappropriately tender to palpation with murky output from the Jackson-Pratt
(JP) drain.

Keep in mind her recent surgery (left sigmoidectomy). Based on her signs and
symptoms and physical examination (increased abdominal pain and murky
output from the JP drain), she likely has an intra-abdominal process such as
an anastomotic leak or abscess. At this time, obtaining a CBC, BMP, lactate,
and upright chest or abdominal radiograph to assess for free air can help
make a definitive diagnosis and guide management.

Inform the surgical team and discuss the patient’s clinical presentation and
intraoperative events. While awaiting laboratory and diagnostic tests,
supportive treatment should be initiated (eg, oxygen therapy, fluid
resuscitation, antibiotics). Continuous monitoring of patient presentation, the
trend in vital signs, and response to interventions are imperative at this time.
III. FAILURE TO RESCUE
Complications and adverse events are known to occur with hospitalized
surgical patients. Although the teams of providers caring for the patient work
to avoid these, the providers need to have a high index of suspicion to care
for the patient. It was once presumed that hospitals that have fewer
complications have less mortality; therefore, they give better care. But there is
a growing body of literature that reveals that this is not always true. Some
hospitals have high reported complication rates but have lower mortality rates.
When investigated why this is true, it was found that those hospitals that have
higher mortality rates may not be as proficient at recognizing and managing
complications as they occur, a phenomenon known as “failure to rescue.”

A. Complicating Factors

All hospitals experience perioperative

emergencies. Effective rescue improves outcomes.

Failure to rescue refers to the inability to save someone’s life after the
development of a complication. Overall, complication rates were found to be
influenced more by patient factors (eg, age, comorbidities, etc.) than hospital
factors, whereas hospital factors predominantly determined failure to rescue
rates. The skills needed to intervene appropriately before the onset of life-
threatening health problems require complex assessment, highly intensive
therapies, targeted interventions, critical evaluation, and immediate
adjustment dependent on patient response. Failure to rescue had the highest
incidence of patient safety indicators and accounted for 62% of all the patient
safety indicators among older patients.

Failure to rescue is a multifactorial issue. Often, clinicians become aware of

problems when the patient is acutely decompensating and needs urgent,
drastic measures. However, a review of the patient’s chart often demonstrates
the patient’s instability was developing hours before the urgent need for
assistance was recognized. To prevent failure to rescue, many institutions
have attempted to develop tools to elucidate subtle changes in the patient’s
status. Examples are the use of early warning scoring systems or nursing
dashboards. These methods give staff, providers, bedside nursing, and
supervising staff quick clinical surveillance tools. The scores, if accurate,
could be used to adjust the setting, staffing, and monitoring used to improve
patient safety (Table 3-2).

Table 3-2 Surgical Acuity Staffing Grid (Sample)

B. Medical Response Teams

Given the consequences of failure to rescue, institutions have tried to improve
surveillance, recognition, and response-to-rescue events. One approach to this
has been the development of Medical Response Teams (MRT). The MRT is
activated for patients in which the healthcare team is experiencing a concern
for their patients, or they meet predetermined criteria. Typically considered a
crisis team, MRTs bring an additional experienced provider with an advanced
skill set to the bedside. This allows for advanced techniques and procedures
to be performed in an expedited fashion as well as ensure the patient is
receiving the most appropriate care level. The Institute for Health Care
Improvement has identified that the use of these teams is one of six changes
needed to prevent death in patients that were deteriorating outside the
intensive care unit (ICU).

MRTs typically are comprised of physicians, nursing, and ancillary staff, such
as respiratory therapists, laboratory technicians, and pharmacists. Each
institution must tailor their team to their available personnel. Typically,
physicians have some training in critical care or emergency medicine. Nursing
team members are usually composed of members that have many years of
bedside critical care experience. Ancillary staff members allow for advanced
procedures and testing to take place.

Many centers have different criteria on when a MRT should be activated.

These are usually centered around physiologic criteria, organ-specific criteria,
or event triggers such as a patient’s failure to respond to a prescribed
therapy. The criteria should be distributed to all staff and allow the staff to
call for additional help and to call early.

IV. DAMAGE CONTROL AND COMPLICATIONS

A. Damage Control Surgery

Damage control is focused on addressing

immediately life-threatening pathologies such as
bleeding and source control.
The concept of damage control as it relates to major surgical procedures and
resuscitation in critically ill patients requiring emergent surgical intervention
represents a giant leap forward; it provides a potential survival advantage to
those patients who are too ill or physiologically deranged to undergo definitive
surgical management at the time of the initial surgical intervention. By not
attempting to force early definitive management, the patient may be more
likely to survive and eventually recover.

The concept of damage control surgery was first publicized over 20 years ago.
The idea parallels the concept of naval damage control in which in the face of
devastating damage, essential maneuvers are rapidly deployed to prevent a
damaged ship from sinking. In essence, similar concepts are performed
during the initial operation of the critically ill patient. The basic idea involves
control of significant bleeding and ongoing contamination and performing only
essential surgical procedures needed for short-term survival. After the
abbreviated initial surgical intervention, the patient is packed open, a
temporary surgical closure is performed, and the patient is admitted to the
ICU for further resuscitation, warming, correction of coagulopathy, and
stabilization. After the patient has been stabilized and physiology has been
normalized, the patient is then taken back to the operating room where
definitive surgical procedures are performed, and the patient is (hopefully)
closed traditionally. Although the concept was initially described for the
trauma patient with massive bleeding, the paradigm has been extended to the
field of emergency surgery with promising results.

B. Damage Control Resuscitation

Similar to damage control surgery, damage control resuscitation has been
described. In response to severe injury and massive hemorrhage, the common
practice had been the aggressive resuscitation with isotonic crystalloid with
the goal of early normalization of blood pressure while preparing for definitive
surgical control of bleeding; this concept was popularized in the 1970s. Based
on military experience in the early 2000s, there was increasing recognition
that this practice was associated with worsening coagulopathy and high
mortality. Instead, an alternative resuscitation strategy was proposed. Rather
than aggressive crystalloid resuscitation to normalize blood pressure, patients
with massive hemorrhage are allowed to be relatively hypotensive, limiting
resuscitation to keep a systolic blood pressure of approximately 90 mm Hg
until definitive surgical control of bleeding is achieved. Further, when
resuscitation is initiated, rather than isotonic crystalloid, a balanced mix of
blood products including packed red blood cells, fresh frozen plasma, and
platelets are used, approximating the components of fresh whole blood.
Adherence to these resuscitation principles was associated with better
outcomes, including decreased mortality, less lung injury, decreased ICU
stays, and decreased ventilator days.

However, with the increased survival in these critically ill patients comes a
whole host of new complications that must be identified and managed. While
the operative issues require specialized surgical and anesthetic expertise,
overall critical care medical and nursing needs can be defined for the non
surgical team.

C. Complications of Damage Control

Vasoactive drug use parallels practice for septic

shock.

Patients treated with a damage control strategy typically have serious

physiologic derangements immediately following their initial damage control
operation. These issues include life-threatening coagulopathy, hypothermia,
septic shock, hypovolemia, acute kidney injury, and significant electrolyte and
metabolic abnormalities. Ongoing fluid losses through the temporary
abdominal closure should be recognized.

1. Coagulopathy
Prompt identification and vigorous correction of coagulopathy are critically
important. Regardless of the method used to identify the coagulopathy, which
might include traditional laboratory tests including PT/PTT/INR/Fibrinogen or
the use of viscoelastic tests, such as thromboelastography (TEG) or rotational
thromboelastometry (ROTEM), providers need to be prepared to administer
blood products aggressively to correct any deficiencies. The role of off-label
use of factor VIIa or prothrombin complex concentrates is controversial in
these situations.

While any coagulopathy is being corrected, volume resuscitation must be

continued to correct any ongoing hypovolemia aggressively. In the case of
acute blood loss with ongoing coagulopathic hemorrhage, a balanced
resuscitation with packed red blood cells, fresh frozen plasma, and platelets is
preferred, especially if viscoelastic testing is not available to guide the
resuscitation. In septic shock, isotonic crystalloid is likely the fluid of choice,
with the possible addition of colloid if large volumes are needed. Care should
be taken to avoid over-resuscitation because this may increase bowel and
tissue edema making subsequent abdominal closure difficult, if not
impossible. The use of dynamic monitoring to guide resuscitation is
recommended. Using lactate as a marker for tissue hypoperfusion and guide
for resuscitation in the postoperative patient may be helpful but does not
singularly replace other markers.

2. Vasopressors
Vasopressor use, if required, should follow standard recommendations for the
treatment of septic shock. However, caution needs to be taken in the face of
any worsening hemodynamic instability or increasing vasopressor
requirements to ensure that the patient has not developed hypovolemia. In the
setting of coagulopathic hemorrhage after injury, volume resuscitation with
blood and blood products should be the first line of resuscitation. Use of
vasopressors should be reserved for specific situations, and even then, only
after ensuring that the patient is not hypovolemic. However, even without any
ongoing hemorrhage, intra-abdominal fluid losses may be markedly
increased. They must be accounted for in the resuscitation, especially in the
setting of severe peritonitis with a temporary abdominal closure device in
place.

3. Electrolytes
Electrolyte abnormalities need to be identified and aggressively corrected.
Calcium is of specific concern because it is crucial for muscle contraction and
hemodynamics; it is an essential cofactor in the coagulation cascade. It is
subject to depletion in the setting of massive transfusion because of citrate
chelation. Other electrolyte deficiencies should be aggressively replaced. In
the setting of acute kidney injury with severe acidosis or hyperkalemia,
providers should consider early renal replacement therapy, typically with
continuous renal replacement therapy or conventional hemodialysis and as
hemodynamics dictate.

4. Nutrition
Once physiology has corrected, consideration should be made for early
enteral nutrition after consultation with the surgical team. However, it is
critical to note that in many cases where the bowel is resected at the time of a
damage control procedure, the intestine is left in discontinuity with the ends
stapled off. In such cases, enteral nutrition or even enteral medication
administration is contraindicated, and the gastrointestinal (GI) tract should
remain decompressed with a gastric tube in place to wall suction. However, if
early enteric nutrition is possible, its use is associated with decreased bowel
edema and greater success at early abdominal closure.

5. Nursing

In addition to the medical issues, important nursing considerations exist in the

care of these patients. Critical care nurses must be familiar with the types of
devices used for temporary abdominal closure at their institution. These can
easily range from commercially available negative pressure wound therapy
devices with closed systems, to closures requiring connection to wall suction,
to improvised closure devices. Each will require slightly different
management. In cases of device failure, evisceration can occur. If this
happens, the exposed bowel should be covered with a moist, sterile dressing
and emergent contact made with the surgical team to arrange for reoperation
or device replacement at the bedside.

6. Analgesia and Sedation

One important consideration is ensuring the administration of adequate
sedation and analgesia. This is important from a patient comfort standpoint,
but also to ensure that patient movement and abdominal muscle contracture is
limited because excessive movement might lead to increased risk of failure of
the temporary closure device. These agents may trigger a hypotensive
response.

7. Monitoring

Close patient monitoring is required. Monitoring both the volume of output

and character of fluid from the closure device is also essential. Increasing or
excessive fluid loss may lead to hypovolemia and indicate the need for
additional volume replacement. A change in fluid character, either more
bloody or bilious, may indicate recurrent intra-abdominal bleeding or the
development of a bowel leak. Either may suggest the need for early
reoperation by the surgical team.
Other important monitoring points include patient temperature and, in some
cases, bladder pressure. Hypothermia is common in patients undergoing
damage control procedures, especially in the setting of massive blood loss and
transfusion. Active external rewarming is essential to correct hypothermia,
especially in cases of ongoing coagulopathy. In cases of worsening physiology,
hemodynamics, or renal function, consideration should be given to monitoring
bladder pressures. It is possible to have an initial or recurrent abdominal or
retroperitoneal compartment syndrome, even with an open abdomen.

D. Reoperation

Radiographs help identify a residual foreign body

in abdominal wall closure.
After the correction of physiologic abnormalities, coagulopathy, sepsis, and
hypothermia, the surgical team will consider the timing of reoperation. The
exact timing will depend on many factors, including the need for additional
surgical procedures such as additional bowel resections or anastomosis
creation, the degree of bowel edema, the respiratory status, the overall
volume status, and patient stability. Ideally, initial reoperation should occur
within 1 to 3 days of the initial procedure. At the time of reoperation, care
needs to be taken to ensure that any packing material left in the patient is
removed, and hospital procedures often dictate that imaging studies be
obtained at the time of closure for verification. Early abdominal closure
should be the goal; delays place the patient at risk for multiple complications,
including the development of enterocutaneous fistula or loss of abdominal
domain where the fascia of the abdominal wall retracts. The presence of
persistent bowel or tissue edema may complicate closure. In such cases,
primary abdominal closure may become difficult, if not impossible. Surgical
options include multiple reoperations or the possibility of a mesh closure with
a planned ventral hernia and the need for subsequent abdominal wall
reconstruction.

V. RISK MODIFICATION
A. Frailty
In the coming decade, up to 20% of the population in the United States is
expected to be older than 65 years. Consistent with the aging population,
emergency surgeons are experiencing an increase in the number of elderly
patients. This is of particular concern because elderly patients have worse
outcomes than younger patients with similar surgical insults or injuries.
Although the increased vulnerability in the elderly may be a function of the
effects of age and comorbidities, it is also postulated to be a result of frailty.
Frailty is a syndrome encompassing multiple domains characterized by
decreased physiologic reserve and reduced resistance to stressors.
Unfortunately, there is a lack of consensus on the operational definition of
frailty and how to assess or measure it. There are several frailty assessment
tools for elderly patients undergoing elective surgery. There remains,
however, a critical need for valid and clinically useful assessment for elderly
trauma and emergency surgery patients whose injuries or other insults may
preclude testing otherwise feasible in the elective surgical patient at a
preoperative appointment, such as gait speed, mobility testing, or a
comprehensive geriatric assessment (Table 3-3).
Recent data suggest that frailty is a more powerful predictor of increased
perioperative mortality, morbidity, and cost than predictions based on age or
comorbidity alone. For example, when compared with robust patients, frail
surgical patients are less likely to be discharged to home, more likely to be
readmitted to the hospital within 30 days, and more likely to have
perioperative complications and mortality.
A significant challenge in the care of the surgical patient lies with the patient’s
journey through various parts of the process: outpatient clinics, preoperative
units, operating room, postoperative recovery facilities, and the surgical ward.
Each of the previously mentioned patient care units has separate personnel
and capabilities. Each unit impacts the patient’s care and communication
between the care teams is vital. Consistent agreement on the end points of the
patient’s management is essential for coordinated care.

Table 3-3 Summary of Commonly Used Preoperative Frailty Scoring

Data taken from Anaya DA, et al. Summary of the Panel Session at the 38th Annual Surgical
Symposium of the Association of VA Surgeons. What Is the Big Deal About Frailty? JAMA Surg.
2014;149(11):1191-1197.

Table 3-4 summarizes steps which can be taken to improve chances of

recovery after surgical procedures. No single element by itself will improve
outcomes from surgery. The approach to perioperative care is multimodal,
using all available aspects of care that improve recovery. It is essential to seek
synergy between one process element and the next. Frequently components of
recovery are guided by different medical and healthcare specialties working
in various departments. Thus, a multidisciplinary approach is necessary.
Many of the listed elements of care are carried out by allied health
professionals alongside physicians and surgeons. Most important in this
process is coordinated review and auditing of all components of the
preoperative preparation and recovery teams to ensure coordinated and
committed care with each subspecialist providing essential elements from
their skill set.
Table 3-4 Steps to Enhanced Recovery after Surgery

Data taken from JAMA Surg 2017; 152:292-298.

B. Frailty Screening
Frailty screening is an example of a quality improvement metric designed to
address factors contributing to increased perioperative morbidity and
mortality. Frailty screening begins with assessing the patient’s cognition,
strength, endurance, fatigue, comorbidities, and nutrition. This information is
gathered by simple patient questionnaires and on preoperative examination.
Interventions aimed at mitigating elements of frailty may be helpful before
surgery. Often, however, the patient’s frailty cannot be reversed. For these
patients, perioperative preparation should include formal discussions with
surgeons, anesthesiologists, and intensivists to alert the patient and health
care team to risks associated with proposed surgery and a prognosis for 6-
month mortality. When appropriate, formal preoperative palliative care
consultation focusing on clarifying goals and expectations for surgery and
recovery, including discussions of ventilator dependence, dialysis, and do not
resuscitate status, should be conducted.

Frail patients are often identified with

questionnaires or demographic data.
With the implementation of frailty screening, 30-day mortality decreased by
over 50% in a population of elective general surgery patients. Improvement in
outcome was highest among patients identified as frail, and 30-day mortality
fell from 12.2% down to 3.8%. Remarkably, mortality rates also decreased
among patients not seen as frail. The magnitude of improvement among frail
patients increased in the 12 months after screening.

C. Sarcopenia and Osteopenia

Because of the limitations of functional testing or completion of medical
questionnaire data in the acute setting, a variety of investigators have sought
surrogate markers with prognostic value such as sarcopenia, defined by low
muscle mass and impaired muscle function. Sarcopenia is a predictor of
ventilator-free days, ICU-free days, discharge disposition, and mortality
among older high-acuity patients. Like sarcopenia, osteopenia is also related
to the pathophysiology of frailty and is associated with poor outcomes. Frailty
is associated with multiple falls and fractures. Low bone density increases the
risk of hip, spine, and extremity fractures. It is possible to repurpose cross-
sectional imaging obtained for various reasons to screen for sarcopenia or
osteoporosis. Thus, opportunistic use of imaging, specifically CT, may be
applied in the acute surgery setting in which a large population of patients
undergo CT imaging as part of routine evaluation. Given that radiologic
evidence of sarcopenia or osteopenia is associated with underlying physical
frailty through shared pathologic pathways, opportunistic screening for
sarcopenia and osteopenia may fill a significant gap in frailty assessment.

Evaluation of osteopenia and sarcopenia in emergency surgery patients

admitted to the ICU who survived to discharge revealed that radiologic
indicators of frailty were strongly predictive of 1-year mortality even after
adjustment for age and other comorbidities. Physical frailty, sarcopenia, and
osteopenia are intertwined on a pathophysiologic level. Traditional frailty
assessment instruments only include criteria for sarcopenia and osteopenia
through shared characteristics such as weakness, weight loss, or falls. It
remains unclear whether radiologic indicators stand alone as a substitute for
traditional frailty evaluation instruments. Current evidence suggests that the
formal addition of sarcopenia improves the prognostic accuracy of traditional
frailty evaluation instruments.

Key Points
Approach to the Surgical Patient, Part 2: Surgical
Emergencies
Changes in end-organ function and key vital signs provide a useful
warning of acute changes in the condition of the surgical patient.
Patient history, review of the surgical notes, and discussion with the
operative surgeon will help guide the diagnosis and management of
acute signs and symptoms.
The ability to identify and stabilize patients after perioperative
complications determine effectiveness in healthcare teams.
The damage control approach identifies and addresses immediate
life-threatening problems. Typical emphasis is on spillage of bowel
contents and bleeding.
Patients requiring damage control interventions are at risk for
coagulopathy and frequently will require serial surgical procedures.
Patient characteristics indicative of increased surgical risk can be
identified during preoperative screening, and patients counseled,
surgical risk modified, and surgical outcomes improved.

Suggested Readings
1. Beckman M, Paul J, Neideen T, Weigelt JA. Role of the open
abdomen in critically ill patients. Crit Care Clin. 2016;32:255-
 264.
2. Cheatham ML, Malbrain ML, Kirkpatrick A, et al. Results from
the International Conference of Experts on Intra-abdominal
Hypertension and Abdominal Compartment Syndrome. II.
Recommendations. Intensive Care Med. 2007;33(6): 951-962.
3. Chovanes J, Cannon JW, Nunez TC. The Evolution of Damage
Control Surgery. Surg Clin North Am. 2012;92(4):859-875.
doi:10.1016/j.suc.2012.04.002.
4. Dracup K, Bryan-Brown CW. From novice to expert to mentor:
Shaping the future. Am J Crit Care. 2004;13(6):448-450.
5. Fitzpatrick ER. Open abdomen in trauma and critical care. Crit
Care Nurse. 2017;37(5):22-45.
6. Ghaferi AA, Birkmeyer JD, Dimick JB. Complications, failure to
rescue, and mortality with major inpatient surgery in Medicare
patients. Ann Surg. 2009;250(6):1029-1034.
7. Hall DE, Arya S, Schmid KK, et al. Association of a frailty
screening initiative with postoperative survival at 30, 180, and
365 days. JAMA Surg. 2017;152(3):233-240.
8. Holcomb JB, Jenkins D, Rhee P, Johannigman J. Damage control
resuscitation: Directly addressing the early coagulopathy of
trauma. J Trauma. 2007;62(2):307-310.
9. Illuzzi E, Gillepsie M. Physical examination in the ICU. In:
Critical Care. Oropello JM, Vladimir K, Pastores SM (eds). Lange,
McGraw-Hill, New York, 2017; pp101-110.
10. Kaplan SJ, Pham TN, Arbabi S, et al. Association of radiologic
indicators of frailty with 1-year mortality in older trauma patients.
Opportunistic screening for sarcopenia and osteopenia. JAMA
Surg. 2017;152(2):e164604.
11. Ljungqvist O, Scott M, Fearon KC. Enhanced recovery after
surgery: A review. JAMA Surg. 2017; 152:292-298.
12. McDonald VS, Thompson KA, Lewis PR, et al. Frailty in trauma:
A systematic review of the surgical literature for clinical
assessment tools. J Trauma Acute Care Surg. 2016;80(5):824-
834.
13. Oropello JM, Vladimir K, Pastores SM. Critical Care: Lange.
McGraw-Hill, New York. 2017.
14. Rotondo MF, Schwab CW, McGonigal MD, et al. “Damage
control”: An approach for improved survival in exsanguinating
penetrating abdominal injury. J Trauma. 1993;35(3):375-382.
15. Silber JH, Williams SV, Krakauer H, Schwartz JS. Hospital and
patient characteristics associated with death after surgery: A study
of adverse occurrence and failure to rescue. Med Care.
1992;30(7):615-629.
16. Thompson JS, Baxter BT, Allison JG, et al. Temporal patterns of
postoperative complications. Arch Surg. 2003;138(6):596-603.
17. Wakeam E, Hyder JA. Raising the Bar for Failure to Rescue:
Critical Appraisal of Current Measurement and Strategies to
Catalyze Improvement. JAMA Surg. 2015;150(11):1023-1024.

Suggested Websites
1. Trauma.org
http://www.trauma.org/archive/resus/DCSoverview.html
2. https://derangedphysiology.com/main/required-reading/trauma-
burns-and-drowning/Chapter%203.0.4/damage-control-surgery
3. https://lifeinthefastlane.com/ccc/damage-control-resuscitation/
4. https://lifeinthefastlane.com/ccc/thromboelastogram-teg/
5. http://www.practical-
haemostasis.com/Miscellaneous/Miscellaneous%20Tests/teg.html
6. https://derangedphysiology.com/main/required-
reading/haematology-and-oncology/Chapter%201.2.0/viscoelastic-
tests-clotting-function-teg-and-rotem
7. ERAS Society Enhanced recovery after surgery.
http://www.erassociety.org.
 Chapter 4
DIAGNOSIS AND MANAGEMENT OF
ACUTE RESPIRATORY FAILURE

Objectives
Define and classify acute respiratory failure.
Describe the pathophysiology and manifestations of acute respiratory failure.
Review the management of acute respiratory failure.

Case Study
A 58-year-old-man presents to the emergency department in the winter with a few
days of worsening dyspnea, productive cough, fever, and malaise. He is an active
smoker with known chronic lung disease, obesity, hypertension, hyperlipidemia,
and diabetes mellitus. He does not see the doctor much, and reports inconsistent
adherence with his medications. The patient is awake but slightly lethargic. He
appears to be in moderate respiratory distress with evident use of accessory muscles
during inspiration and expiration and a respiratory rate of 30 breaths/min. Audible
crackles are present in the right posterior lung fields with scattered expiratory
wheezes. You are called to assess the patient and initiate treatment.
– How would you prioritize the immediate needs for this patient?
– What tests would be useful to stratify the severity of this patient’s condition?
– Which respiratory support should be considered?
– What pharmacologic treatment(s) should be initiated?
I. INTRODUCTION
Acute respiratory failure (ARF) is one of the leading causes of admission to the
ICU. It is defined as a lack of capacity of the respiratory system and/or other vital
organs, such as the brain and heart, to meet the patient’s oxygenation, ventilation,
or metabolic requirements. The pulmonary system is involved in two crucial
functions: elimination of carbon dioxide (CO2) and oxygenation of the blood. There
are three types of respiratory failure: hypoxemic, hypercapnic, and mixed.
Hypoxemic respiratory failure, historically known as type 1, is defined by a room
air PaO2 of ≤ 60 mm Hg (≤ 6.7–8 k Pa) or an abnormal ratio of PaO2 to
fraction of inspired oxygen (PaO2:FIO2, or P:F ratio; discussed later). This
abnormality of PaO2 should exist in the absence of intracardiac right- to-left
shunting. Hypercapnic respiratory failure, or type 2, is defined by a PaCO2 ≥ 50
mm Hg (≥ 6.7 k Pa) that is not caused by respiratory compensation for metabolic
alkalosis, usually with a pH < 7.35. Mixed respiratory failure has features of both
hypercapnia and hypoxemia and is a common form of respiratory failure in critically
ill patients. Respiratory failure is considered chronic once the renal system attempts
compensation with the retention of bicarbonate. This usually occurs over days of
persistent hypercapnia and the resulting respiratory acidosis. Frequently, in patients
with chronic lung disease, ARF may be superimposed on chronic respiratory
insufficiency. In such circumstances, the acute component is distinguishable from
the chronic component by the degree of respiratory acidosis (as defined by an
abnormal pH) in relation to PaCO2 and elevated bicarbonate values and knowledge
of baseline oxygen requirements.

II. CAUSES OF ACUTE RESPIRATORY FAILURE

Acute respiratory failure develops in a variety of clinical settings. It may result from
primary pulmonary insults or from other systemic non-pulmonary disorders, as
summarized in Table 4-1. Diseases of the central nervous system, neuromuscular
system, upper and lower airways, pulmonary parenchyma, pulmonary vasculature,
thoracoabdominal cavity, and cardiovascular system may all give rise to ARF.

Hypoxemic respiratory failure may be seen in disorders that interfere with the
oxygenation of the blood as it circulates through the alveolar capillaries. This may
occur in patients with severe pneumonia, acute respiratory distress syndrome
(ARDS), or acute pulmonary edema. Hypercapnia most often results from
inadequate alveolar ventilation, which results in ineffective CO2 clearance. This can
be seen in patients with severe airflow obstruction, central respiratory failure, or
neuromuscular respiratory failure.

Table 4-1 Causes of Respiratory Failure

Abbreviations: ARDS, acute respiratory distress syndrome; COPD, chronic obstructive pulmonary disease;
CVA, cerebrovascular accident; NMB, neuromuscular blockade.
Reproduced with permission Pamplin J, Borgman M, eds. Fundamental Critical Care Support: Resource
Limited. Mount Prospect, IL: Society of Critical Care Medicine; 2020.

The following are common ICU scenarios that lead to ARF:

Chronic obstructive pulmonary disease (COPD) exacerbations are
characterized by increased thick mucopurulent secretions as well as
wheezing secondary to bronchospasm. They are often associated with
both hypoxemic and hypercapnic acute respiratory failure (ie, mixed
ARF).
 Pneumonia is most commonly associated with hypoxemic respiratory
failure, although it also can be associated with hypercapnic respiratory
failure, especially in the setting of other chronic lung diseases such as
COPD.
ARDS is a manifestation of a severe systemic inflammatory response
caused by pulmonary or non-pulmonary injury or disease. Hypoxemic
respiratory failure predominantly occurs because of an increased shunt
fraction from alveolar filling.
Traumatic brain injury is associated mainly with hypercapnic respiratory
failure, although it can be complicated by hypoxemic respiratory failure
in the setting of concurrent aspiration, pulmonary contusions, neurogenic
pulmonary edema, or chronic pulmonary disease.
Medication or substance overdose usually occurs from central nervous
system-depressing agents, such as benzodiazepines, opioids, or
barbiturates. It presents with hypercapnic respiratory failure secondary to
a centrally mediated decreased respiratory drive resulting in alveolar
hypoventilation.
Decompensated congestive heart failure is associated with predominantly
hypoxemic failure secondary to alveolar filling and increased shunt;
however, hypercapnic respiratory failure may also occur in severe
exacerbations or in the presence of pulmonary disease.

III. PATHOPHYSIOLOGY OF ACUTE RESPIRATORY FAILURE

A. Hypoxemia
Hypoxemia signifies a decrease in the partial pressure of oxygen (PaO2) in the
blood. Hypoxia defines a state in which the supply of oxygen to the body as a whole
or a specific region is inadequate. Although the usual definitions of hypoxemic
respiratory failure include pulse oximetry (SpO2) and PaO2, additional
measurements of oxygenation, mechanisms of hypoxemia, and the degree of its
impact include: the alveolar-arterial (A-a) gradient, the ratio of PaO2 to the fraction
of inspired oxygen (FIO2) known as the P:F ratio, and the oxygenation index (OI).
Regardless of how hypoxemic respiratory failure is defined or monitored, the
important clinical context is how the degree of hypoxemia results in tissue hypoxia.

Alveolar-arterial gradient:

The A-a gradient is the oxygen gradient between the alveolar oxygen partial
pressure (PAO2) and the content of dissolved oxygen in the arterial supply (PaO2).
A normal A-a gradient for a young healthy adult is usually 5–10 mm Hg, but
increases with age. An age-adjusted approximation for the A-a gradient = (Age/4)
+ 4. The calculation for A-a gradient is:

A-a gradient = PAO2 – PaO2

PaO2 is measured by obtaining an ABG analysis, whereas PAO2 is calculated by

the following equation:

PAO2 = FIO2 × (PATM – PH2O) – (PaCO2/R)

FIO2 is the fraction of inspired oxygen (0.21 at room air)

PATM is the atmospheric pressure (760 mm Hg at sea level)

PH2O is the partial pressure of water (47 mm Hg at 37°C)

PaCO2 is the partial pressure of CO2 obtained from the ABG analysis

R is the respiratory quotient (approximately 0.8)

P:F Ratio:

The PaO2:FIO2 (P:F) ratio, in which PaO2 is measured as mm Hg and FIO2 is the
fraction of inspired oxygen, is a measurement of oxygenation that accounts for the
amount of supplemental oxygen that the patient is requiring. It is a simple
calculation that is most commonly used in patients with hypoxemic respiratory
failure, specifically ARDS, to classify the severity of their disease process and trend
it over time. A normal P:F ratio is usually 300–500. Based on the Berlin definition
of ARDS, the P:F ratio stratifies the severity of the hypoxemia and provides
indications for certain advanced management therapies. The most accepted
definition of ARDS is the Berlin definition, which was updated in 2012. To be
classified as having ARDS, a patient must meet all three of the following criteria:
 The P:F ratio can be helpful for following trends in a
patient’s condition and evaluating ventilation
strategies.

Onset within 7 days after a known clinical insult or new or worsening

symptoms
Bilateral diffuse alveolar opacities on chest imaging (chest radiograph or
CT scan)
P:F ratio < 300*
Mild : 201 to 300
Moderate: 101 to 200
Severe: < 100
*P:F ratio is measured at a minimum PEEP setting for CPAP of 5 cm H2O.

Oxygenation Index (OI):

The OI is a measurement of oxygenation dysfunction that takes into account mean
airway pressure while a patient is on mechanical ventilation.

OI = [100 × (mean airway pressure (cm H2O) × FIO2]/PaO2

An OI of ≥ 25 can indicate severe hypoxemia. The OI has some advantages over

the P:F ratio. The two main techniques to improve alveolar oxygenation for a patient
on positive pressure ventilation are to increase the FIO2 and the airway pressure
(the latter commonly by increasing positive end-expiratory pressure [PEEP]). Thus,
two different patients with the same PaO2 and FIO2 can have different mean
airway pressures but the same P:F ratios; therefore, their different OIs will more
accurately predict the discrepancy in oxygenation dysfunction.
For Example:

Which patient has a higher likelihood of worse outcomes?

 Patient 1: PaO2 65 mm Hg, FIO2 80%, PEEP 10, PIP 30, MAP 20*,
P:F 0.8 = OI 21

Patient 2: PaO2 65 mm Hg, FIO2 80%, PEEP 18, PIP 40, MAP 29*,
P:F 0.8 = OI 26

Answer: Patient 2 with an OI of > 25 has more severe hypoxemia with

evidence of worse lung compliance, and ultimately a higher mortality rate
compared with Patient 1.
Abbreviations: PIP, peak inspiratory pressure; Ti, inspiratory time.
*Mean airway pressure (MAP) based on Ti 1.0, respiratory rate 30 breaths/min, pressure based on
presumed lung compliance differences.

Mechanisms of Hypoxemia:

The four main mechanisms of hypoxemia are ventilation/perfusion mismatch,

hypoventilation, diffusion impairment, and reduced inspired oxygen tension (PIO2).
The most common underlying physiologic abnormality in hypoxemic respiratory
failure is a mismatch of alveolar ventilation and pulmonary perfusion , as
illustrated in Figure 4-1. The mismatch of ventilation and perfusion, where
ventilation is decreased relative to perfusion, is called low matching is
particularly important to oxygenation of blood as opposed to elimination of CO2
(discussed in Section IV) because of the kinetics of the hemoglobin oxygen
dissociation curve. Although there is normally a heterogeneous amount of
ventilation and perfusion among the upper, middle, and lower lung zones,
significant decreases in either or contribute to a mismatch with a net
result of hypoxemia. Lung areas with high ratios, which provide a high PaO2,
cannot compensate for areas with a low ratio (providing low PaO2) as the
hemoglobin molecule is already about 90% saturated at a PaO2 of about 60 mm
Hg. The admixture of poorly oxygenated blood returning from abnormal alveoli
dilutes oxygenated blood from more normal lung units, resulting in systemic
hypoxemia. The hypoxemia caused by mismatch is usually easily corrected by
supplemental oxygen.
 Figure 4-1. Ventilation and Perfusion Matching in the Lung

A, At the end of the pathologic continuum, areas of limited ventilation relative to perfusion
produce shunt effect and hypoxemia. B, Ventilation and perfusion are matched in the normal
lung. C, At the opposite of the continuum, areas of better ventilation than perfusion produce dead
space effect.

Diseases that cause progressive obstruction of distal airways, alveolar filling, or

atelectasis (eg, pneumonia, aspiration, pulmonary edema) result in decreased
oxygen availability in the distal airways for uptake through the pulmonary
capillaries. Subsequent hypoxic pulmonary vasoconstriction results in decreased
blood flow to these abnormal lung units. Although this decline has a lower effect
than the decrease in oxygen availability, it results in a greater proportion of
deoxygenated blood (venous admixture) that is returned to the left side of the heart.

One extreme of mismatch is shunt because there is perfusion of the

unventilated lung. In diseases that cause diffuse alveolar flooding (eg, ARDS),
refractory hypoxemia may be the result of shunt physiology. Treatment of
hypoxemia caused by mismatch should be directed toward treating the
underlying cause such as infections, reversing airway obstruction, reopening
(recruiting) atelectatic lung zones, and preventing closure (de-recruitment) of the
affected lung units. Oxygen therapy and/or mechanical ventilation are cornerstones
in providing support until such time that the cause of mismatch has been
reversed.
Other causes of hypoxemia include:
 Decreased diffusion of oxygen across the alveolocapillary membrane
complex because of interstitial edema, inflammation, fibrosis, etc.
Alveolar hypoventilation
High altitude with low inspired partial pressure of oxygen
Diffusion abnormality is rarely the primary cause for hypoxemia because oxygen
transport across the alveolocapillary membrane is generally perfusion limited rather
than diffusion limited; however, in cases such as increased cardiac output and
tachycardia, diffusion may be limited when the transit time across pulmonary
capillaries is reduced. Therapy for diffusion abnormalities, in addition to
maintaining adequate circulating volume, includes treatment of the cause of
interstitial pathology (ie, diuretics for cardiogenic pulmonary edema, corticosteroids
for inflammatory disorders). Ensuring adequate minute ventilation will correct
hypoxemia that is solely the result of hypoventilation. High altitude is a rare cause
of acute hypoxemia in patients. As a compensatory treatment strategy, providing
oxygen supplementation (FIO2) while the cause of the hypoxemia is investigated
and corrected may improve oxygenation.

B. Hypercapnia
Hypercapnic respiratory failure is caused by either excess CO2 production or
decreased effective alveolar ventilation. Alveolar minute ventilation (VA) is
determined by the tidal volume (VT), the respiratory rate frequency (f), and
physiologic and anatomic dead space (VD).

VA = (VT – VD)f

Hypercapnia has a multitude of causes as listed in Table 4-1. In general, healthy

individuals do not display symptoms of hypercapnia until the PaCO2 rises about 70
to 80 mm Hg, whereas patients with chronic hypercapnia may be able to tolerate
PaCO2 levels as high as 90 to 120 mm Hg before becoming symptomatic.
Hypercapnic respiratory failure, therefore, has a different PaCO2 threshold for
each patient but can be summarized as the condition in which insufficient CO2
removal by the lungs necessitates medical therapy and/or ventilatory support.
Hypercapnia, resulting from either decreased VT or the respiratory rate frequency,
may occur with drug ingestions or anesthetics that lead to depression of the
medullary respiratory centers. An elevated PaCO2 normally increases the
ventilatory drive. Therefore, hypercapnic respiratory failure implies that the patient
is unable to sustain minute ventilation (f × VT).
Treatment of decreased VT or respiratory rate may require reversal of sedation or
other drugs, endotracheal intubation with mechanical ventilation to rest fatigued
muscles, supplemental nutrition, respiratory stimulants, or treatment of other
possible primary causes. For neuromuscular disorders such as myasthenia gravis
and Guillain-Barré syndrome, serial measurement of ventilatory mechanics, such as
negative inspiratory force and forced vital capacity, can dictate when mechanical
ventilation is warranted. Either a negative inspiratory force below −20 to 25 cm
H2O or forced vital capacity < 10 mL/kg, should raise concern that a patient’s
ventilatory mechanics are sufficiently impaired and mechanical ventilation is
needed. Desaturation or hypoxemia cannot be relied on because they are secondary
to alveolar hypoventilation, and therefore a late finding of respiratory failure.

The more rapidly the negative inspiratory pressure

and forced vital capacity deteriorate, the lower the
threshold for intubation and mechanical ventilation.

Increased physiologic dead space (VD) may also produce hypercapnia and is
another type of mismatch illustrated in Figure 4-1. When gas flow to and from
airways remains adequate but blood flow is diminished, CO2 does not have the
opportunity to diffuse out of the pulmonary circulation, and CO2-rich blood is
returned to the left atrium. Increased dead space ventilation may occur in
respiratory muscle fatigue from any cause, leading to rapid shallow breathing.
Increased VD may also be seen in hypovolemia, pulmonary embolism, poor cardiac
output, or when the regional airway pressure is relatively higher than the regional
perfusion pressure, reducing pulmonary blood flow in that area.

Strategies to reduce dead space may include reduction in peak or mean airway
pressures, if the patient is receiving mechanical ventilation, augmentation of
intravascular volume and/or cardiac output, or treatment of other causes for limited
pulmonary blood flow. It may be possible to compensate for hypercapnia caused by
high VD by modifying parameters to increase minute ventilation during mechanical
ventilation while the cause of hypercapnia is sought and corrected. Because of the
high solubility of CO2, a diffusion barrier rarely ever occurs. Increased CO2
production may contribute to hypercapnia secondary to either excess carbohydrate
nutritional calories or extreme hypercatabolic conditions (eg, burns,
hyperthyroidism, persistent fever).

C. Mixed Respiratory Failure

Patients commonly demonstrate characteristics of both pathophysiologic categories
of ARF during the course of illness. An understanding of each underlying
pathophysiology is necessary to plan the appropriate therapeutic support. Several
related disease processes often act synergistically to compound respiratory failure.
For example, the patient with chronic pulmonary disease and a large dead space
often has associated heart failure, which increases mismatching and worsens
hypoxemia. In a patient with severe ARDS, pulmonary interstitial and alveolar
edema result in increased intra-pulmonary shunt and dead space, and decreased
functional lung size because of alveolar collapse; subsequently, the shunt
contributes primarily to hypoxemia while increased deadspace causes hypercapnia,
resulting in mixed respiratory failure.

IV. MANIFESTATIONS OF ACUTE RESPIRATORY FAILURE

A. Clinical Presentation of Respiratory Distress
Clinical manifestations of respiratory distress commonly include signs and
symptoms of hypoxemia, hypercapnia, or both. These include:
Altered mental status ranging from agitation to somnolence
Evidence of increased work of breathing, such as nasal flaring in infants,
use of accessory respiratory muscles,
intercostal/suprasternal/supraclavicular muscle retraction, tachypnea,
hyperpnea, or a paradoxical or dysynchronous breathing pattern (Figure
4-2)
Bradypnea
 Cyanosis of mucosal membranes (eg, tongue, mouth) or nail beds
Diaphoresis, tachycardia, hypertension, and other signs of catecholamine
release

Figure 4-2. Normal Versus Abnormal Respiration

A, The abdominal wall moves outward as the diaphragm moves downward in normal inspiration.
B, With respiratory muscle fatigue, the diaphragm becomes flaccid and moves upward during
inspiration resulting in inward movement of the abdominal wall.

B. Diagnostic Tests

Waveform capnography (end-tidal CO2 [ETco2])

may be used as a surrogate for PaCO2

Pulse oximetry can be used to rapidly evaluate oxygenation in a patient with

respiratory distress by estimating the arterial oxyhemoglobin saturation. However,
pulse oximetry provides no assessment for hypercapnia. Arterial blood gas analysis
is commonly used in severely ill patients to determine the two primary measures of
respiratory failure, the PaO2 and PaCO2, as well as pH. Additional tests, such as
electrolytes, hematocrit, and drug levels, may provide clues to the underlying
etiology of ARF. Chest radiography and bedside ultrasonography in combination
with these laboratory tests is invaluable in suggesting the underlying
pathophysiology of ARF.
Waveform capnography (end-tidal CO2 [ETCO2]) is a measure of the partial
pressure of exhaled CO2 and may be used as a surrogate for PaCO2 (Figure 4-3).
Although ETCO2 may not accurately reflect actual PaCO2 because of alterations in
dead space ventilation (areas of the lung in which ventilation occurs but there is no
perfusion), ETCO2 trends are useful for monitoring patient ventilation, especially
when ABG analysis is limited or unavailable. In addition, capnography provides
reassurance that an endotracheal tube (ETT) or tracheostomy is in place,
particularly during transport.
 Figure 4-3. Waveform Capnography

A, Normal. B, Status asthmaticus. C, Trigger dyssynchrony. D, Worsening hypoventilation.

V. MANAGEMENT CONSIDERATIONS
A. Oxygen Supplementation
Most patients with ARF require supplemental oxygen. Oxygen transfer from alveolar
gas to capillary blood occurs by diffusion across the alveolar-capillary membrane
and is driven by the oxygen partial-pressure gradient between the partial pressure
of alveolar oxygen (PaO2) and the PO2 of the pulmonary capillary blood. In most
cases of ARF, the PaO2 can be substantially increased by use of supplemental
oxygen, thus increasing the gradient across the membrane and improving the PaO2.

Supplemental oxygen can be provided by a variety of devices (Figure 4-4). The

effectiveness of each is determined by its capacity to deliver sufficient oxygen at a
high enough flow rate to match the patient’s spontaneous inspiratory flow rate.
Matching between the flow capacity of the oxygen device and the patient’s
inspiratory flow demand determines how much room air is entrained by the
nonintubated patient breathing in an open system. Any entrained room air (FIO2 =
0.21) will dilute (decrease) the FIO2 of the delivered gas in such a way that the
tracheal FIO2, and hence PaO2, may be considerably lower than the FIO2
delivered from the oxygen source. Therefore, oxygen-supplement systems are
usually classified as high oxygen (capable of delivering up to 100% oxygen),
controlled oxygen (set oxygen percentage), or low oxygen. Similarly, the devices are
also categorized as either high flow, moderate flow, or low flow, reflecting the flow-
delivery capacity of the gas at the preset FIO2 level. Table 4-2 provides an
overview and compares some commonly used supplemental oxygen delivery
devices.

Table 4-2 Comparison of Supplemental Oxygen Delivery Devices

Reproduced with permission Pamplin J, Borgman M, eds. Fundamental Critical Care Support: Resource
Limited. Mount Prospect, IL: Society of Critical Care Medicine; 2020.

Supplemental oxygen should be considered a

temporizing intervention while the primary etiology
of hypoxemia is diagnosed and treated.

For example, a tachypneic and hyperpneic patient will have a high inspiratory flow
rate during each breath. In such cases, hypoxemia is less likely to respond well to
oxygen supplementation by nasal cannula because it is a low-oxygen, low-flow
system and cannot match the patient’s high inspiratory flow rate. Room air will be
entrained during inspiration, and the tracheal FIO2 will be reduced. A high-oxygen,
high-flow system should be selected for this type of patient.

Figure 4-4. Oxygen Delivery Devices

1. Low-Flow Nasal Cannula
Short prongs of the nasal cannula are inserted into the nares. Oxygen (100%) is
delivered through the cannula, but at a rate between 0.5 and 5 L/min. The
resulting FIO2 depends on the patient’s minute ventilation and, therefore, cannot
be precisely controlled, but the maximal tracheal FIO2 is not likely to exceed 0.4 to
0.5 (40% to 50%). Higher flow rates do not result in much higher FIO2 levels and
have a drying and irritating effect on nasal mucosa. The nasal cannula is
comfortable and well tolerated by many patients with ARF in whom precise control
of FIO2 is not necessary. It is a low-flow, low-oxygen device.

2. Aerosol Face Mask

The commonly used aerosol face mask combines a variable oxygen setting and
moderate flows. The mask, which has large side holes, is attached by large-bore
tubing to a nebulizer that blends 100% oxygen and room air to deliver gas at a
preset FIO2 level. Flow matching can be evaluated by observing the patient during
spontaneous breathing. If the entire aerosol mist disappears from the mask during
inhalation, the patient’s inspiratory flow demands are probably exceeding the
capacity of the nebulizer and room air is being entrained. The aerosol face mask is
a variable oxygen, moderate-flow device.

3. Air-Entrainment Face Mask

Air-entrainment masks (also called Venturi masks) deliver oxygen through a jet-
mixing device that increases the velocity of oxygen and causes a controlled
entrainment. The FIO2 can be more precisely controlled from 0.24 to 0.5 (24% to
50%) at high-flow rates simply by selecting the interchangeable jet nozzle and
adjusting the oxygen flow rate. It is a high-flow, controlled-oxygen device.

4. Reservoir Face Mask

A reservoir mask is frequently used for improving

oxygenation in patients with severe hypoxemia until
further evaluation and treatments are accomplished.
The reservoir face mask incorporates a reservoir bag from which the patient
breathes. This bag is filled with 100% oxygen from a supply source. The flow rate
is adjusted so that the bag remains completely or partially distended throughout the
respiratory cycle. When the mask is properly applied, oxygen delivery to the
nonintubated patient can be maximized but rarely exceeds an FIO2 of 0.6 to 0.9.
The reservoir face mask is a high-oxygen, high-flow device.

5. Resuscitation Bag-Mask Unit

Although not commonly considered an oxygen-supplement device, bag-mask units

are usually included with other emergency equipment and, therefore, are readily
accessible. When the mask is held firmly over the patient’s face, room air
entrainment is largely excluded. If the oxygen flow to the bag is kept high (≥ 15
L/min), a high-oxygen supply is provided at sufficient flow. The resuscitation bag
need not be compressed to supply oxygen. It is a high-oxygen, high-flow device.

B. Advanced Oxygen Supplementation

1. High-Flow Nasal Cannula

High-flow nasal cannula (HFNC) systems involve delivery of heated and humidified
oxygen at high flow rates. Standard oxygen therapy delivers dry and cold air into
the respiratory tract, which may promote inflammation, increase airway resistance,
and affect mucocilliary clearance. Conversely, heated and humidified air delivered
via the HFNC has been shown to reduce airway resistance and airway inflammation
while promoting secretion clearance.
HFNC may also improve respiratory mechanics because of the higher flow rates that
it is capable of delivering. For example, in the setting of ARF, a patient’s minute
ventilation can far exceed 20 L/min. Whereas the nonrebreather mask can only
achieve a flow of 15 L/min, the HFNC is capable of matching the patient’s needs by
reaching oxygen delivery at a flow of up to 60 L/min in adults. Furthermore, these
high flow rates can generate a modest PEEP in the airway. Although debated, in
general, up to 1 cm H20 of PEEP is generated for every 10 L/min of flow the
system delivers, which improves oxygenation. Lastly, the high inspiratory flow rates
wash out the CO2-rich exhalation air in the upper airway. As the pharyngeal dead
space is reduced, the actual oxygen concentration reaching the alveoli is higher than
with conventional oxygen therapy.
When setting the initial parameters for HFNC, flow rate should be titrated first
(typically by 10 L/min increments) followed by FIO2. Temperature may be set from
31°C (87.8°F) to 37°C (98.6°F) as tolerated by patient. If adequate saturation
and/or improvement in work of breathing is not achieved when reaching 60 L/min
with FIO2 50%, endotracheal intubation should be considered.

Potential contraindications to HFNC include concomitant COPD because evidence

has demonstrated that noninvasive positive pressure ventilation (NIPPV) has
mortality benefit. If a patient requires endotracheal intubation, although has a do-
not-intubate status, HFNC may be appropriate from both a therapeutic and a
palliative perspective. The last indication, backed by consistent evidence, is the use
of HFNC as a preoxygenation tool when performing rapid sequence intubation.
HFNC has consistently shown to increase safe apnea time.

2. Noninvasive Positive Pressure Ventilation

NIPPV is a form of mechanical ventilation that provides respiratory assistance

through a mask or helmet without a secure or invasive airway. Both oxygenation and
ventilation can be augmented in the already breathing patient through the delivery
of positive pressure and FIO2, ranging from ambient air at 21% up to 100%. Some
advantages and disadvantages of NIPPV are listed in Table 4-3.

Table 4-3 Advantages and Disadvantages of NIPPV

NIPPV encompasses several different modalities. The two modes most frequently
used in patients with ARF are bilevel positive airway pressure (BiPAP) and
continuous positive airway pressure (CPAP). Each mode has unique indications but
share the same contraindications (Table 4-4). Overall, NIPPV can decrease
mortality, endotracheal intubations, and ICU length of stay in a variety of clinical
scenarios. However, it has been shown to increase mortality if used incorrectly. All
types of NIPPV are contraindicated in patients who are not able to follow
commands, cannot handle oral secretions appropriately, underwent recent
esophageal surgery, have facial deformities, require restraints, and/or are
hemodynamically unstable. As with HFNC, if work of breathing and/or oxygenation
do not improve after an initial trial of NIPPV, endotracheal intubation should not be
further delayed.

Table 4-4 Contraindications to NIPPV

BiPAP may be indicated in several clinical scenarios. NIPPV has potential benefit
for several patient types but is not ideal for all. Traditionally, patients with
exacerbations of congestive heart failure or COPD can respond well with NIPPV as
a bridge while the underlying process is addressed. Other situations in which
NIPPV may provide benefit over mechanical ventilation or avoid the need for
mechanical ventilation include immunocompromised patients with respiratory
failure, patients with asthma exacerbation, postextubation, respiratory failure in
patients with cystic fibrosis, intubation refusal, and palliative care. The use of
NIPPV in ARDS is controversial. In some studies, it has been shown to decrease
the rate of endotracheal intubation but does not influence overall mortality.

The initial setup for NIPPV and close monitoring of the patient within the first 1 to
2 hours are the most crucial aspects for ensuring success of NIPPV. Suggestions for
initiation and monitoring NIPPV are highlighted in Table 4-5. The patient should
be properly monitored in an environment in which a nurse, respiratory therapist, or
physician has continuous direct observation of the patient and proper monitoring
with heart rate, blood pressure, pulse oximetry, and ideally ETCO2. Pre-NIPPV
baselines for pH, PaCO2 (or SpO2), PCO2 (or ETCO2), respiratory rate, and
patient comfort must be established, and clear ideal trajectory identified in these
numbers and observations to indicate success or failure. Reassessment after
initiating NIPPV should occur within 30 to 60 minutes. In general, if there is no
improvement within 4 to 6 hours (or if there is earlier clinical decline), invasive
mechanical ventilation should be strongly considered. Sedation should be used
cautiously during NIPPV to avoid respiratory depression. Consider gastric
decompression with a nasogastric tube if a helmet is used or the patient requires
very high delivered pressures (above 15 cm H2O). The patient’s oral intake should
be limited in the initial period in the event that gastric insufflation causes emesis or
the patient fails NIPPV and requires invasive mechanical ventilation.

Table 4-5 Initiation, Early Titration, and Assessment of NIPPV

Abbreviations: BiPAP, bilevel positive airway pressure; CPAP, continuous positive airway pressure; EPAP,
expiratory positive airway pressure; ETCO2, end-tidal carbon dioxide; FIO2, fraction of inspired oxygen; IPAP,
inspiratory positive airway pressure; NIPPV, noninvasive positive pressure ventilation; PaO2, partial arterial
oxygen pressure; PaCO2, partial arterial carbon dioxide pressure; PEEP, positive end-expiratory pressure;
SpO2, oxygen saturation; VA, alveolar minute ventilation; VT, tidal volume.
Reproduced with permission Pamplin J, Borgman M, eds. Fundamental Critical Care Support: Resource
Limited. Mount Prospect, IL: Society of Critical Care Medicine; 2020.

The initial parameters that are set include the inspiratory positive airway pressure
(IPAP), expiratory airway pressure (EPAP), FIO2, and back-up respiratory rate.
The IPAP may be adjusted to manipulate ventilation parameters, while the EPAP
(in conjunction with the FIO2) may be adjusted to control oxygenation. A difference
of at least 4 cm of water (cm H2O) between the IPAP and EPAP is recommended.
Parameters are titrated to promote a patient ventilation of 5–8mL/kg, improve
oxygenation to 88–92%, while being comfortably tolerated. Initial reasonable
BiPAP settings would be an IPAP of 8 cm H2O, EPAP of 4 cm H2O, FIO2 of
50%, and a back-up respiratory rate of 12. If additional minute ventilation is
required, increase IPAP accordingly; conversely, EPAP and FIO2 may be titrated
to improve oxygenation.

Patients with COPD who have been endotracheally intubated can be extubated
earlier to BiPAP ventilation. This not only decreases days on mechanical
ventilation, but also ICU length of stay and even mortality. CPAP is primarily
indicated in hypoxemic respiratory failure secondary to acutely decompensated
congestive heart failure (CHF). CPAP may be beneficial by several mechanisms.
First, it maintains an elevated PEEP, therefore increasing mean airway pressure
and, as a consequence, oxygenation. Secondly, in patients with CHF, as positive
pressure is delivered, intrathoracic pressure increases. As a result, preload
decreases, thereby reducing lung edema while decreasing afterload and promoting
an increase in cardiac output. CPAP is the equivalent of EPAP in BiPAP. As
discussed earlier, a starting point of 5 cm H2O of CPAP may be adequate if the
patient’s saturation and work of breathing improve, although more typically a
pressure of 8–10 cm H2O may be required.

C. Pharmacologic Adjuncts
Many diseases that cause ARF produce similar anatomic and physiologic
derangements, including bronchial inflammation, mucosal edema, smooth muscle
contraction, and increased mucus production and viscosity. Each of these processes
may contribute to obstruction of airway gas flow, increased airway resistance,
mismatch, and elevated VD. Some pharmacologic agents may be helpful in the care
of such patients and may directly alter shunt or dead-space effects.

1. β2-Agonists

Inhaled β2-agonists are important therapy in patients with ARF secondary to many
causes. Stimulation of β2-adrenergic receptors causes bronchial and vascular
smooth-muscle relaxation. These agents are typically administered by metered-dose
inhaler or by intermittent or continuous nebulization (Table 4-2). On rare
occasions, in very critically ill patients with obstructive airway disease, β2-agonists
are administered by both inhalation and subcutaneous injection. Long-acting
inhaled agents do not have a role in the management of patients with acute
respiratory failure. Racemic epinephrine aerosol is an established therapy for upper
airway obstruction in children with croup and is also used for laryngeal edema in
adults.

2. Anticholinergic Agents
Ipratropium bromide competes with acetylcholine at the bronchial receptor site,
resulting in bronchial smooth-muscle relaxation. This agent is delivered by metered-
dose inhaler or nebulization (Table 4-6). Ipratropium has a more delayed onset of
action than β2-agonists and has more consistent bronchodilatory effects in COPD
than in asthma. The addition of ipratropium to albuterol appears to have an additive
benefit in approximately 30% of patients with asthma. Tiotropium is a long-acting
anticholinergic bronchodilator that has sustained effects in patients with COPD;
however, its use in acute exacerbations is not recommended.

Table 4-6 Pharmacologic Agents for Obstructive Airway Disease

Abbreviations: q, every; MDI, metered-dose inhaler; NS, normal saline
aIn patients with severe asthma, frequency of administration of inhaled β-agonists should be guided by response
to therapy and risk for adverse effects. Therapy is routinely initiated with three treatments every 20 minutes.
Further therapy adjustments are then based on response. Continuous nebulization may also be employed.
Caution should be exercised when considering use of continuous nebulized β2-agonists, particularly in older
patients and those with underlying cardiac disease.

3. Corticosteroids

Providing corticosteroid therapy has a clear benefit for critically ill patients with
respiratory failure who are at risk of an exacerbation of asthma or COPD. Although
the central role of inflammation in obstructive airway disease is well established,
corticosteroids may also decrease β-receptor tachyphylaxis. Intravenous and oral
routes are equal in efficacy. Limited consensus exists on dosing schedules in
asthma. Doses of methylprednisolone of 80 mg/24 h have been as effective as >
360 mg/24 h. Some clinicians use doses equivalent to those given for asthma when
treating COPD, whereas others begin with doses equivalent to 1 mg/kg/24 h,
adjusting as patient response dictates. Careful monitoring of corticosteroid adverse
effects is warranted. Acute myopathies have been described after the administration
of moderate to high dosages of corticosteroids in patients with COPD and/or
asthma. After the acute exacerbation, inhaled corticosteroids are often useful
adjuncts to therapy and may allow a reduction in systemic corticosteroid dosage.
However, routine use of inhalational agents is not recommended in the setting of
acute severe bronchospasm. In ARDS, the use of corticosteroids is not well
understood, but may have some benefit in the late phase, between 7 and 13 days
after onset.

4. Antibiotics

Bacterial infection (bronchitis/pneumonia) frequently precipitates ARF. Antibiotics

should be used when there is clinical suspicion that a bacterial respiratory infection
is present (eg, change in sputum characteristics, pulmonary infiltrates on the chest
radiograph, fever, leukocytosis), and they should be chosen to effectively treat the
usual pathogens. Therapy should be subsequently adjusted when culture and
sensitivity data become available.

Several randomized trials have compared clinical outcomes in patients hospitalized

with acute exacerbation of COPD and have shown antibiotic treatment has been
associated with a decreased risk of adverse outcomes. When the decision is made to
use antibiotics, it is important to distinguish a simple from a complicated case of
acute exacerbation of COPD and a 5-day course is usually recommended.

D. Miscellaneous Agent and Treatments

Agents to hydrate or otherwise alter the composition, elasticity, or viscosity of
mucus have been used, although their efficacy has not been consistently
demonstrated except in selected patient groups (eg, patients with cystic fibrosis).
Examples of these agents include mucolytics such as acetylcysteine or propylene
glycol, bronchorrheic agents such as saturated solution of potassium iodide or
glyceryl guaiacolate, and alkalinizing agents such as aerosolized sodium
bicarbonate.

Postural drainage, chest physical therapy, nasotracheal suctioning, incentive

spirometry, intermittent positive pressure breathing, and cough/deep-breathing
exercises have long been used. Also available are newer measures such as positive
expiratory pressure therapy, vest devices (high-frequency chest oscillator), and
mattress percussion devices. Many of these modalities may be applied to treat
specific symptoms of ARF or the cause of respiratory failure. The effectiveness and
positive impact of the contributions of the bedside nurse or the respiratory care
practitioner and the avoidance of intubation/mechanical ventilation should not be
underestimated.

Key Points
Diagnosis and Management of Acute Respiratory Failure
Acute respiratory failure is classified as hypoxemic, hypercapnic, or
mixed. Arterial blood gas measurements are the primary assessment tool
for determining this classification.
The most common pathophysiologic mechanism for hypoxemic acute
respiratory failure is ventilation/perfusion mismatch.
Acute hypercapnic respiratory failure is primarily the result of a change
in one or more determinants of the alveolar minute ventilation equation:
tidal volume, respiratory frequency, and physiologic dead space.
Oxygen supplementation is commonly used to treat hypoxemia. The
oxygen supply device that is chosen must be capable of matching the
oxygen and respiratory flow demands of the patient.
Pharmacologic and therapeutic adjuncts should be considered when
treating patients with acute respiratory failure.

Suggested Readings
1. Cannon J, Colombo C, Pamplin J, et al. Joint Trauma System Clinical
Practice Guideline. Acute Respiratory Failure. U.S. Army Institute of
Surgical Research. Publication date January 23, 2017.
https://jts.amedd.army.mil/assets/docs/cpgs/JTS_Clinical_Practice_Guid
elines_(CPGs)/Acute_Respiratory_Failure_23_Jan_2017_ID06.pdf.
Accessed January 30, 2019.
 2. Chiumello D, Brochard L, Marini J, et al. Respiratory support in
patients with acute respiratory distress syndrome: an expert opinion.
Crit Care. 2017;21(240):1-8.
3. Dolovich MB, Ahrens RC, Hess DR, et al. Device selection and
outcomes of aerosol therapy: Evidence-based guidelines: American
College of Chest Physicians/American College of Asthma, Allergy and
Immunology. Chest. 2005;127(1):335-371.
4. Lodeserto FJ, Lettich TM, Rezaie SR. High-flow Nasal Cannula:
Mechanisms of Action and Adult and Pediatric Indications. Cureus.
2018;10(11):e3639. Published 2018 Nov 26.
doi:10.7759/cureus.3639
5. Manser R, Reid D, Abramson M. Corticosteroids for acute severe
asthma in hospitalized patients. Cochrane Database Syst Rev. 2001;
(1):CD001740. doi:10.1002/14651858.CD001740.
6. Marino PL. The ICU Book. 4th ed. Philadelphia, PA: Wolters Kluwer
Health; 2014:391-464 and 487-586.
7. Pontoppidan H, Geffin B, Lowenstein E. Acute respiratory failure in the
adult: 1. N Engl J Med. 1972;287:690-698.
8. Pontoppidan H, Geffin B, Lowenstein E. Acute respiratory failure in the
adult: 2. N Engl J Med. 1972;287:743-752.
9. Pontoppidan H, Geffin B, Lowenstein E. Acute respiratory failure in the
adult: 3. N Engl J Med. 1972;287:799-806.
10. Rochwerg B, Brochard L, Elliott MW, et al. Official ERS/ATS clinical
practice guidelines: noninvasive ventilation for acute respiratory failure.
Eur Respir J. 2017;50:1602426
[https://doi.org/10.1183/13993003.02426-2016].
11. Spinelli E, Mauri T, Beitler J, Pesenti A, Brodie D. Respiratory drive in
the acute respiratory distress syndrome: pathophysiology, monitoring,
and therapeutic interventions. Intensive Care Medicine.
2020;46(4):606-618.
12. Sponsler K, Markly D, Labrin J. What is the appropriate use of
antibiotics in AECOPD. The Hospitalist. 2012 Jan 26. http://the-
hospitalist.org/issue/january-2012.
 Chapter 5
SURGICAL AIRWAY EMERGENCIES

Objectives
Recognize emergency tracheostomy complications and take immediate action
to re-establish the airway and adequate ventilation.
Consider the clinical setting of postoperative neck hematoma and take
immediate actions to control the airway and provide conditions for surgical
reintervention.
Learn symptoms of upper airway obstruction caused by angioedema.
Review techniques for needle and surgical cricothyroidotomy.

Case Study
A 65-year-old man with a medical history of myocardial infarction and chronic
obstructive pulmonary disease underwent a left carotid endarterectomy under
regional anesthesia. On arrival to the intensive care unit (ICU), he had an infusion
of sodium nitroprusside, with a mean arterial pressure of 110 mm Hg. He was
conscious, with no neurologic deficit, and eupneic, with supplemental O2 by nasal
cannula and SpO2 of 98%.

Two hours after arrival, the patient had a sudden drop of mean arterial pressure,
below 50 mm Hg. He was unresponsive with a respiratory rate of 32 breaths/min,
with an SpO2 of 80%. Inspiratory and expiratory stridor was noted. While assisting
respirations with a bag-valve-mask, the surgical dressing was noted to be displaced
by a large firm mass under the suture line.
– What is the cause of the sudden worsening of this patient’s status?
 – What are the risk factors for this complication?
– What should be your immediate interventions?

I. INTRODUCTION
It is reported that up to 20% of all critical incidents in the ICU are related to the
airway and such incidents may occur at intubation, extubation, or during treatment.
This chapter focuses on airway issues specific to surgical patients.

Tracheostomy complications can challenge providers and acutely endanger patients.

Providers should recognize which surgical procedures can put patients at the risk of
surgical airway emergencies as the result of a postoperative neck hematoma. Also, it
is important for providers to recognize upper airway obstruction resulting from
angioedema (AE). An inadequate consciousness level may compromise the airway
immediately after transfer from the postanesthetic care unit. Finally, this chapter
reviews the indications, anatomy, and emergency surgical airway (needle/surgical
cricothyroidotomy).

II. TRACHEOSTOMY EMERGENCIES AND EARLY

COMPLICATIONS
Several complications and emergencies are related to a tracheostomy procedure.
However, the three most common tracheostomy emergencies are:
1. Loss of airway: tube dislodgement, false lumen
2. Tube obstruction: mucus plugging, other tube malfunction
3. Bleeding: tracheoinnominate artery fistula, stoma hemorrhage

Early recognition of each of these conditions is the key to managing the airway
successfully and adequately ventilating and oxygenating the patient until definitive
surgical treatment is employed to restore the airway.
 If a patient with a tracheostomy has trouble
breathing, check whether the tube is in the correct
position.

One of the early and potentially life-threatening tracheostomy complications and

emergencies is tube displacement within the early post-procedure period (<7
days), before the stoma has matured and the tracheostomy tract has healed. The
normal anatomy after tracheostomy is shown in Figure 5-1. The structure of the
tracheostomy tube is shown in Figure 5-2. The loss of airway could be the result of
the complete displacement of the tracheostomy tube (decannulation) or partial
displacement (dislodgement) or when the tip of the tube is displaced into a false
passage anterior to the trachea into the subcutaneous tissue. When dislodgement
happens, quick diagnosis and immediate response are crucial to success.
Figure 5-1. Normal Anatomy after Tracheostomy
 Figure 5-2. Parts of a Tracheostomy Tube

The risk factors include:

Loose tube ties

Insufficient length of tracheostomy tube for patient anatomy
Soft-tissue or airway edema
Obesity
Excessive movement of the tube because of inadequate sedation and
patient agitation
Persistent coughing
The tube being pulled because of the weight of an unsupported ventilator
circuit
 The surgical technique used for tracheostomy can be a predisposing
factor if the tracheostomy incision is too big for the tube size used

A. Management
It takes about 7 to 10 days for the stoma to heal and the tracheostomy tract to
remain open or mature. If the tube is dislodged or accidentally removed before that
time, the stoma and tissue planes can easily collapse. An attempt to reinsert the
tube blindly will likely be unsuccessful because of the risk of creating a false lumen.
Therefore, the dislodgement of the tracheal tube during the first week post-
procedure is a medical emergency and should be treated as such.

If a tube is removed during the first week after tracheostomy, blind placement
should not be attempted through the tract. Equipment and supplies, including
oxygen bag-mask, suction catheter, and laryngoscope or bronchoscope should be
immediately requested to insert an endotracheal tube by the supraglottic (oral or
nasal) route to secure the airway first before any attempts to reinsert a new
tracheostomy tube under controlled conditions.
When a suction catheter cannot be inserted through the tracheostomy tube beyond
the tube (5–7 cm), it could be a sign of dislodgement, indicating that the tube could
be in a false passage or obstructed by a mucus plug (discussed in next section).

Consider bag-valve-mask ventilation and intubation

(oral or nasal) if a new tracheostomy (within 7 days)
is accidentally dislodged because reinsertion through
the stoma may be difficult.

When suspecting a false tract, the provider should not forcefully manually bag
ventilate the patient through the suspected dislodged tube, especially when
significant resistance is felt during bagging. Forceful bagging can push air into the
subcutaneous tissues and cause subcutaneous emphysema and crepitus in the neck,
face, and upper chest area. This subcutaneous air can make securing the airway
more difficult.
B. Preventive Measures

It is essential to secure the tracheostomy adequately

to avoid accidental dislodgement.

In the postoperative period, the management of a tracheostomy can help prevent

tube dislodgements and avoid potentially catastrophic consequences. Such
measures include keeping tracheostomy ties secure and tight (no more than a single
finger should fit under the ties), removing any traction to the ventilator tubes and
circuit, keeping the tracheostomy tube in the midline and neutral position,
minimizing transport of the patient as much as possible, and adequate sedation to
avoid excessive coughing or agitation by the patient.
When the tracheostomy tube is completely removed from the stoma (decannulation)
and if the stoma is not matured (less than a week old), then the likelihood of
successful tube reinsertion without causing a false lumen is very low. Therefore, the
immediate treatment of decannulation in an immature stoma is bag-mask ventilation
and endotracheal intubation (ETI).

C. Tube Obstruction: Mucus Plugging, Tube Malfunction

If a tracheostomy is in the right place, but a patient

still has trouble breathing, see whether anything is
plugging the tube or not.

When a patient with a tracheostomy tube is in respiratory distress, the first step is to
rule out any obstruction of the tube. To do so, remove the inner cannula and make
sure it is patent. If the cannula is clogged with secretions, debris, and mucus plugs,
it should be cleaned and replaced with a new one. If the patient continues to be in
distress, an attempt to pass a suction catheter down the tracheostomy tube must be
made. If the catheter easily passes and tracheal secretions can be suctioned, the
tube is properly in place, and a primary patient problem should be pursued. If
there is resistance during the passage of the suction catheter, but the catheter can
be passed through, the tube may be partially obstructed with secretions.

Conversely, if a suction catheter cannot be passed at all or cannot be passed

beyond the length of the tracheostomy tube, consideration should be given to a
completely obstructed tube with thick dried secretions or a tube that is lodged in a
false lumen. The management at this point depends on the maturity of the stoma. If
the stoma is more than a week old (mature), then the entire tracheostomy tube must
be removed and replaced. If the stoma is fresh (less than a week old), then bag-
mask ventilation with a deflated cuff (or removed) tracheostomy tube is the safest
intervention, followed by ETI and revision of the tracheostomy later under a
controlled condition. The algorithm for managing tube obstruction is shown in
Figure 5-3.
 Figure 5-3. Tracheostomy Tube Obstruction Troubleshooting

Information taken from Morris LL, Whitmer A, McIntosh E. Tracheostomy Care and
Complications in the Intensive Care Unit. Critical Care Nurse. 2013;33(5):18-29.

D. Bleeding: Stoma Hemorrhage, Tracheoinnominate Artery Fistula

One of the perioperative complications of a new tracheostomy is stoma hemorrhage.
A small amount of bleeding after the procedure is expected and usually self-limited,
but if bleeding at the site continues and is excessive, it should be a serious concern.
In such circumstances, the surgeon should be contacted as soon as possible while
attempting to stop bleeding by applying local pressure.
Another rare but most deadly complication is a tracheoinnominate artery fistula. In
this situation, the innominate artery is eroded through the trachea, causing severe
bleeding resulting in exsanguination or suffocation as a result of blood clot
formation in the airway and aspiration of blood into alveoli. Risk factors for this
complication that often happens 3 to 4 weeks after tracheostomy are:
Pressure necrosis from high pressures tracheostomy tube cuffs
Improper placement of the cannula tip (being pulled due to direct weight
of the ventilator circuit)
Hyperextension of the head causing pressure on the trachea from the tip
of the tube
Radiotherapy of the neck
Prolonged use of a corticosteroid

In the case of a tracheoinnominate fistula, overinflate

the cuff, provide intubation and direct digital
compression, and call surgeons for repair.

Although this is an infrequent complication (a reported incidence of 0.7%), the

mortality rate is almost 100%. Successful management requires quick thinking and
immediate action, including overinflation of the cuff to tamponade the hemorrhage,
and translaryngeal intubation for oxygenation with direct digital compression,
followed by immediate surgery for repair. Another treatment option could be
endovascular embolization.

III. POSTOPERATIVE NECK HEMATOMA

Formation of a neck hematoma (NH) compressing the upper airway may occur after
various neck surgeries (Table 5-1). A retropharyngeal hematoma may occur after
anterior cervical spine surgery.
Many NHs can be treated conservatively, but the patient should be monitored for
signs of airway and hemodynamic compromise. A hematoma that is rapidly
expanding may directly compress the tracheal lumen below the level of the cricoid
cartilage or cause supraglottic edema because of venous and lymphatic congestion,
or both. Symptoms may be absent until the lumen is <5 mm, but compression may
rapidly become life-threatening. In these circumstances, there is a need for
emergency airway management and reoperation.

Common Neck Procedures in which Postoperative Hematomas May

Table 5-1
Occur

Emergency reintubation may be difficult because of a small tracheal lumen,

tracheal deviation, and laryngeal edema. Multiple intubation attempts may result in
oropharyngeal and laryngeal edema or bleeding, further complicating visualization
of upper airway anatomy.

The key to the management of a postoperative neck

hematoma includes early detection, close
observation, airway management, and appropriate
surgical intervention.
At pressures of 257 mm Hg, equivalent to the maximum possible pressure in the
neck (ie, systolic blood pressure), there was an average compression of 20.8% of
the original anterior-posterior tracheal diameter. Pressures in hematomas observed
after neck surgery would be insufficient to cause airway obstruction due to direct
pressure on the trachea. Therefore, the most likely cause of airway obstruction
would be supraglottic edema secondary to venous obstruction.
Respiratory compromise and airway obstruction may occur after anterior cervical
spine surgery. Symptoms developed, on average, 36 hours postoperatively,
attributable to pharyngeal edema.

Risk factors for airway complication are:

Exposing more than three vertebral bodies
Blood loss >300 mL
Exposures involving C2, C3, or C4
Surgical time >5 hours
Myelopathy, spinal cord injury, pulmonary problems, smoking, anesthetic risk
factors, and the absence of a drain did not correlate with an airway complication.

A. Characteristics of Postoperative Neck Hematomas by Procedures

1. Carotid Endarterectomy

Carotid hematoma after carotid endarterectomy (CEA) is a devastating and

relatively common complication, although the incidence of significant hematoma is
reduced. A 10-year retrospective analysis identified patients requiring airway
management for neck exploration within 72 hours after CEA. Neck exploration for
hematoma was required in 1.4% of patients, and most of these required airway
management immediately before neck exploration surgery. The average interval
between the completion of CEA and return to the operating room for hematoma
evacuation was 6.0 hours. Tracheal intubation was accomplished with both
fiberoptic visualization and direct laryngoscopy. In instances of poor direct
visualization of the glottis, decompression of the airway by opening of the surgical
incision may facilitate intubation of the trachea.

2. Cervical Endocrine Surgical Procedures

Airway compromise from postoperative neck hematoma remains the most feared
complication after cervical endocrine surgical procedures, such as thyroidectomy
and parathyroidectomy. These events are rare but potentially lethal because of the
potential for airway compromise, leading to hypoxia and cardiorespiratory arrest.
Critical decision-making is required to simultaneously protect the airway, manage
the wound, and control the bleeding. Reintubation can be more challenging than
the initial intubation. If neck swelling is recognized, the patient should be evaluated
quickly for symptomatology suggestive of airway compromise, such as hypotension
or hypoxia.

3. Cricopharyngeal Dysfunction and Zenker Diverticulum Surgery

After cricopharyngeal dysfunction and Zenker diverticulum surgery correction, a
drain is left for 24 hours to avoid hematomas in the neck region. One of the
complications of the procedure may be the development of hematomas of the
cervical region that can jeopardize the airway patency and require immediate
surgical revision.

B. Management
The first 12 hours are the most critical in managing a patient after CEA surgery. In
addition to the usual care required for a patient recovering from general anesthesia,
the essential factors are observation of the patient’s neurologic status, blood
pressure control (either hypotension or hypertension must be appropriately treated),
and close wound observation. An expanding hematoma should be identified early,
and the patient should be returned promptly to the operating room to identify the
bleeding source and evacuation of the hematoma.
Bleeding is a potentially fatal postoperative complication following central
compartment neck surgery and occurs in less than 2% of cases. Reoperation for
bleeding is an objective measure of this complication and is a quality indicator in
thyroid and parathyroid surgery. The suggested algorithm for the management of
the airway after a postoperative NH is shown in Figure 5-4.

Figure 5-4. Algorithm for Airway Management after Postoperative Neck

Hematoma
Reprinted from Surgery, 160(6), Christakis I, et al., Commentary on: Clinical practice algorithm
for the treatment of cervical hematoma after an endocrine surgical procedure, 1712-1714,
Copyright (2016), with permission from Elsevier.
The American Society of Anesthesiologists (ASA) has developed guidance for
airway management in this setting. If the patient is cooperative, stable, and able to
maintain spontaneous breathing, airway patency, and adequate oxygen saturation,
awake intubation is recommended. Should a life-threatening obstruction occur,
personnel who are able to perform a surgical airway should be prepared to
intervene immediately. Suspicion that the postoperative NH is expanding may be an
indication to open the wound. Spontaneous ventilation should be maintained with
the induction of general anesthesia. The tracheal tube should be placed below the
level of the obstruction and may require fiberoptic confirmation. Use of a
supraglottic airway device is not recommended. Video-assisted laryngoscopy and
flexible scope intubation can be helpful choices if they allow airway visualization.

C. Risk Factors for Postoperative Neck Hematoma

In one recent prospective comparative study, perioperative clopidogrel, combined
with aspirin, was not associated with greater bleeding complications across all
categories of major arterial surgery. Vascular surgeons are regularly confronted with
complex decisions concerning the cessation or continuation of clopidogrel because
an increasing number of vascular patients are on dual antiplatelet therapy (APT).

The main factors associated with reintervention were:

Previous APT
Non-patch surgical techniques
Neurologic instability (shunt use), probably associated with less accurate
hemostasis

Global bleeding is related to the use of P2Y12 inhibitors (ie, clopidogrel)

preoperatively. Postoperative hypertension is also associated with a higher risk of
bleeding. The relationship between airway management technique to patient
outcome has not been systematically studied.
The routine use of an intraoperative drain has not been shown to reduce the
incidence of postoperative neck hematoma. Bleeding rarely occurs from the suture
line. More often, a diffuse ooze is present, requiring reversal of anticoagulation.
Drainage of the hematoma and correction of its cause prevent chronic draining
wounds, infection, and the rare occurrence of pseudoaneurysm formation. The last
issue is more frequent when vessel closure is performed with patch angioplasty.
Given the paucity of evidence-based guidelines on the appropriate use of
perioperative clopidogrel, there appears to be an apparent lack of consensus among
vascular specialists on this issue. A 2009 survey of 399 European surgeons found
that 43% and 55%, respectively, would stop the P2Y12 inhibitor before CEA for
symptomatic and asymptomatic patients.
Antiplatelet/anticoagulant drugs and coagulopathies groups are reported to be risk
factors for NHs requiring reoperation after thyroidectomy. The rate of NH after
thyroidectomy is increased four fold in patients of both groups. No significant
differences for the subgroups of low-dose aspirin, P2Y12 inhibitors, prophylactic
heparin use, and coagulopathies group were reported.

Anticoagulation/antiplatelet therapy is one of the risk

factors for postoperative NH.

The subgroup receiving vitamin K antagonists (eg, warfarin) reported a tenfold

higher incidence than the control group. Half of the NHs reported in both groups
developed after 24 hours from surgery. A strict postoperative and post-discharge
surveillance is mandatory for these patients, given the late NH occurrence.
Outpatient surgery is contraindicated.
Protamine reduced serious bleeding in patients that had used heparin before or
during surgery and requiring reoperation during CEA without increasing the risk of
myocardial infarction, stroke, or death.

D. Therapy

Incising surgical sutures to decompress the NH at the

bedside should be considered if the patient’s airway
is immediately threatened.
A clearly defined, sequential approach to a patient with NH is critical because
preoxygenation may be difficult. Any delay in securing the airway may lead to
rapidly progressing hypoxemia. If the patient is completely asymptomatic, the
surgical team should be informed, the patient should be taken to the operating room
for wound exploration, and staff should be on high alert to open the wound at
bedside if the patient becomes symptomatic. If the patient is symptomatic upon
initial evaluation, it is advisable to actively manage the patient’s airway and
breathing by bag-valve-mask, ETI, and possible cricothyroidotomy while
simultaneously decompressing the hematoma by incising the sutures, including
those approximating the strap muscles. This often can be done either by the on-call
surgical team or under their direction. No local anesthetic is needed, and sterile
technique (gloves and topical preparation) should be used as urgency permits. The
number of ETI attempts allowed before switching to a different technique should be
discussed (no more than two, according to the guidelines from the Difficult Airway
Society).

Be prepared for cricothyroidotomy when securing the

airway of a patient with a NH.

If the ETI is unsuccessful and the face mask and laryngeal mask airway are
inadequate for maintaining ventilation and oxygenation, other noninvasive airway
ventilation techniques should be considered (eg, rigid bronchoscope, esophageal-
tracheal Combitube ventilation, transtracheal jet ventilation). If all of the techniques
listed previously fail, the most qualified provider should perform an emergency
cricothyroidotomy.

If the emergency setting is outside of the operating room, the first responder to a
patient with a NH may have limited experience obtaining a surgical airway. An
emergency surgical airway can be difficult but is usually preferred despite potential
complications. Most providers cannot perform this maneuver effectively within 3
minutes and will take longer. In this situation, a delayed surgical airway can result
in the death of the patient. Cricothyroidotomy can be performed via a percutaneous
or surgical approach. The current airway management guidelines of the “can’t
intubate-can’t ventilate” scenario include using cannula cricothyroidotomy with
percutaneous transtracheal jet ventilation or using surgical cricothyroidotomy.
IV. ANGIOEDEMA

Case Study
A 64-year-old African American woman arrives at the emergency department (ED)
reporting swelling of the tongue and subjective dyspnea of abrupt onset. Her
medical history includes type 2 diabetes mellitus, hypertension, and diastolic
congestive heart failure with prescriptions of beta-blockers and an ACE inhibitor for
many years; in addition, her surgical history consists of a non-diagnostic exploratory
laparotomy 20 years ago. Evaluation of the patient reveals a limited view of the oral
cavity because of tongue swelling, but no stridor or dysphonia is present initially.
Pulse oximetry and vital signs are normal. The patient received therapy with H2
blockers, short-acting nebulized bronchodilators, and systemic steroids. Two hours
later, the patient has no symptomatic improvement and now has drooling and
increasing anxiety.

While waiting for the Ear-Nose-Throat service on-call, the patient receives racemic
epinephrine, and preparations are made for a difficult airway/surgical airway
situation.

What is the cause of this upper airway obstruction scenario?

Why has the standard therapy failed to prevent progression and clinical
deterioration?
What is the appropriate pharmacologic intervention if the patient does
not require an artificial airway yet?

Incidence

Angioedema (AE), also referred to as angioneurotic edema, is a complication with

potential life-threatening consequences since the initial recognition by Osler of
hereditary AE (HAE) in 1885. The early recognition and management of AE are of
great importance to the practitioner in the acute setting and for those in the ED and
the perioperative setting.
 Recognize AE as one of the differential diagnoses of
upper airway obstruction.

The population affected is mostly older individuals and African Americans (AA) in
origin. AE has increased in prevalence according to the Nationwide Emergency
Department Sample (NEDS) 2006–2010 from 29.3 to 35.8 of 100,000 people.
Data obtained from the National Inpatient Samples (NIS) 2000–2009 showed an
increase in total hospitalizations associated with AE, from 3.4 per 100,000 to 5.4
per 100,000, and increased hospitalization rates for individuals of AA origin.

Among hospitalized patients with significant drug-induced AE, the condition is

associated with cardiovascular and antihypertensive agents, particularly angiotensin-
converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs),
even if the drug has been taken for years.

A. Pathophysiology and Classification

AE is the clinical manifestation of edema in the subcutaneous and submucosal
tissues as a result of increased vasodilation and vascular permeability. This process
is triggered by inflammatory activation using a histamine-mediated pathway (HMP)
or a bradykinin-mediated pathway (BMP). The presentation of urticaria/wheals is
generally associated with activation of the HMP while its absence is associated with
activation of BMP.
The pathophysiology of AE depends on the inflammatory pathway activated.

HMP: Typically represented by Type1 hypersensitivity reaction, upon

presentation of an antigen to T-cells (CD4-TH2), stimulates B-cells to
synthesize immunoglobulins, particularly IgE antigen-specific with the
release of histamine and on a late phase response, leukotrienes, and
others. This usually occurs within seconds or minutes after exposure in
the initial stage.
BMP: The release of bradykinin, a vasodilatory mediator, promotes
endothelial cell activation and, consequently, tissue edema. Bradykinin is
released by multiple cells. The mechanisms that promote its production
and prevent its degradation can cause AE. Bradykinin production is
 directly associated with activation of the coagulation cascade, contact, or
complement pathways.

The classification of AE is related to the clinical presentation and the underlying

mechanism involved in the inflammatory response, as defined in Table 5-2.

Table 5-2 Angioedema Classification

Abbreviations: HMP, histamine-mediated pathway; AE, angioedema; BMP, bradykinin-mediated pathway

B. Diagnosis
The initial evaluation and medical history of the patient are essential in the
approach to the patient with AE. Prior medical history, age of the first event,
ethnicity, drug exposure, and family history are relevant.
In women, evaluation of the prescription of hormonal therapy (oral contraceptive
pill, hormone replacement therapy) and pregnancy status are important. In the
perioperative setting, a history of prior adverse drug effect, prior diagnosis of HAE,
and chronic therapy and compliance are important because advanced preparation
of the perioperative period is fundamental. AE can occur in patients without known
drug allergies.

In addition, special populations with special needs or therapies, ie, patients with
hypertension/congestive heart failure and therapies associated with the use of
ACEI/ARB, in the pregnant patient, in labor, or breastfeeding, calls for the need for
alternative maintenance preventive medication in case of HAE.
Triggers associated with HAE attacks include:

Trauma
Medical procedures
Use of estrogen-containing agents
ACEI/ARB
NSAIDs

C. Clinical Manifestations
The clinical manifestations of AE are dependent on the mediator pathway induced
by the trigger cause. The histamine pathway activation is related to a history of
atopy, episodes of anaphylaxis, urticaria, or drug sensitization. If activation of the
bradykinin pathway is suspected, it is vital to evaluate family history (ie, HAE),
history of malignancy, and the use of known trigger drugs, in particular, ACEIs and
ARBs.

Symptoms associated with AE include:

Urticaria (more frequent with HMP) (with pruritus or not)
Swelling of larynx, tongue, lips, eyelids (dysphonia, dysphagia, drooling)
Swelling of distal extremities and urogenital (more frequent with BMP)
Abdominal pain (more frequent with BMP)

The evaluation of patients with AE in the emergency setting would benefit in the
grading of severity because this aids in assessing risk and influences appropriate
disposition.
The suggested staging scale is divided into four stages. The clinical manifestations
correlate with the necessity of a higher level of care.

Stage I presents as facial rash, facial edema, and lip edema, with
outpatient treatment.
 Stage II presents as soft palate edema and is treated on the hospital floor.
Stage III presents as tongue edema and most often requires ICU level of
care.
Stage IV presents as laryngeal edema and requires ICU treatment.
Patients in this stage are more likely to require an artificial airway.
The evaluation of drug-induced AE relies on identifying drug exposure and clinical
presentation (time of onset, drugs used, the potential for pharmacologic interaction,
etc). An example is the use of NSAIDs, more likely associated with histamine
pathway activation, in contrast to the use of ACEI/ARB alone or in association with
others (ie, rTPA) and is associated with activation of the bradykinin pathway.
Finally, recognizing pseudoangioedema in patients with swelling that resembles AE
is very important because it impacts the management and subsequent prognosis.
Examples of pseudoangioedema are acute contact dermatitis, drug rash with
eosinophilia and systemic symptoms (DRESS), hypothyroidism, superior vena cava
syndrome, and subcutaneous emphysema, among others.

D. Pharmacologic Management
In all cases, consideration should be given to performing a laboratory diagnostic
work-up. It is suggested to evaluate IgE levels, tryptase concentration, C4
concentration, C1q level, C1INH concentration, and C1INH function studies.

Secure the airway first for life-threatening upper

airway obstruction due to AE and then consider
pharmacotherapy.

AE is an emergent, life-threatening situation. To address upper airway obstruction,

the application of the Upper Airway Emergency Protocol is recommended (see
Section V - EMERGENCY SURGICAL AIRWAY). Once the airway has been
evaluated and secured, in addition to hemodynamic stabilization, if necessary, the
patient would benefit from standard therapy based on epinephrine, anti-histaminic
(H1 and H2 blockers), and systemic steroids.
Pharmacologic agents commonly used for the therapy of AE associated with
histamine release are:

1. Epinephrine

In the patient with hemodynamic instability or with manifestations of upper airway

compromise, the administration of SQ/IM epinephrine in doses of 0.01 mg/kg of a
1:1,000 solution and up to 0.5 mg is warranted.

2. Antihistaminic Therapy

The use of antihistaminic therapy uses both H1 and H2 receptor blockers. H1

blockers, like diphenhydramine (or chlorpheniramine), taking advantage of the
availability in IV form, are suggested. Be aware of potential adverse effects such as
somnolence, urinary retention, and delirium in susceptible individuals like the
elderly. Alternatively, the use of non-sedating H1 blockers is acceptable, if
tolerated, and in non-severe cases. The use of H2 blockers is common practice in
the acute setting. The use of H2RA with H1 blockers is standard of care to block
histamine from multiple pathways.

3. Systemic Steroids

Corticosteroids are of common use for the acute management of AE. In the acute
setting, the use of methylprednisolone in doses of 60–120 mg IV is suggested. Oral
corticosteroids could be used, if tolerated, in non-severe cases. Individuals allergic
to methylprednisolone or prednisone could alternatively benefit from the use of
dexamethasone. If the type of AE is not known, there is no contraindication for the
administration of epinephrine, antihistamines, and systemic steroids. Bradykinin-
mediated AE would typically not respond to the therapy suggested previously, and
progression may occur.

4. Specific Therapy

The use of specific therapy in the acute setting is relevant in individuals with HAE
Type 1 and 2 (HAE-1 and HAE-2), HAE-nC1INH, and HAE associated with
ACEI/ARB. Consensus recommendations for the therapy of these types of HAE in
the acute setting are included in Table 5-3.

5. Plasma-derived C1INH
C1 esterase inhibitor (human) is indicated for the acute treatment and the
prophylactic therapy of HAE in adults and children and the treatment of HAE-
C1INH deficiency. The medication is administered intravenously. The adverse drug
effects include hypersensitivity (including anaphylaxis), thromboembolic events, and
risk of transmission of infectious pathogens from the donor’s plasma. This product
is obtained from human plasma. Although donations are screened, tested, and
inactivated, there is a risk that it may contain infectious agents that can transmit
diseases from donor to patient. Patients should be monitored for arterial and venous
thromboembolic events, particularly those with preexisting risks from thrombosis
like immobility, morbid obesity, and hormone use.

Drugs Used for Short- and Long-Term Prophylaxis of Hereditary

Table 5-3
Angioedema

*MASP denotes mannose-binding lectin-associated serine protease.

6. Ecallantide
Ecallantide is a plasma kallikrein inhibitor that reduces the kallikrein-mediated
production of bradykinin. It is indicated and approved for the treatment of acute
HAE attacks in patients older than 12 years of age. The administration is by a set of
three 10-mg SQ injections under direct supervision; all three injections may be
administered in the same or different locations. An additional divided 30-mg dose
may be administered within 24 hours if AE persists. Adverse drug effects include
hypersensitivity reactions (including anaphylaxis), which can occur in up to 3% of
cases. Some patients may develop antibodies to the medication, which may increase
the risk of hypersensitivity reactions. Other adverse reactions occurring in ≥ 5% of
patients include headache, diarrhea, neutropenia, and pruritus.

7. Icatibant

Icatibant is a selective bradykinin-B2 receptor antagonist which blocks the vascular

effects of bradykinin. It is indicated for the acute treatment of HAE in adults older
than18 years of age. Expert opinion favors its use in acute AE associated with
ACEI/ARB use, particularly if given within the first few hours of symptom onset
before swelling has peaked. The administration is by single 30-mg SQ injection,
which may be repeated every 6 hours if the patient does not have an adequate
response or if symptoms reappear up to a maximum dose of 90 mg per day. It is
common for patients to develop an injection site reaction, which occurs in up to
97% of patients. Up to 4% of patients may develop antibodies to the medication.
Other adverse effects include increased liver function tests, dizziness, and fever, all
of which occur in less than 5% of patients.

8. Fresh Frozen Plasma

In areas where direct therapy is not available, fresh frozen plasma administration
may be the only therapy available for acute HAE attacks, including AE associated
with ACEI/ARB use. It appears effective in most incidences of bradykinin-mediated
AE. Administer an IV of 2 units for <90 kg or 3 units for >90 kg, with repeated
dosing, if required. Consideration has to be given to the risk of transmissible
diseases and transfusion reactions.

E. Perioperative Management
 Plasma-derived C1INH, androgens, and FFP can be
used for prophylaxis of AE for patients at high risk.

In the setting of perioperative or preprocedural (medical, surgical, or dental),

prophylaxis is recommended if any mechanical impact will occur in the upper
respiratory/digestive tract of patients with HAE. The drug of choice is the
administration of plasma-derived C1INH. Consideration for the administration of
fresh frozen plasma (FFP) should be given if resources are limited. These
procedures are to be performed in a controlled environment because these
interventions are not 100% effective.

In the management of an obstetric patient with HAE, it is advised to prefer vaginal

delivery. When needed, an artificial airway can be prepared for difficult airway
management, and if a cesarean section is needed, consider the administration of
plasma-derived C1INH.

F. Management of Drug-Induced Angioedema

The management of drug-induced AE in the acute setting depends on the
assessment of the airway involvement and the recognition of the offending drug and
its pathophysiologic action. In the event of drugs triggering the HMP, it is
recommended to use the standard acute pharmacologic therapy discussed
previously.

Alternatively, interference with arachidonic acid metabolism (ie, NSAIDs)

could trigger AE.
Drugs interfering with bradykinin metabolism, increasing bradykinin
level (ie, rTPA and ACEI/ARB) have the potential for additive adverse
effect when used in combination.
Consideration should be given to the increased risk for AE in patients
older than 40 years of age, of African American descent, and females.
Expert opinion for the treatment of ACEI/ARB-induced AE in the acute
setting is the use of icatibant or ecallantide when available.

G. Other Types of Management

Acquired-AE is infrequent with a reported prevalence of 1:100,000 to 1:500,000
in the general population. Clinical manifestations are the same as HAE, although it
is often associated with lymphoproliferative disorders or antibodies against C1INH.
The treatment in the acute setting is the same as in HAE.

Idiopathic AE refers to patients with clinical manifestation of AE in which no

identifiable causality is related to recurrent attacks. Management in the acute setting
is standard pharmacologic therapy and supportive care in a monitored environment
if indicated.

V. EMERGENCY SURGICAL AIRWAY

The emergency surgical airway is indicated in the presence of acute airway
obstruction (AAO) or predictably difficult airway (nasal or oral) in addition to the
“cannot intubate-cannot ventilate (CICV)” scenario. The situational emergency
could significantly compromise the morbidity and mortality associated with the
procedure. A multidisciplinary team approach, advanced evaluation, and risk
assessment, with appropriate planning (when possible) with more than one initiative
available, is recommended.

A. Acute Airway Obstruction

The most common manifestations associated with AAO that could require
emergency surgical airway are stridor, dysphagia, hoarseness, dyspnea, neck mass,
and pain. In the patient with AAO, in addition to clinical evaluation, the use of
direct laryngoscopy (direct visualization vs. indirect video laryngoscopy) or naso-
endoscopic evaluation allows an estimate of the level of compromise of the patient’s
airway (Figure 5-5). If possible, imaging via computed tomography or
ultrasonography scanning would be helpful if timing and safety allow.
 Figure 5-5. Modified Cormack-Lehane Score Classification
(Laryngoscopy)

Reproduced with permission Madden MA, ed Pediatric Fundamental Critical Care Support. 2nd
ed. Mount Prospect, IL: Society of Critical Care Medicine; 2013. Copyright © 2013 the Society of
Critical Care Medicine.

Before attempting intubation, clinicians should assess the patient’s airway to predict
the difficulty of intubation. When such difficulties are encountered, surgeons who
can implement an emergency surgical airway may need to be on standby.
Conditions associated with airway difficulty are listed here.

Abnormal facial anatomy/development

Small mouth or large tongue

Dental abnormality
Prognathia
 Obesity
Advanced pregnancy
Acromegaly
Congenital syndromes

Inability to open mouth

Masseter muscle spasm (dental abscess)

Temporomandibular joint dysfunction
Facial burns
Postradiotherapy fibrosis
Scleroderma

Cervical immobility/abnormality

Short neck/obesity
Poor cervical mobility (eg, ankylosing spondylitis)
Previous cervical spine surgery
Presence of cervical collar
Postradiotherapy fibrosis

Pharyngeal or laryngeal abnormality

High or anterior larynx

Deep vallecula: inability to reach base of epiglottis with blade of scope
Anatomic abnormality of epiglottis or hypopharynx (eg, tumor)
Subglottic stenosis

Injury
Traumatic debris
Obstructing foreign bodies
 Basilar skull fracture
Bleeding into airway or adjacent swelling/hematoma
Fractures of maxilla/mandible
Cervical spine instability (confirmed or potential)
Laryngeal fracture or disruption

Infections
Epiglottitis
Abscess
Croup, bronchiolitis
Laryngeal papillomatosis
Tetanus/trismus

Connective tissue/inflammatory disorders

Rheumatoid arthritis: temporomandibular joint or cervical spine

involvement, cricoarytenoid arthritis
Scleroderma
Sarcoidosis

Endocrine disorders

Goiter: airway compression or deviation

Hypothyroidism: acromegaly: large tongue

Data from Lavery GG, Craig TR. Airway management in the critically ill adult. In:
Parrillo JE, Dellinger RP, eds. Critical Care Medicine. 4th ed. Philadelphia, PA:
Elsevier Saunders; 2014:11–30.

The Mallampati classifications are a helpful tool for assessing the potential for
difficult intubation (Figure 5-6). Any airway obstruction caused by edema of the
glottis, fracture of the larynx, or severe oropharyngeal hemorrhage presents an
immediate challenge. The restriction of cervical spinal motion in most patients with
blunt trauma increases the difficulty of establishing an airway.
Figure 5-7 displays the difficult airway algorithm. The inability to intubate the
trachea indicates an alternative airway plan, including a laryngeal mask airway,
laryngeal tube airway, or surgical airway. A surgical airway (ie, cricothyroidotomy
or tracheostomy) is indicated through the vocal cords. A surgical cricothyroidotomy
is a preferable way to establish the airway because it is easier to perform, is
associated with less bleeding, and requires less time than an emergency
tracheostomy.

Figure 5-6. Mallampati Classifications

Reproduced with permission Killu K, Sarani B, eds. Fundamental Critical Care Support, 6th ed.
Mount Prospect IL: Society of Critical Care Medicine; 2017. Copyright © 2017 the Society of
Critical Care Medicine.
 Figure 5-7. Management of the Difficult Airway

Abbreviations: LMA, laryngeal mask airway; ET, esophageal-tracheal

Reproduced with permission Killu K, Sarani B, eds. Fundamental Critical Care Support, 6th ed.
Mount Prospect IL: Society of Critical Care Medicine; 2017. Copyright © 2017 the Society of
Critical Care Medicine.

B. “Cannot Intubate – Cannot Ventilate”

 To manage the difficult airway, judgment, skill, and
teamwork are all critical.

“Cannot intubate-cannot ventilate (CICV)” is an uncommon but life-threatening

situation. Efficient teamwork with dedicated team members is crucial in overcoming
this predicament. Clinicians who are skilled at cricothyroidotomy (needle or
surgical) should be involved in the team.

C. Anatomy
The cricothyroid muscles are attached to the cricothyroid membrane, which is
diamond-shaped and lies between the thyroid and the cricoid cartilages. In adults,
the cricothyroid membrane is 1 centimeter in height and 2 to 3 centimeters wide.
The membrane between the cricothyroid muscles is only 1 centimeter. It is critical
to recognize the location of the cricothyroid membrane when performing
cricothyroidotomy (Figure 5-8).
 Figure 5-8. Anatomy for Cricothyroidotomy

Locate the cricothyroid membrane first for the

cricothyroidotomy.

The cricoid cartilage is the only circumferential structure among other structures
composing the trachea. It supports the upper airway and is attached to muscles and
ligaments. The vocal cords are attached to the inner anterior part of the thyroid
cartilage and located about 1 centimeter cephalad to the upper edge of the
cricothyroid membrane.

D. Needle Cricothyroidotomy
Needle cricothyroidotomy is accomplished by inserting a needle through the
cricothyroid membrane into the trachea to provide oxygen on a short-term basis (for
30 to 40 minutes) until a definitive airway can be placed. The percutaneous
transtracheal oxygenation (PTO) technique is performed by placing a large-caliber
plastic cannula (12- to 14-gauge in adults and 16- to 18-gauge in children) through
the cricothyroid membrane into the trachea below the level of the obstruction
(Figure 5-9 A and 5-9 B). The cannula is then connected to oxygen flow at 15
L/min (50 to 60 psi) with a Y-connector or a side hole cut in the tubing between the
oxygen source and the plastic cannula. Intermittent insufflation, 1 second on and 4
seconds off, can be achieved by placing the thumb over the open end of the Y-
connector or side hole.

Figure 5-9 A - D. Percutaneous Cricothyroidotomy

Figure 5-9 A. Identify the cricothyroid membrane and the midline.

Insert a 14-gauge intravenous cannula and syringe through the skin and
membrane. Continuously apply negative pressure until air enters the
syringe.
Figure 5-9 B. Stop at this point and push the cannula off the needle into
the trachea. Insert the J wire into the cannula advancing only to the
estimated level of the carina. Remove the cannula over the wire leaving
the wire in place.
Figure 5-9 C. Thread the cricothyroidotomy cannula on to the J wire and
advance into the trachea over the wire in a controlled fashion. Remove
the wire assuring it is intact.
 Figure 5-9 D. Secure the cannula adequately. The insertion of the
cannula into the trachea allows apneic (low-pressure) ventilation or jet
(high-pressure) ventilation.

Of note, the use of PTO should be minimized in patients with head injuries because
CO2 slowly accumulates as a result of inadequate exhalation. Moreover, significant
barotrauma, including pulmonary rupture with tension pneumothorax, can occur
following PTO if there is complete foreign body obstruction of the glottic area.
Careful attention must be paid to the preservation of effective inhalation and
exhalation. Commercial kits are available that include small-diameter cannulae with
a flange that can be used similar to a tracheostomy tube temporarily (Figure 5-9 C,
and 5-9 D).

Needle cricothyroidotomy provides a temporal

airway. Tracheostomy needs to be followed as a
definitive airway.
E. Surgical Cricothyroidotomy

Surgical cricothyroidotomy with a cuffed

endotracheal tube can provide a definitive airway.

Surgical cricothyroidotomy is accomplished by making a skin incision that extends

through the cricothyroid membrane (Figure 5-10 A-D). This establishes a definitive
airway, which allows positive-pressure ventilation for considerable periods and
protects against pulmonary aspiration.

Figure 5-10 A - D. Surgical Cricothyrotomy

Figure 5-10 A. Make a 1.5-cm vertical skin incision over the cricothyroid
membrane. (A vertical incision is recommended because it allows the
surgeon to extend the incision up and down when the patient’s anatomic
landmarks are obscured to determine the level of the cricothyroid
membrane. Also, it avoids injury to the anterior jugular veins, which are
located just lateral to the midline).
Figure 5-10 B. Incise the superficial fascia and subcutaneous fat.
Figure 5-10 C. Divide the cricothyroid membrane transversely with a
short blade, blunt forceps, or the handle of a scalpel.
 Figure 5-10 D. Insert a small endotracheal or tracheostomy tube
(preferably 5- to 7-mm internal diameter) or tracheostomy tube
(preferably 5- to 7-mm outer diameter) through the membrane between
the thyroid and cricoid cartilages.

Choose needle cricothyroidotomy rather than

surgical cricothyroidotomy for pediatric patients
younger than 12 years of age.

When an endotracheal tube is used, it must be adequately secured to prevent

malpositioning, such as slipping into the bronchus or complete dislodgement.

For pediatric patients younger than 12 years of age, surgical cricothyroidotomy is

not recommended to avoid damage to the cricoid cartilage, which is the only
circumferential support for the upper trachea.
Key Points
Surgical Airway Emergencies
When tracheostomy tube dislodgement or decannulation happens, quick
diagnosis and immediate response are the keys to success.
The age of the stoma following a tracheostomy is the most crucial
determinant factor in what course of action is to be taken to secure the
airway and deliver adequate oxygenation.
In cases of rapid expansion of a neck hematoma, the neck incision should
be reopened and the clot evacuated before attempting reintubation.
Complete airway obstruction may, in extreme circumstances, necessitate
emergency cricothyrotomy or tracheostomy.
Angioedema is one of the airway-threatening events in perioperative
patients. It is essential to know the risk factors for angioedema.
Once symptoms of angioedema are recognized, epinephrine,
antihistamines, and steroids are choices for treatment in the acute setting.
Plasma-derived C1inhibitor is indicated for patients with HAE with
C1NH deficiency. The most severe manifestation is upper airway
obstruction due to laryngeal edema. If this is the case, the difficult airway
algorithm should be followed. Healthcare providers should anticipate an
emergency surgical airway.
Needle or surgical cricothyroidotomy may be necessary for the presence
of acute airway obstruction, difficult airway, and “cannot intubate-cannot
ventilate” situation. Teamwork with a multidisciplinary team member
involving clinicians skilled at airway management is critical.

Suggested Readings
1. Bernstein JA, Cremonesi P, Hoffmann TK, Hollingsworth J.
Angioedema in the emergency department: A practical guide to
 differential diagnosis and management. Int J Emerg Med.
2017;10(1):15.
2. Bove MJ, Morris LL. Complications and emergency procedures. In:
Morris LL, Afifi MS, eds. Tracheostomies: The Complete Guide. NY:
Springer Publishing Co LLC; 2010:277-302.
3. Christakis I, Perrier ND. Commentary on: Clinical practice algorithm for
the treatment of cervical hematoma after an endocrine surgical
procedure. Surgery. 2016;160(6):1712-1714.
4. Friedman Y, Sobek S. Tracheostomy. In: Parrillo JE, Dellinger RP,
eds. Critical Care Medicine. 4th ed. Philadelphia, PA: Elsevier
Saunders; 2014:202-212.
5. Hagberg CA, Kaslow O. Difficult airway management algorithm in
trauma: Updated by COTEP. ASA Monitor 2014; 78:56. Available at
www.asahq.org.
6. Lavery GG, Craig TR. Airway management in the critically ill adult. In:
Parrillo JE, Dellinger RP, eds. Critical Care Medicine. 4th ed.
Philadelphia, PA: Elsevier Saunders; 2014:11-30.
7. Maurer M, Magerl M, Ansotegui I, et al. The international WAO/EAACI
guideline for the management of hereditary angioedema – the 2017
revision and update. Allergy. 2018;73(8):1575-1596.
8. Moellman JJ, Bernstein JA, Lindsell C, et al. A consensus parameter for
the evaluation and management of angioedema in the emergency
department. Acad Emerg Med. 2014;21(4):469-484.
9. Morris LL, Whitmer A, McIntosh E. Tracheostomy care and
complications in the intensive care unit. Crit Care Nurse.
2013;33(5):18-30.

Suggested Websites
1. https://www.researchgate.net/figure/Suggested-clinical-practice-
algorithm-for-management-of-the-airway-in-patients-
who_fig1_303597347. Accessed on July 19, 2018.
2. Open Access Atlas of Otolaryngology, Head & Neck Operative Surgery
https://vula.uct.ac.za/access/content/group/ba5fb1bd-be95-48e5-81be-
586fbaeba29d/Cricothyroidotomy%20and%20needle%20cricothyroto
my.pdf
3. Open Access Atlas of Otolaryngology, Head & Neck Operative Surgery
https://vula.uct.ac.za/access/content/group/ba5fb1bd-be95-48e5-81be-
586fbaeba29d/Percutaneous%20dilational%20tracheostomy%20surgic
al%20technique.pdf%20
 Chapter 6
MECHANICAL VENTILATION

Objectives
Discuss the indications and techniques for noninvasive positive
pressure ventilation.
Describe the clinical parameters that should be reviewed to decide
whether the patient is failing to respond to noninvasive methods and
requires invasive mechanical ventilation.
Describe the characteristics of different types of breaths and modes of
mechanical ventilation.
Outline ventilator settings and monitoring needs for the initiation of
mechanical ventilation.
Describe interactions between ventilatory parameters and
modifications needed to avoid harmful effects of mechanical
ventilation.
Review the guidelines for initial ventilator management that apply to
specific clinical situations.

Case Study
A 67-year-old woman with severe chronic obstructive pulmonary disease
presents to the hospital and reports an upper respiratory tract illness and
increasing shortness of breath of 2 days’ duration. She has been using her
home nebulizers without relief. Her vital signs show a blood pressure of
140/90 mm Hg, heart rate of 122 beats/min, respirations of 32 breaths/min,
and a temperature of 37.2°C (99.0°F). Physical examination is remarkable
for use of accessory muscles of respiration and diffuse wheezing bilaterally.
She is alert but unable to speak in full sentences. An arterial blood gas
analysis demonstrates a pH of 7.49, PCO2 of 29 mm Hg, and a PO2 of 48
mm Hg. Bronchodilator therapy is started, and the woman is given IV
steroids.
– What type of respiratory support should be initiated?
– What settings should be selected for respiratory support?
– What are the goals of respiratory support?

I. INTRODUCTION
When hypoxic or hypercapnic respiratory failure cannot be treated by other
means, advanced support with positive pressure ventilation may be needed. A
ventilator is a device used to assist or replace the work of the respiratory
system. Positive pressure ventilation can be delivered noninvasively via a
mask or helmet or invasively via an endotracheal tube or tracheostomy.
Generally accepted indications for initiating positive pressure ventilatory
support are summarized in Table 6-1.

Table 6-1 Indications for Positive Pressure Ventilatory Support

II. NONINVASIVE POSITIVE PRESSURE VENTILATION
A. What Is Noninvasive Positive Pressure Ventilation?
Noninvasive positive pressure ventilation (NPPV) refers to a form of
mechanical ventilation that provides respiratory assistance without an invasive
artificial airway. The potential beneficial effects of NPPV are similar to those
of invasive mechanical ventilation and include decreased work of breathing,
improved oxygenation, and improved gas exchange. In addition, this type of
ventilation avoids many of the complications associated with intubation and
invasive mechanical ventilation. Potential advantages and disadvantages of
NPPV are listed in Table 6-2.

Table 6-2 Advantages and Disadvantages of Noninvasive Positive Pressure

 Ventilation

B. How Does NPPV Work?

NPPV uses two levels of positive airway pressure, combining the modalities of
pressure support ventilation (PSV) and continuous positive airway pressure
(CPAP) (discussed later). By convention, the PSV modality is referred to as
IPAP (inspiratory positive airway pressure), and the CPAP modality is
referred to as EPAP (expiratory positive airway pressure). CPAP alone can
also be delivered noninvasively but does not provide support of ventilation.
CPAP allows spontaneous breathing from a gas source at an elevated baseline
system pressure (higher than atmospheric pressure) and is functionally
equivalent to positive end-expiratory pressure (PEEP). The difference
between these two pressure levels (ΔP) determines tidal volume generated.
NPPV can be delivered using a standard ICU ventilator or a portable device.
The benefits of using an ICU ventilator include delivery of a more precise and
higher concentration of oxygen, the separation of inspiratory and expiratory
tubing to prevent rebreathing CO2, better monitoring and alarm features, and
improved detection of air leaks. Alarm setups may need to be altered on
standard ventilators because the alarms are typically triggered by exhalation,
and noninvasive ventilation inherently has more gas leakage compared with
ventilation via an endotracheal tube. Ventilators specifically designed to
provide patient-triggered noninvasive pressure support or patient-triggered
volume-cycled breaths are optimal.

C. What Types of Interfaces Are Available?

The ventilator connects to a tightly fitted face mask, nasal mask, nasal plugs,
or a helmet (Figure 6-1). Many patients with acute respiratory failure are
mouth breathers, so the face mask is preferred because it is associated with
smaller leaks than the nasal plugs and nasal mask. The nasal passages may
offer significant resistance to airflow, limiting the benefits of NPPV. Some gas
leakage is anticipated with both masks and can be compensated for by
increasing pressure settings or increasing the set tidal volume (VT) level.
When a nasal mask is used, the patient’s mouth should be kept closed or chin
straps should be employed to reduce leakage.

The use of the helmet as an interface for the NPPV device has been
increasing recently. The levels of PEEP that can be delivered through the
helmet can be higher than those that can be obtained with other interfaces or
with a high-flow nasal cannula. Benefits of the helmet include comfort, where
the patient can move more freely, or the ability to partially preserve some
intake, like drinking through a straw if needed. In addition, less skin injury
and lacerations are noted. Assessing the tidal volume is usually difficult when
using a helmet because of varying distention. Disadvantages could include
noise, accumulation of CO2 in the helmet, and desynchrony between the
patient and the ventilator because of less sensitivity of triggering.

Figure 6-1. Devices for Delivery of Noninvasive Positive Pressure

Ventilation

Examples of noninvasive positive pressure ventilation delivery devices: A, face mask; B,

total face mask; C, nasal mask with chin strap; and D, helmet.
D. Which Patients Benefit From NPPV?
Before NPPV is initiated, patient characteristics and the potential for
successfully treating the underlying respiratory condition should be evaluated.
Table 6-3 lists conditions leading to respiratory failure that are likely to
improve with use of NPPV. Of these, acute exacerbations of chronic
obstructive pulmonary disease and cardiogenic pulmonary edema are the two
conditions best studied and they have accepted indications for the application
of NPPV. An approach to initiating NPPV after appropriate patient evaluation
is outlined in Table 6-4. NPPV is best used in the alert, cooperative patient
whose respiratory condition is expected to improve in 24 to 48 hours.
Potential candidates should be hemodynamically stable, able to control airway
secretions, and able to synchronize with the ventilator. If a provider skilled in
the application of NPPV is not available, if the patient is too sick for this
support, or if NPPV has failed to benefit the patient, it is critical to move
quickly to invasive mechanical ventilation.

Respiratory Conditions Likely to Respond to Noninvasive Positive

Table 6-3
Pressure Ventilation

Table 6-4 Initiation of Noninvasive Positive Pressure Ventilation

Abbreviations: ABG, arterial blood gas; EPAP, expiratory positive airway pressure; IPAP, inspiratory
positive airway pressure; NPPV, noninvasive positive pressure ventilation; VT, tidal volume

E. Which Patients Should Not Receive Noninvasive Mechanical

Ventilation?
In general, NPPV should not be initiated in the following circumstances:
uncooperative patients; patients with difficulty clearing secretions, recurrent
emesis, or post-cardiac or respiratory arrest; and patients with hemodynamic
instability. A more detailed list of contraindications for the use of NPPV is
presented in Table 6-5.

Contraindications to Use of Noninvasive Positive Pressure

Table 6-5
Ventilation
F. How Are Patients Monitored on NPPV?

Avoid inspiratory pressures greater than 20 cm

H2O because gastric distension can occur.

Patients receiving NPPV must be monitored closely in a proper setting, and

continuous pulse oximetry and cardiac monitoring are suggested. Close
clinical follow-up assessments are required, including evaluations of the pH,
PaO2, and PaCO2. Consider transition to invasive ventilation when a clear
trend toward improvement has not been observed over the first 1 or 2 hours,
or when the therapeutic goals have not been achieved within the first 4 to 6
hours. Sedation should be used cautiously and with adequate monitoring
when NPPV is initiated. Additional measures that may be considered include
application of a protective nose and mouth patch to protect any pressure
injuries and gastric decompression if a face mask or helmet is used. Oral
intake should be restricted until the patient has stabilized and intubation is no
longer a consideration. An algorithm for assessing NPPV is presented in
Figure 6-2.

Figure 6-2. Assessment of Noninvasive Positive Pressure

Ventilation

Abbreviations: ARF, acute respiratory failure; NPPV, noninvasive positive pressure

ventilation
 Case Study (continued)
Noninvasive positive pressure ventilation is initiated. Two hours after
initiation, the patient exhibits persistent marked accessory muscle use and
altered mental status. Vitals signs now show a heart rate of 130 beats/min,
blood pressure of 160/90 mm Hg, respiratory rate of 32 breaths/min, and
temperature of 36.6°C (98°F). Arterial blood gas demonstrates a pH of
7.27, PCO2 of 60 mm Hg, and PO2 of 90 mm Hg. Patient is now somnolent.

– Should this patient be intubated and invasive mechanical ventilation

initiated?
– What are the initial settings on invasive mechanical ventilation?
– How should patients on invasive mechanical ventilation be monitored?

III. DECISION TO INTUBATE

The decision to initiate invasive mechanical ventilation is a crucial and time-
sensitive one. Delay in intubation, inability to identify a difficult airway, and
inability to anticipate possible hemodynamic consequences of intubation can
reduce the likelihood of good patient outcomes. In general, consideration of
three quick bedside questions can help facilitate a prompt decision to proceed
with invasive mechanical ventilation, especially when transitioning from
noninvasive ventilation.

Is there failure in airway maintenance or protection (eg, inability to

handle secretions)?
Is there failure to achieve desired goals with current respiratory
support (oxygenation, ventilation, or work of breathing)?
Is the illness anticipated to worsen in the next 24 to 48 hours?

IV. INVASIVE MECHANICAL VENTILATION

Mechanical ventilation via an endotracheal tube is commonly used to support
critically ill patients. It is a definitive intervention with the goal of obtaining
acceptable oxygenation and ventilation with a secure airway.

Each mechanical ventilation respiratory cycle can be divided into two phases:
inspiration and expiration (Figure 6-3A).

The respiratory cycle is the time from the initiation of one breath until the
initiation of the next breath. Triggering (A) signals the transition from
expiration to inspiration; cycling (C) indicates the transition from inspiration to
expiration. Other components of the total respiratory cycle (ABCD) include
inspiratory pause (BC), inspiration (ABC), and expiration (CD). Spontaneous
breaths do not include an inspiratory pause. The spontaneous respiratory
cycle (ACD) is demonstrated in Figure 6-3B.

Figure 6-3. Respiratory Cycle During Mechanical Ventilation and

Spontaneous Breathing
Inspiration is the point at which the exhalation valve closes and fresh gas
under pressure from the ventilator enters the chest. The amount of gas
delivered during inspiration is determined by any of three targets that can be
set on the ventilator: volume, pressure, and/or flow.

Cycling is the changeover from the end of inspiration to the expiratory phase.
It occurs in response to one of three parameters: elapsed time, delivered
volume, or a decrease in flow rate. During expiration, the ventilator gas flow
is stopped, and the exhalation circuit is opened to allow gas to escape
passively from the lungs. Expiration continues until the next inspiration
begins.

Triggering is the changeover from expiration to inspiration. Triggering a

ventilator-delivered breath depends on the patient’s interaction with the
ventilator:

Assisted breath: The patient initiates a breath, and this inspiratory

effort produces a drop in airway pressures or a diversion of
constant gas flow in the ventilator circuitry. A signal triggers the
ventilator to deliver a breath. This is an example of partial
ventilator control.
Unassisted, mandatory, or controlled breath: In the absence of
patient interaction with the ventilator, breaths are delivered based
on elapsed time (eg, at a set rate of 10 breaths/min and no
detection of patient effort, the ventilator will be triggered every 6
seconds). This is an example of full ventilator control.

Spontaneous breaths (no ventilator assistance) are also possible in

synchronized intermittent mandatory ventilation (SIMV) and bilevel
ventilation. The most common ventilator breaths are described later. CPAP
allows spontaneous breathing at a higher baseline pressure.

V. TYPES OF TARGETED/CYCLED BREATHS

A. Volume-Cycled Breath
A volume-cycled breath, often called volume assist-control breath, ensures
the delivery of a preset tidal volume (unless the peak pressure limit is
exceeded). On most ventilators, the setting of peak inspiratory flow rate and
the choice of inspiratory flow waveform (square, sine, or decelerating)
determine the length of inspiration. Some ventilators change the peak
inspiratory flow rate to maintain constant inspiratory time on switching
between a constant flow (square) and decelerating flow (ramp) waveforms.
With volume-cycled breaths, worsening airway resistance or lung/chest-wall
compliance results in increases in peak inspiratory pressure to maintain the
set tidal volume (unless the peak pressure limit is exceeded and the ventilator
will discontinue the remainder of the breath to avoid excessively high
inspiratory pressures).

B. Time-Cycled Breath
A time-cycled breath, often called pressure assist-control breath, applies a
constant pressure for a preset time. The application of pressure throughout
inspiration results in a square (constant) pressure-over-time waveform during
inspiration and a decelerating inspiratory flow waveform as the pressure
gradient falls between the ventilator and the patient (since pressure rises as
the lung fills). Flow in this breath format is variable and this leads to variable
tidal volume depending on lung compliance. Flow depends on the resistance
of the lung, the compliance of the lung, and patient effort. With this type of
breath, changes in airway resistance or lung/chest-wall compliance will alter
tidal volume (ie, worsening of airway resistance or lung compliance results in
a decrease in tidal volume).

C. Flow-Cycled Breath
A flow-cycled breath, usually called a pressure support breath, is a
spontaneous mode of ventilation. The patient initiates every breath and the
ventilator delivers support with the preset pressure value. With this support,
the patient self-regulates the respiratory rate and tidal volume. The set
inspiratory pressure support level is kept constant with a decelerating flow.
The patient triggers all breaths. A change in the mechanical properties of the
lung/thorax and/or patient effort affects the delivered tidal volume. The
pressure support level must be regulated to obtain the desired ventilation.

Pressure support breaths are terminated when the flow rate decreases to a
predetermined percentage of the initial peak flow rate (typically 25%). As the
patient’s inspiratory effort decreases, the flow decreases, marking the
proximity of the end of inspiration.

VI. MODES OF MECHANICAL VENTILATION

The mode of ventilation describes how one or more types of ventilator breaths
interface with the patient to provide ventilatory support. When mechanical
ventilation is initiated, the optimum ventilatory support for a given clinical
circumstance and the specific needs of the patient must be determined.
Commonly used modes of ventilation include assist-control (AC) ventilation,
SIMV, and PSV. The various modes are achieved by using some combination
of the three types of ventilator breaths and may be combined with the
application of PEEP.

A. Assist-Control Ventilation
AC ventilation can be delivered with either volume-cycled (volume assist-
control) or time-cycled (pressure assist-control) breaths. We will emphasize
volume control because it is the most commonly used mode.

In volume AC, the preset VT is guaranteed at a preset flow rate and with a set
minimum respiratory rate. The patient can initiate breaths and trigger the
ventilator, and the ventilator will assist to achieve the preset VT delivered at
the preset flow. Thus, patients receive the minimum number of ventilator
breaths (set rate), but the total number of breaths is higher if the patient
triggers the ventilator with additional inspiratory efforts.
With proper use of AC, the work of breathing may be significantly decreased.
However, if the ventilator and the patient are not in synchrony or if the
ventilator inspiratory flow rates are not matched to the patient’s demand, this
mode may result in an increase in the patient’s work of breathing.
The total number of breaths during AC ventilation may be higher than the
minimum set rate, based on the patient’s respiratory drive and ability to
trigger the ventilator. This mode has also been called continuous mandatory
ventilation (CMV). However, CMV more accurately represents a situation in
which the patient does not trigger additional breaths (ie, absent respiratory
drive, as when the patient is paralyzed [discussed next]).

The other breath type of AC is pressure control. Pressure and inspiration time
are set, allowing the breath to be delivered at a certain rate per minute. In
pressure control, the set pressure is the controlling parameter and time is the
signal that ends the inspiration. The delivered tidal volume is determined by
these set parameters and the compliance of the lungs. The flow is determined
by the set pressure, the inspiratory:expiratory ratio (I:E ratio), lung resistance
and compliance, and the patient’s efforts. As the patient’s compliance
decreases or resistance increases, the tidal volume will decrease. If
compliance increases or resistance decreases, then tidal volume will increase.

B. Pressure Support Ventilation

PSV provides a preset level of inspiratory pressure assist with each ventilator-
detected patient effort. This inspiratory assist is selected to overcome the
increased work of breathing imposed by the disease process, endotracheal
tube, inspiratory valves, and other mechanical aspects of ventilatory support.
The set amount of pressure that is applied augments each patient-triggered
breath. All breaths are flow cycled (usually, the assist will decelerate when
flow falls < 25% of the initial flow rate generated by the patient-initiated
breath). The patient controls the respiratory rate and exerts a strong influence
on the duration of inspiration, flow rate, and VT. In addition, the delivered
VT is influenced by pulmonary compliance and resistance. Rapid changes in
these parameters potentially alter the VT and work of breathing. PSV may be
coupled with SIMV (see next section), primarily as a means to diminish excess
work of breathing for spontaneous breaths occurring between mandatory
breaths.
 PSV augments the patient’s own respiratory effort
and is best adjusted by observing changes in the
patient’s respiratory rate, VT, and comfort.

The amount of pressure support is titrated according to the patient’s VT

measured by the ventilator during expiration. Suggested parameters include a
setting that achieves one or more of the following goals:
A VT of 6 to 8 mL/kg, depending on patient needs
A slowing of spontaneous breathing rate to an acceptable range (<
30 breaths/min)
The desired minute ventilation
Appropriate apnea alarms and a backup ventilation setting are essential.
Potential benefits of PSV include the comfort and tolerance this ventilatory
mode offers some patients. In addition, PSV may reduce the work of
breathing by diminishing patient-ventilator asynchrony. Typically, as pressure
support is increased in patients with lung disease, the patient’s work of
breathing and respiratory rate decrease and VT increases. With PSV, an
endotracheal tube cuff leak may interfere with appropriate cycling because
flow may never drop to the preset threshold for cycling (ie, 25% of the peak
flow rate).

C. Synchronized Intermittent Mandatory Ventilation

SIMV delivers either volume-cycled or time-cycled breaths at a preset
mandatory rate. Volume cycling is most commonly used for the mandatory
breaths. This type of ventilation may not be suited for the critically ill patient
who requires a set VT to be delivered with every breath and are fully
dependent on the ventilator support. Breaths may be triggered by the patient
or by the time elapsed. If the patient-initiated breath falls within a certain
period of time before the onset of the mandatory breath, the ventilator
synchronizes its support by delivering the mandatory breath early, thus
essentially converting a controlled breath to an assisted one. The number of
breaths that will be synchronized in this fashion is the preset (mandatory)
rate. When no effort is detected, the ventilator delivers the preset VT at the
preset (time-elapsed) rate. When the patient initiates breaths over the set
mandatory rate spontaneously, these breaths are usually supported by the
ventilator (assisted breaths) with the addition of pressure support. Notice the
difference from assist control—volume control ventilation, in which each
breath (patient- or ventilator-initiated) had the same guaranteed VT.

It is recommended that PSV be used in

conjunction with SIMV to decrease the patient’s
work of breathing during spontaneous breaths.

In SIMV, the addition of pressure support to these spontaneous patient-

initiated breaths is recommended, using a value that offsets the resistance of
the endotracheal tube. Synchronization allows for enhanced patient-ventilator
synchrony by delivering the preset machine breaths in conjunction with the
patient’s inspiratory effort for each mandatory breath.
The SIMV mode allows patients to contribute to and determine a portion of
their ventilatory requirement. The negative inspiratory pressure generated by
spontaneous breathing may lead to increased venous return to the right side
of the heart, which may improve cardiac output and cardiovascular function.
When no pressure support is added, potential increases in work of breathing
may delay weaning from mechanical ventilation.

D. Controlled Mechanical Ventilation

 Do not confuse the CMV (assist-control) setting
on modern ventilators for controlled mechanical
ventilations.

CMV delivers unassisted ventilator breaths at a preset rate. All breaths are
mandatory and are either volume-cycled or time-cycled. No additional
spontaneous assisted breaths are initiated beyond the set number of
controlled breaths. Current ventilators do not allow direct setting of CMV, and
this mode can be achieved only in patients who are not capable of
spontaneous respiratory effort, such as those who are heavily sedated or
receiving neuromuscular blockade during surgery under anesthesia.

E. CPAP and Weaning

CPAP is seldom used as initial support for acute respiratory failure in a
patient who is intubated and is not considered a mode of mechanical
ventilation. Here continuous positive pressure is applied throughout the
respiratory cycle with the patient breathing spontaneously around the applied
pressure. Therefore, respiratory rate and VT depend entirely on the patient’s
inspiratory effort (without help from the ventilator) as the patient inspires
against the resistance of the endotracheal tube. CPAP with low levels of
pressure support (typically 5–7 cm of water) may be used for weaning during
the final stages of invasive ventilation when patients are being assessed for
their potential readiness for extubation.
Airway pressure and flow tracings of spontaneous respiration, CPAP, and the
different modes of mechanical ventilation are illustrated in Figure 6-4.

Figure 6-4. Airway Pressure and Flow Tracings

The advantages and disadvantages of the various modes of invasive
mechanical ventilation are summarized in Table 6-6. In choosing a mode of
ventilation, it is important to consider specific goals, the most important of
which are adequacy of ventilation and oxygenation, reduction in the work of
breathing, and the assurance of patient comfort and synchrony with the
ventilator.

Table 6-6 Potential Advantages and Disadvantages of Selected Modes of

 Mechanical Ventilation

Abbreviations: AC, assist-control; ET, endotracheal; VT, tidal volume; WOB, work of breathing

VII. CHOOSING A MODE AND INITIAL VENTILATOR

SETTINGS
Choosing a mode of mechanical ventilation depends on the reason it is
required and the underlying disease process. In general, AC is used as the
initial mode for a patient needing invasive mechanical ventilation.
When initiating ventilatory support in adults, a fraction of inspired oxygen
(FIO2) of 1.0 is used to ensure maximal amount of available oxygen during
the patient’s adjustment to the ventilator and during the initial attempts to
stabilize the patient’s condition. In addition, the high level of oxygen offers
support for complications that may have occurred before and during
intubation. The usual recommended VT level is 6 to 8 mL/kg of the predicted
body weight. Higher VT levels should be avoided to reduce the possibility of
lung injury. An appropriate respiratory rate should be set to achieve the
desired minute ventilation. Normal minute ventilation (VT × respiratory rate)
is approximately 7 to 8 L/min, but certain conditions may require levels that
more than double this baseline. Minute ventilation should be adjusted to
produce the PaCO2 level that allows an acceptable acid-base (pH) status for
the patient’s clinical condition. As a general rule, FIO2, mean airway
pressure, and PEEP affect the PaO2, whereas the respiratory rate, dead
space (VD), and VT affect alveolar minute ventilation and PaCO2.

To estimate predicted body weight

Males:
50 + 2.3 (height in inches – 60)
50 + 0.91 (height in cm – 152.4)
Females:
45.5 + 2.3 (height in inches – 60)
45.5 + 0.91 (height in cm – 152.4)

Although a normal or close to normal pH status may allow resumption of

optimal functioning of the cellular metabolism essential to the recovery of a
critically ill patient, in some circumstances (acute respiratory distress
syndrome and severe obstructive lung disease), the goals of mechanical
ventilation are not to normalize blood gases. Hypercapnia and respiratory
acidosis are tolerated in such situations to achieve goals such as minimizing
dynamic hyperinflation and avoiding ventilator-associated lung injury. Hence,
individual ventilator settings and their titration contribute to a dynamic
process that must be tailored to the patient’s changing needs. Guidelines for
the initiation of mechanical ventilation are listed in Table 6-7.

Table 6-7 Guidelines for the Initiation of Mechanical Ventilation

Abbreviations: ARDS, acute respiratory distress syndrome; PBW, predicted body weight; PEEP,
positive end-expiratory pressure; SpO2, oxyhemoglobin saturation as measured by pulse oximetry; VT,
tidal volume

VIII. CONTINUING CARE DURING MECHANICAL

VENTILATION
After mechanical ventilation has been initiated, the following parameters
should be assessed and titrated to achieve the desired goals. Many important
interrelationships exist among ventilator settings, and the consequences of
making any change must be appreciated. This interdependency of parameters
may lead to beneficial or harmful effects in the respiratory and/or
cardiovascular systems. Critical care consultation should be obtained for
continuing ventilator management.

A. Inspiratory Pressures
During positive pressure volume assist-control ventilation, airway pressure
rises progressively to a peak inspiratory pressure (Ppeak; Figure 6-5), which
is reached at end inspiration. The Ppeak is the sum of the pressure required
to overcome airway resistance and the pressure required to overcome the
elastic properties of the lung and chest wall. Ppeak, sometimes referred to as
peak airway pressure, is affected by many other variables, such as the flow
rate, diameter of the endotracheal tube, secretions, and diminished bronchial
diameter. When an inspiratory hold is applied at the end of inspiration, gas
flow ceases, all dynamic factors are eliminated, and the pressure drops to a
measurement called the inspiratory plateau pressure (Pplat). The Pplat
reflects the pressure required to overcome the elastic recoil within the lung
and chest wall and, contrary to the Ppeak, is a static pressure. The Pplat is
the best estimate of peak alveolar pressure, which is an important indicator of
alveolar distension. Accurate measurement of Pplat requires the absence of
any patient effort and an inspiratory hold for a minimum of 0.5 seconds
(usually 1 second).

Potential adverse effects from high inspiratory pressures include barotrauma,

volutrauma, and reduced cardiac output. Barotrauma (pneumothorax,
pneumomediastinum) and volutrauma (lung parenchymal injury caused by
overinflation), although linked to high Ppeak, correlate best with Pplat. The
relation of Ppeak and Pplat is illustrated in Figure 6-5. This figure
demonstrates airway pressure tracings for typical volume assist-control
ventilation under conditions of normal compliance and resistance, increased
airway resistance, and decreased respiratory system compliance.
As mentioned earlier, an example of the relationship of Ppeak and Pplat to
alveolar distension is demonstrated by the effect of endotracheal tube size on
Ppeak and Pplat. As the internal diameter of an endotracheal tube is
decreased in a patient receiving (fixed volume) ventilation, the same VT will
result in higher Ppeak, yet Pplat (obtained during inspiratory hold) and
alveolar distension remain unchanged as the pressure is dissipated across the
resistance of the endotracheal tube. The same VT, regardless of the type of
breath, produces the same alveolar distension at end inspiration. To avoid
injury in patients receiving mechanical ventilation, Pplat should be maintained
< 30 cm H2O. When compliance is decreased, both Ppeak and Pplat rise
for a fixed VT. As resistance is unchanged, the difference between peak
pressure and plateau pressure is not affected.
Figure 6-5. Relationship of Peak Inspiratory Pressure and
Inspiratory Plateau Pressure
 Abbreviation: PEEP, positive end-expiratory pressure

Elevated Pplat may be reduced by the following interventions:

Decrease PEEP, which may also decrease oxygenation and worsen
alveolar collapse (if PEEP is used to improve oxygenation and
alveolar stability).
Decrease VT, which may lead to hypercapnia because of a
reduction in minute ventilation.
Avoid and decrease auto-PEEP (see next section) with interventions
that prolong the expiratory time, understanding that this may lead
to hypercapnia.

B. Relation of Inspiratory Time to Expiratory Time and Auto-PEEP

If the expiratory time is too short to allow full exhalation, the previously
delivered breath is not completely expired and the next lung inflation is
superimposed on the residual gas in the lung. This results in lung
hyperinflation and PEEP above the preset level on the ventilator. This
increase in end-expiratory pressure is called auto-PEEP, or intrinsic,
inadvertent, or occult PEEP. Auto-PEEP can be quantified by using manual
methods or through electronic programs within some ventilators during an
expiratory hold maneuver. However, it is most easily diagnosed qualitatively
by viewing the flow-versus-time graphic waveform tracing available on most
mechanical ventilators because the expiratory flow fails to reach the zero flow
level before the initiation of the next breath (Figure 6-6). The potentially
harmful physiologic effects of auto-PEEP on peak, plateau, and mean airway
pressures are the same as those of preset PEEP. In addition, high levels of
PEEP may decrease venous return to the heart, resulting in hypotension and
higher PCO2 because of increased dead space, and adversely affect
oxygenation (especially with asymmetric lung disease).
 Figure 6-6. Flow-Time Waveform Demonstrating Auto-PEEP

Abbreviation: PEEP, positive end-expiratory pressure

Auto-PEEP may be reduced by the following interventions:

Decrease respiratory rate by changing the set rate or sedating the
patient. These interventions result in fewer inspirations per minute
and thus increase the total expiratory time available; this is the
most effective way of decreasing auto-PEEP.
Decrease VT, which requires less time to deliver a smaller breath
and allows more time for exhalation.
Increase flow rate, delivering the VT faster and allowing more time
in the cycle for exhalation. This intervention has little impact unless
the initial flow rate was set at an extremely low level. It will also
lead to an increase in the airway pressure.
Change the inspiratory waveform from decelerating (ramp) to
constant (square), which delivers VTin a shorter time, allowing
 more time for exhalation.

As discussed previously, the first two interventions may lead to hypercapnia

because of a reduction in minute ventilation; however, the benefits of a
decrease in auto-PEEP despite the lower minute ventilation may lead to little
change in PaCO2. When severe air trapping occurs, allowing sufficient
expiratory time may improve ventilation and CO2 removal. Hypercapnia and
a controlled reduction in pH (permissive hypercapnia) may be acceptable in
some clinical conditions but requires expert consultation. This approach may
not be suitable for patients with intracranial hypertension because
hypercapnia causes cerebral vasodilation and further increases in the
intracranial pressure.

C. FIO2
High levels of inspired oxygen may be harmful to lung parenchyma after
prolonged exposure. Although the precise threshold for concern is not known,
it is desirable to reduce the FIO2 to ≤ 0.5 (50% oxygen) within the first 24
hours. However, hypoxemia is always considered a greater risk to the patient
than high FIO2 levels. The primary determinants of oxygenation during
mechanical ventilation are FIO2 and mean airway pressure. Other minor
determinants include VT, inspiratory-expiratory ratio, inspiratory flow rate,
PEEP, auto-PEEP, use of inspiratory pause, and the inspiratory flow
waveform pattern (volume breaths). In the patient with acute respiratory
distress syndrome (ARDS), PEEP becomes a major determinant of mean
airway pressure. The interrelationships of these various parameters, as
already demonstrated, often lead to complex adjustments within the
mechanical ventilation plan.

D. Minute Ventilation and Alveolar Minute Ventilation

Minute ventilation, defined as the amount of gas exchanged by an individual
in 1 minute, is calculated as the respiratory rate multiplied by mean VT. The
primary determinant of CO2 exchange during mechanical ventilation is the
alveolar minute ventilation, calculated as:

VA = (VT − VD)f

in which VD is dead space and f is the respiratory rate. The VT, the
respiratory rate, and their interrelationships with other ventilatory parameters
have already been discussed. Physiologic VD represents, in general, lung
units that are relatively well ventilated but under-perfused. The physiologic
effect of high amounts of VD is hypercapnia (impaired CO2 clearance). Dead
space may result from the pathologic process in the lung or from mechanical
ventilation complicated by high airway pressures, low intravascular volume, or
low cardiac output.
As previously discussed, adequate ventilation is assessed by consideration of
both the PaCO2 and the pH. Hyperventilation resulting in a low PaCO2 level
may be an appropriate short-term compensatory goal during metabolic
acidosis while the primary etiology is corrected. Similarly, a patient with
chronic hypercapnia has an increased baseline PaCO2 and maintains a near-
normal pH by renal compensation (increased bicarbonate retention). Patients
with chronic compensated hypercapnia should receive sufficient minute
ventilation during mechanical ventilation to maintain the PaCO2 at their usual
(baseline) level, and utmost attention should be paid to the pH to avoid severe
alkalemia and loss of retained bicarbonate.

E. Humidification
Gases delivered by mechanical ventilators are typically dry, and the upper
respiratory tract is bypassed by artificial airways, resulting in loss of heat and
moisture. Heating and humidification of gases are routinely provided during
mechanical ventilation to prevent mucosal damage and minimize inspissation
of secretions. Available systems include passive humidifiers (artificial nose) or
active, microprocessor-controlled heat and humidifying systems (heated
humidifiers). The passive humidifiers are contraindicated in the presence of
copious secretions, minute ventilation > 12 L/min, air leaks > 15% of
delivered tidal volume, or blood in the airway.

F. Use of Positive End-Expiratory Pressure

Adjustment of PEEP is the cornerstone strategy employed for disease states
that cause alveolar collapse or airway closure (eg, ARDS). It causes alveolar
recruitment and prevents repeated opening and closing of the alveoli
(atelectrauma). Titration of PEEP for hypoxemic respiratory failure secondary
to ARDS can be performed according to the PEEP/FIO2 combinations given
in Table 6-8.

Table 6-8 Suggested Combinations of PEEP and FIO2 to Reach Goal PaO2

Abbreviations: PEEP, positive end-expiratory pressure; FIO2, fraction of inspired oxygen

In patients with severe obstructive lung disease, applying external PEEP and
setting it close to the auto-PEEP value can help offset the work of breathing to
trigger the ventilator. Seeking expert consultation is prudent if higher levels of
PEEP are required to maintain oxygenation.

G. Prophylactic Therapies
Mechanical intubation is a risk factor for venous thromboembolism, gastric
stress ulceration, and nosocomial pneumonia. Measures to prevent venous
thromboembolism include the prophylactic use of anticoagulation (unless
contraindicated) and/or pneumatic compression devices. Using a proton pump
inhibitor or histamine 2-receptor blocker is warranted for stress ulcer
prevention. The risk of ventilator-associated pneumonia (ventilator bundle) is
reduced by elevation of the head of the bed to ≥ 30°, oral hygiene, and
daily evaluations for liberation from mechanical ventilation.

IX. SEDATION, ANALGESIA, AND NEUROMUSCULAR

BLOCKADE
Endotracheal intubation and mechanical ventilation can be uncomfortable and
anxiety provoking. To improve the patient’s comfort and synchrony with the
ventilator, anxiolytics, sedatives, and analgesics may be administered.
Neuromuscular blocking agents should be used with caution, and expert
consultation should be sought before initiation. Guidelines for the use of these
agents are outlined in the Society of Critical Care Medicine’s Clinical
Practice Guidelines for Sustained Neuromuscular Blockade in the Adult
Critically Ill Patient and in Clinical Practice Guidelines for the
Management of Pain, Agitation, and Delirium in Adult Patients in the
Intensive Care Unit. Caution also should be exercised with use of sedation in
nonintubated patients with acute respiratory insufficiency or impending
respiratory failure.

X. VENTILATORY GUIDELINES FOR SPECIFIC CLINICAL

SITUATIONS

Case Study
A previously healthy 36-year-old man presents to the hospital and reports a
cough, sputum production, and a fever of 2 days’ duration. An admission
chest radiograph reveals a developing infiltrate in the left lower lobe. The man
is admitted to the general ward and started on antibiotics for community-
acquired pneumonia. Less than 24 hours later, the patient continues to
deteriorate and requires oxygen at 10 L/min. He is not in obvious respiratory
distress; however, pulse oximetry reveals severe hypoxemia (83% to 89% on
supplemental oxygen, 10 L/min). Sputum cultures show Streptococcus
pyogenes (group A) colonies, and a new chest radiograph reveals new, diffuse
bilateral alveolar infiltrates. The patient is intubated because of worsening
hypoxemia.
– What initial ventilator settings would you use for this patient?
– What steps should be taken to minimize barotrauma during ventilation?
– What parameters should be measured and monitored?

A. Acute Respiratory Distress Syndrome

ARDS causes a decrease in lung compliance, making the lungs stiff and
difficult to inflate, and produces hypoxemic respiratory failure. Guidelines for
mechanical ventilation in ARDS are outlined in Tables 6-8 and 6-9. High
Ppeak and Pplat complicate mechanical ventilation because of the low lung
compliance or high airway resistance. Lower VT2 (4–6 mL/kg of predicted
body weight) is required, and the Pplat should be maintained at the desired
level of ≤ 30 cm H2O; permissive hypercapnia may be required to
accomplish that goal. The FIO2 is increased as necessary to prevent
hypoxemia but reduced as soon as other ventilatory interventions are
effective. Because of increased shunt in ARDS, hypoxemia may be severe.
PEEP is the most effective way to improve oxygenation and is typically
applied in the range of 8 to 15 cm H2O, based on the severity of hypoxemia.
Higher PEEP levels may be indicated in severe lung injury. Although patients
with ARDS are somewhat less likely to develop auto-PEEP because expiratory
time requirements are reduced as a result of decreased lung compliance
(stiffness), its presence should be monitored, especially at higher inspiratory-
expiratory ratios. Table 6-9 outlines the recommended strategy for ventilating
patients with ARDS. Table 6-8 outlines the recommended FIO2 and PEEP
combinations.

Table 6-9 Mechanical Ventilation in Acute Respiratory Distress Syndrome

Abbreviations: PBW, predicted body weight; PEEP, positive end-expiratory pressure; Pplat, plateau
pressure; VT, tidal volume

Case Study
A 28-year-old woman with a history of asthma is intubated and admitted to
the ICU for an acute asthma exacerbation. Peak airway pressure on admission
was 40 cm H2O, and Pplat was 25 cm H2O immediately after intubation;
however, 6 hours later, peak airway pressures have arisen to 55 cm H2O
while the Pplat has remained the same.
– What is the likely etiology of her high peak airway pressures in the
setting of unchanged plateau pressures?
– What adjunctive therapies, in addition to ventilator support, does this
patient need to reduce the elevated airway pressures?
– Which parameter (ie, peak airway pressure or Pplat) has been
associated with a higher risk of barotrauma in an intubated patient?
B. Obstructive Airway Disease
Mechanical ventilation for patients with asthma and chronic obstructive
pulmonary disease is designed to support oxygenation and assist ventilation
until airway obstruction has improved. After initial intubation, airway
secretions and persistent small airway obstruction may manifest as elevated
peak airway pressures and a normal Pplat. This suggests an airway
obstruction (not worsening compliance), and bronchodilators and steroids
should be used aggressively to help alleviate this obstruction while mechanical
ventilation supports the patient. As airflow improves, the patient will tolerate
higher VT levels and longer inspiratory times.
Mechanical ventilation in these patients may also produce hyperinflation,
auto-PEEP, and resultant hypotension. Therefore, careful attention is needed
to balance cycle, inspiratory, and expiratory times. The initial VT should be 6
to 8 mL/kg, and the minute ventilation should be adjusted to a low normal
pH. With volume ventilation, the inspiratory flow rate should be set to
optimize the inspiratory-expiratory ratio and allow complete exhalation. Such
management reduces breath stacking and the potential for auto-PEEP.

C. Asymmetric Lung Disease

Asymmetric lung disease or injury that occurs after aspiration, contusion, or a
localized pneumonia may cause abnormal distribution of ventilation and gas
exchange during mechanical ventilation. Because the conditioned gas from
the ventilator follows the path of least resistance along the bronchi, the VT is
distributed primarily to the less-affected (more-compliant) lung and may
overexpand it. Overdistension of the less-affected lung and poor expansion of
the diseased/injured lung worsen ventilation-perfusion relationships in both
lungs, and hypoxemia and hypercapnia may occur, persist, or worsen, in
addition to causing injury to the normal lung. Standard settings and principles
of ventilator support should be initiated. However, if this is unsuccessful,
expert consultation should be obtained to facilitate further efforts at patient
management. Putting the less-involved lung in the gravitationally dependent
(decubitus) position may be helpful in directing pulmonary blood flow to lung
units receiving better ventilation. Other techniques, such as differential lung
ventilation, could be considered, and immediate expert consultation may be
required.

D. Heart Disease
The major goals of ventilatory support in patients with myocardial ischemia
are to decrease the work of breathing and ensure adequate oxygen delivery to
the heart. Decreasing the work of breathing will reduce the consumption of
oxygen by respiratory muscles, thus increasing oxygen availability to the
heart. Patients with cardiogenic pulmonary edema who are mechanically
ventilated receive additional benefit from the decrease in preload as a result
of increased intrathoracic pressure. Left ventricular afterload also decreases
through application of positive juxtacardiac pressure during systole.

E. Neuromuscular Disease
Patients with peripheral neuromuscular disease typically have an intact
respiratory drive and normal lungs. These patients may require a higher VT
level to avoid the sensation of dyspnea. Adjustments are made in other
ventilatory parameters to ensure a normal arterial pH.

XI. MONITORING MECHANICAL VENTILATORY SUPPORT

Patients who receive mechanical ventilatory support require continuous
monitoring to assess the beneficial and potential adverse effects of treatment
(Table 6-10). Arterial blood gas measurements provide valuable information
about the adequacy of oxygenation, ventilation, and acid-base balance. This
information is essential during the initial phases of ventilatory support and
during periods of patient instability. If available, a pulse oximeter and end-
tidal capnometer (for measuring end-tidal CO2) can be used to further
monitor the patient’s progress.

Table 6-10 Recommendations for Monitoring Mechanical Ventilatory Support

Ventilators are equipped with sophisticated alarms and monitors to assist with
patient management and detection of adverse events. When initiating
ventilatory support, the respiratory care practitioner usually establishes alarm
parameters for low and high minute ventilation, high inspiratory pressures,
and low exhaled volumes and pressures. Many ventilators allow for the
measurement of auto-PEEP.
The low-pressure alarm is intended to alert the clinician to a leak in the circuit
or to ventilator disconnection. A high-pressure alarm warns that the set
maximum peak airway pressure has been exceeded; this alarm is usually set
10 cm H2O above the patient’s baseline peak airway pressure. If a patient
receiving volume ventilation develops mucous plugging or a marked change in
airway resistance or lung compliance, the peak pressure will rise acutely. If
the peak pressure alarm sounds with volume ventilation, it implies that the
patient is not receiving the set VT because inspiration ends when the pressure
alarm limit is exceeded. Conversely, in pressure preset modes of ventilation,
changes in airway resistance or lung compliance will trigger the low exhaled
volume alarm.

XII. HYPOTENSION ASSOCIATED WITH INITIATION OF

MECHANICAL VENTILATION
A. Tension Pneumothorax
When hypotension occurs immediately after initiation of mechanical
ventilation, tension pneumothorax should be one of the first considerations.
This diagnosis is based on a physical examination that finds decreased or
absent breath sounds and tympany to percussion on the side of the
pneumothorax. Tracheal deviation away from the side of the pneumothorax
may be observed, although it is uncommon after placement of an
endotracheal tube. Treatment includes emergent decompression by inserting
a large-bore catheter or needle into the second or third intercostal space in
the midclavicular line. Treatment should not be delayed awaiting a chest
radiograph. The insertion of a catheter or needle is both diagnostic and
therapeutic: it improves blood pressure and reverses the findings of physical
examination. The insertion of the catheter or needle must be followed by
chest tube placement.

B. Conversion from Negative to Positive Intrathoracic Pressure

Normal intrathoracic pressure is slightly negative relative to the atmosphere.
When positive pressure ventilation is initiated, intrathoracic pressure becomes
positive. As intrathoracic pressure rises, right atrial pressure rises and the
intravascular pressure gradient for return of blood from the large
extrathoracic veins into the right heart decreases. As a result, blood return to
the heart may be reduced. Left ventricular preload, stroke volume, cardiac
output, and blood pressure then may decrease in sequence. Underlying
intravascular volume depletion exacerbates the deleterious effects of the
increased intrathoracic pressure on cardiac output and blood pressure.
Treatment of this common complication includes volume resuscitation by
means of rapidly infused fluid boluses to raise extrathoracic venous pressure
and increase venous return to the right heart until the blood pressure
increases. Oxygen saturation should be monitored to avoid overly aggressive
fluid resuscitation. Use of ventilation techniques associated with high mean
airway pressure may exacerbate the deleterious hemodynamic consequences
of mechanical ventilation.

C. Auto-PEEP
As previously discussed, auto-PEEP occurs when the combination of
ventilator settings and patient physiology results in an inadequate expiratory
time. Excessive end-expiratory pressure may increase intrathoracic pressure
and cause hypotension because of decreased venous return to the heart.
Although auto-PEEP may occur in any patient, those with obstructive airway
disease are particularly predisposed to this condition because of the need for
a prolonged expiratory phase.

D. Acute Myocardial Ischemia/Infarction

Stress from the cause of acute respiratory failure, as well as the stress of
intubation itself, may lead to increased myocardial oxygen demand and to
acute myocardial ischemia, infarction, and subsequent hypotension. Patients
at high risk should be evaluated with serial electrocardiograms and
myocardial markers of injury.

XIII. READINESS AND WEANING FROM INVASIVE

MECHANICAL VENTILATION
Mechanical ventilation is not without complications, including and not limited
to, superimposed infections, laryngeal injury, diaphragmatic dysfunction, and
others.
The need to assess the readiness of a patient to wean from mechanical
ventilation should be done on a daily basis and those patients that can be
freed from mechanical ventilation should be disconnected from the machines
as soon as possible without risking complications.
A few clinical parameters and criteria can be used as indicators for readiness
to wean. Below are some criteria used:
The main cause of the respiratory failure that lead to the intubation
and mechanical ventilation has improved significantly or resolved.
Adequate mental status to maintain an airway (including the ability
to clear secretions)
Adequate oxygen saturation > 90%, PO2 > 60 mm Hg with
FIO2 40–50%
 PEEP around 5–8 cm H2O

pH > 7.25
Able to initiate inspiratory effort
Appropriate mentation to protect airway
Minimal secretions with strong cough
Hemodynamically stable and no escalation of resuscitation or
vasopressors
Weaning patients from mechanical ventilation to extubation can be a
challenging process. Formal discontinuation assessment should be done when
the patient is placed on a spontaneous breathing trial (SBT), and not receiving
significant support from the machine. The SBT should continue for about 30
minutes, and no more than 2 hours. There are few predictors and parameters
that should be examined and achieved before the decision is made to
extubate the patient. The use of Negative Inspiratory Force (NIF), Force Vital
Capacity (FVC), or the Respiratory Shallow Breathing Index (RSBI) have been
used by many clinicians. Expert consultation should be considered when
deciding to extubate the patient.
As many as one in every five patients with planned extubation might require
re-intubation. This failure is highly dependent on the correct evaluation of
previously described parameters. Most extubation failures occur within the
first 24 hours up to 72 hours after extubation.

Key Points
Mechanical Ventilation
The primary goals of noninvasive and invasive positive pressure
ventilation are to support ventilation and oxygenation, and to
reduce work of breathing while ensuring patient comfort.
 NPPV is best used in the alert, cooperative patient whose
respiratory condition is expected to improve in 24 to 48 hours.
The advantages and disadvantages of the different modes of
invasive mechanical ventilation must be considered when
determining the optimal ventilatory support for the patient’s clinical
condition.
Guidelines for initiating mechanical ventilation should be carefully
followed, with adjustments made based on patient assessment and
monitoring.
The complex interactions of inspiratory pressures, inspiratory-
expiratory ratio, FIO2, and PEEP must be appreciated to evaluate
the potential benefits and harmful effects in each patient.
The primary determinants of oxygenation are FIO2 and mean
airway pressure, whereas alveolar ventilation primarily affects CO2
exchange.
During mechanical ventilation, a patient must be closely monitored
using the ventilator alarm systems, continuous pulse oximetry,
attentive physical assessment, measurement of inspiratory Pplat (as
clinically appropriate), and intermittent arterial blood gases and
chest radiographs as needed.
High inspiratory plateau pressures are associated with a higher
incidence of ventilator-induced lung injury and should be
maintained below 30 cm H2O.

Hypotension occurring immediately after initiation of invasive

mechanical ventilation should prompt evaluation for tension
pneumothorax, decreased venous blood return because of
intrathoracic pressure, auto-PEEP, or myocardial ischemia.

Suggested Readings
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lower tidal volumes as compared with traditional tidal volumes for
acute lung injury and the acute respiratory distress syndrome. N
Engl J Med. 2000;342:1301-1308.
2. Caples SM, Gay PC. Noninvasive positive pressure ventilation in
the intensive care unit: a concise review. Crit Care Med.
2005;33:2651-2658.
3. Fink M, Abraham E, Vincent J, et al, eds. Chapter 66: Controlled
mechanical ventilation. In: Textbook of Critical Care. 5th ed.
Philadelphia, PA: WB Saunders Co; 2005.
4. Fink M, Abraham E, Vincent J, et al, eds. Chapter 67: Patient-
ventilator interaction. In: Textbook of Critical Care. 5th ed.
Philadelphia, PA: WB Saunders Co; 2005.
5. Hess DR, Kacmarek RM. Essentials of Mechanical Ventilation.
2nd ed. New York, NY: McGraw-Hill Companies; 2002.
6. Kallet RH, Jasmer RM, Pittet JF, et al. Clinical implementation of
the ARDS Network protocol is associated with reduced hospital
mortality compared with historical controls. Crit Care Med.
2005;33:925-929.
7. Leisching T, Kwok H, Hill NS. Acute applications of noninvasive
positive pressure ventilation. Chest. 2003;124:699-713.
8. MacIntyre N. Ventilatory management of ALI/ARDS. Semin
Respir Crit Care Med. 2006;27:396-403.
9. MacIntyre N, Branson RD. Mechanical Ventilation. Philadelphia,
PA: WB Saunders Co; 2000.
10. MacIntyre NR, Cook DJ, Ely EW Jr, et al. Evidence-based
guidelines for weaning and discontinuing ventilatory support: a
collective task force facilitated by the American College of Chest
Physicians; the American Association for Respiratory Care; and
 the American College of Critical Care Medicine. Chest.
2001;120(6 Suppl):375S.
11. Marini JJ. Dynamic hyperinflation and auto-PEEP end-expiratory
pressure: lessons learned over 30 years. Am J Respir Crit Care
Med. 2011;184:756-762.
12. Marini JJ, Gattinoni L. Ventilatory management of acute
respiratory distress syndrome: a consensus of two. Crit Care
Med. 2004;32:250-255.
13. Murray MJ, Cowen J, DeBlock H, et al. Clinical practice
guidelines for sustained neuromuscular blockade in the adult
critically ill patient. Crit Care Med. 2002;30:142-156.
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quantitative systematic review of randomized controlled trials.
Anesth Analg. 2004;99:193-200.
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Suggested Website
1. Society of Critical Care Medicine/Guidelines. www.SCCM.org.
 Chapter 7
MONITORING OXYGEN BALANCE
AND ACID-BASE STATUS

Objectives
Outline the determinants of oxygen balance.
Recognize disorders of oxygen delivery.
Assess oxygen balance.
Discuss hemodynamic monitoring and volume responsiveness.
Explain the use of acid-base status in monitoring the seriously ill
patient.
Discuss acid-base disturbances.
Describe disease processes that cause metabolic acidosis.

Case Study
A 67-year-old woman with a medical history of hypertension, diabetes
mellitus, and systolic heart failure (left ventricular ejection fraction [LVEF
20%]) presented to the hospital with altered mental status and shortness of
breath. The patient’s pulse is 123 beats/min, blood pressure 84/54 mm Hg,
respiratory rate 28 breaths/min, and oxygen saturation on pulse oximetry
(SpO2) 89% while breathing room air. She was found to have a lower
gastrointestinal bleed.
 – What monitoring devices should be implemented?
– What blood tests should be obtained to determine whether the oxygen
balance is adequate?

I. INTRODUCTION
Monitoring devices are not therapeutic and information from monitoring
devices must be integrated with patient assessment and clinical judgment to
determine optimal care. In addition, the clinician must be aware of the
limitations and risk-benefit ratio of a monitoring system. Monitoring may be as
simple as measuring the pulse or temperature or as complex as invasive
hemodynamic techniques with direct and calculated measurements.
Physiologic stress leads to early effects on the heart rate, respiratory rate,
vascular tone, and blood pressure. Significant abnormalities of these vital
signs may suggest the need for more intensive monitoring. More invasive
monitoring strategies carry a higher risk of complications, but should be
considered if they provide sufficient new information to guide therapy. This
chapter will emphasize only basic monitoring techniques that can be initiated
in most care environments.

The goals of monitoring in seriously ill patients are to recognize physiologic

abnormalities and to guide interventions. These actions help to ensure
adequate blood flow and oxygen delivery for maintenance of cellular and
organ function. Tissue oxygenation cannot be directly measured or monitored
at the bedside in a predictable and reliable manner. However, estimates of
the adequacy of oxygenation can be made based on knowledge of the oxygen
balance, which is determined by oxygen delivery and oxygen consumption.
An understanding of these principles is required to appreciate the usefulness
and limitations of various monitoring tools.

II. PRINCIPLES OF OXYGEN DELIVERY

Organs consume oxygen to make energy and therefore organs require oxygen
to function properly. In addition, oxygen delivery requires the driving force of
the cardiovascular system. Oxygen delivery is defined as the amount of
oxygen presented to the tissues. Oxygen consumption is defined as the
amount of oxygen needed to meet the body’s metabolic demands. At
baseline, the body delivers 4–5 times more oxygen than what is needed by
the tissues. This extra delivery is the oxygen reservoir that is available for
sharp increases in consumption, such as running away from a threat (Figure
7-1). In critical illness, physiologic derangements that result in an absolute
decrease in the oxygen delivered or an increase in tissue oxygen demand may
compromise this margin of safety. In addition, adequate oxygen delivery does
not always guarantee appropriate oxygen utilization. For example, infection
leading to sepsis can decrease the mitochondria’s ability to effectively use
oxygen at the tissue level. Efforts to improve oxygen delivery are more easily
manipulated in the critically ill patient than oxygen consumption. Oxygen
delivery is dependent on the oxygen content of arterial blood and the ability
of the body to carry it to the tissues (cardiac output).

Oxygen delivery (DO2) = cardiac output (CO) × arterial oxygen content

(CaO2)

Invasive and/or more complex noninvasive monitoring is required for exact

measurement of cardiac output. However, an understanding of the variables
that determine oxygen content in the blood and cardiac output, along with
less invasive monitoring, may guide appropriate treatment.

A. Oxygen Content of Arterial Blood

Arterial oxygen content (CaO2) is defined as the amount of oxygen bound to
hemoglobin plus the amount of oxygen dissolved in arterial blood plasma. The
components of arterial oxygen content are related by the formula:

CaO2(mL O2/dL) = [Hemoglobin (g/dL) × 1.34 × SaO2(%)] + [0.0031 ×

PaO2(mm Hg)]

SaO2 is the arterial oxyhemoglobin saturation and PaO2 is the partial

pressure of oxygen dissolved in arterial blood. Each fully saturated gram of
hemoglobin transports 1.34–1.39 mL of oxygen, depending on the affinity of
hemoglobin for oxygen. Hemoglobin is the major contributor of oxygen for
tissue demands and releases bound oxygen based on cellular uptake of
dissolved oxygen as blood flows through the capillaries. The ability of
hemoglobin to release more oxygen when supply is inadequate or cellular
demand is increased is one of the main compensatory mechanisms to sustain
cellular function. The oxyhemoglobin dissociation curve shows the
relationship of hemoglobin saturation and partial pressure of oxygen (PaO2)
(Figure 7-1).

The major determinants of oxygen delivery are

hemoglobin, SaO2, and cardiac output.
Figure 7-1. Oxyhemoglobin Dissociation Curve

The oxyhemoglobin dissociation curve relates the PO2 to oxyhemoglobin saturation. Near-
maximal saturation of hemoglobin occurs at a PO2 of 60 mm Hg (8.0 k Pa). PO2 values
above this point provide only a modest increase in oxyhemoglobin saturation. Note,
however, that a rapid decrease in oxyhemoglobin saturation occurs when the PO2 drops
below 60 mm Hg (8.0 k Pa).

Stored packed red blood cells rapidly lose a

substance called 2,3-diphosphoglycerate (2,3
DPG). This results in an impairment in oxygen
transport to tissues.
When the PaO2 drops to approximately 40 mm Hg (5.3 kappa) in the
capillaries, the decrease in oxyhemoglobin saturation to 75% reflects the
amount of oxygen released to the tissues. During physiologic stress,
oxyhemoglobin saturation at the tissue level may decrease to <20%,
reflecting the release of additional oxygen to tissues. Acidosis, fever, and
increased CO2 production will shift this curve to the right, resulting in a lower
affinity of oxygen for hemoglobin and greater delivery of oxygen to the
tissues. Lower temperature, higher pH, and lower CO2 will shift the curve to
the left and increase the affinity of oxygen for hemoglobin. In other words, a
shift to the right will result in more oxygen being delivered to the tissues.

Calculated CaO2 reflects oxygen that is

available in the arterial circulation and not
necessarily the oxygen that is delivered to or
consumed by specific tissues.

Arterial oxygen content can be estimated by using the direct measurement of

the hemoglobin concentration and arterial oxyhemoglobin saturation in
intermittent blood samples because dissolved oxygen (0.0031 × PaO2)
contributes minimally to oxygen content. Although hemoglobin is not
monitored continuously, oxyhemoglobin saturation measured by pulse
oximetry (SpO2) allows continuous assessment of this determinant of arterial
oxygen content.

B. Cardiac Output
In addition to the oxygen content of arterial blood being optimum, an
appropriate cardiac output is needed to ensure delivery of oxygen to the
tissues. Monitoring tools aside, the evaluation of a critically ill patient begins
with a thorough clinical examination (Table 7-1). Cardiac output (in mL/min
or L/min) is the product of heart rate and stroke volume (Figure 7-2).
Table 7-1 Clinical Assessment of Determinants of Cardiac Output

Figure 7-2. Cardiac Output as the Product of Heart Rate and

Stroke Volume

Persistent tachycardia should be considered as a

possible compensatory mechanism to increase
oxygen delivery.
Stroke volume is the quantity of blood pumped out of the left heart with each
beat and is determined by the difference between the end-diastolic volume
and end-systolic volume of the ventricle. Variables that determine stroke
volume are preload, afterload, and contractile function. The first
compensatory mechanism to increase oxygen delivery is often an increase in
heart rate. Patients who are unable to increase their heart rate (eg, beta-
blockade or fixed pacing) will have a limited ability to compensate.

Although the heart rate is easily measured and evaluated, an evaluation of

stroke volume requires special noninvasive, minimally invasive, or invasive
methods. The option of measuring cardiac output by assessing stroke volume
depends on the training, expertise, and resources available. The pulmonary
artery catheter is used as an invasive method of measuring intermittent or
continuous cardiac output but requires critical care expertise. Minimally
invasive hemodynamic methods measure cardiac output using analysis of the
arterial waveform or aortic blood flow. Devices that analyze the arterial
waveform to determine pulse pressure, stroke volume, and cardiac output
require an arterial catheter, and some also require placement of a central
venous catheter. Esophageal Doppler devices estimate cardiac output from
measurement of blood flow in the descending aorta. Noninvasive
hemodynamic monitors use principles of bioimpedance or bioreactance to
determine stroke volume and cardiac output.

The clinician must be aware of the limitations that affect measurement

accuracy and interpretation of any chosen technique. If cardiac output is not
directly measured, an indirect assessment of variables involved in determining
cardiac output can be determined clinically (Table 7-2) and knowledge of
hemodynamic principles can be useful.

Table 7-2 Devices to Measure Cardiac Output or Stroke Volume

1. Contractility
Contractility is the ability of myocardial fibers to shorten during systole. It is
highly dependent on preload and afterload and is difficult to measure as an
independent variable. Systemic factors that can affect contractility in the
critically ill patient are endogenous sympathetic activation, acidosis, ischemia,
inflammatory mediators, and vasoactive agents. An increase in contractility
would result in a larger stroke volume. Echocardiographic measurement of
the ejection fraction provides some information to the clinician on
contractility.

2. Preload

Preload is a measure or estimate of the ventricular volume at the end of

diastole (end-diastolic volume) and is determined by venous return and
ventricular compliance. The distensibility or stretch (compliance) of the
ventricle and the volume load (venous return) it can accept are the basis for
the Frank-Starling curve. In general, a greater end-diastolic volume leads to
increased stretch on the myocardium, resulting in a larger stroke volume and
therefore, better cardiac output. The curve is actually bell-shaped and too
much fluid, thus elevated preload, can lead to overstretch of the ventricle,
leading to decreased stroke volume as a result of the loss of effective
contractility (Figure 7-3). Because it is difficult to measure volume, preload is
most often estimated from the ventricular end-diastolic pressure, which is
transmitted and reflected in the atrial pressure. The atrial pressure is
estimated by the measurement of pressure in a central vein or the pulmonary
artery. Thus, the right ventricular preload is estimated by measurement of the
central venous pressure (CVP) and the left ventricular preload by the
measurement of pulmonary artery occlusion pressure (PAOP). These
pressures indirectly reflect the end-diastolic volume as well as the compliance
of the ventricular wall. Using bedside ultrasonography, assessment of the size
and variability of the inferior vena cava with respiration may aid in the
assessment of right ventricular preload. However it should not be used
independently because it is not sensitive or specific enough to predict volume
responsiveness.

Figure 7-3. Relationship Between Ventricular Preload and Stroke

Volume:

When end-diastolic volume of the ventricle (preload) increases, stroke volume usually
increases proportionately.

Pressure and volume are not linear, CVP and

PAOP should not be used alone to determine
 volume status. Trends are more beneficial than
isolated values.

The relationship between the measured pressure and volume in the

ventricular chambers depends on the compliance or distensibility of the
ventricle. During myocardial ischemia, sepsis, valvular dysfunction, and even
tachycardia, the ventricles may become less compliant and may not fully relax
during diastole. This diastolic dysfunction reduces the ventricular volume at
end diastole but may be associated with a higher filling pressure; therefore,
the clinician may misinterpret pressure measurements to indicate adequate
volume loading. Changes in intrathoracic pressures (eg, tension
pneumothorax, positive pressure ventilation) may also affect the filling
pressures.

3. Afterload

Afterload is the myocardial wall tension required to overcome the resistance,

or pressure load, that opposes ejection of blood from the ventricle during
systole. The higher the afterload, the more tension the ventricle must develop,
the more work is performed, and the less efficient the contraction may
become. Afterload is usually estimated from the systemic mean arterial
pressure (left ventricle) and mean pulmonary artery pressure (right ventricle)
by calculations of systemic and pulmonary vascular resistance.

III. ASSESSMENT OF OXYGEN BALANCE

In addition to oxygen delivery, oxygen consumption by the tissues affects
oxygen balance (Figure 7-4). Several factors can increase oxygen
consumption in a critically ill patient including but limited to: pain, agitation,
anxiety, seizures, piloerection, shivering, fever, and increased work of
breathing. However, less is known about the factors that determine oxygen
utilization at the cellular and tissue levels, and no direct routine measures of
oxygen consumption are available. Indirect calculated measurement of oxygen
consumption requires invasive or complex techniques. These measures reflect
global oxygen utilization and do not provide information on oxygen utilization
by specific tissues or organs.

Figure 7-4. Oxygen Balance

Measuring global oxygen balance may be useful in monitoring the critically ill
patient. The goal of resuscitation in a critically ill patient is to ensure an
appropriate oxygen balance. When there is not an oxygen balance, and
consumption is higher than delivery for an organ, the organ is ischemic.
Ischemia leads to organ failure as the organ shifts from aerobic to anaerobic
metabolism. Minimally invasive measurements of global oxygen balance
include central venous oxyhemoglobin saturation (ScvO2) and lactate
concentrations.

Normal SvO2 is >65%.

Normal ScvO2 is >70%.

ScvO2 can be obtained continuously or intermittently from a catheter placed

in the internal jugular or subclavian vein and correlates with the mixed
venous oxyhemoglobin saturation (SvO2) obtained from a pulmonary artery
catheter in the pulmonary artery. The SvO2 measures the oxyhemoglobin
saturation of blood from the whole body that has been mixed in the
pulmonary artery. These measures of venous oxyhemoglobin saturation
represent the amount of oxygen still bound to hemoglobin after traversing the
tissue capillaries and returning to the right heart; the difference between the
SaO2 and SvO2 estimates the amount of oxygen used (Figure 7-5). In normal
individuals, the SvO2 is >65% and the ScvO2 is 2% to 3% lower. However,
in patients with shock and/or hypoperfusion, the ScvO2 may be 5% to 7%
higher than the SvO2 because of greater desaturation of venous blood from
the gastrointestinal tract contributing to SvO2. Low values of ScvO2 suggest
an imbalance in the oxygen supply and demand. This imbalance may be
caused by decreases in cardiac output, hemoglobin concentration, SaO2, or
increases in tissue oxygen consumption. Patients may have more than one
abnormality contributing to oxygen imbalance. A normal ScvO2 may still be
associated with tissue hypoxia in conditions such as severe sepsis and certain
poisonings (eg, cyanide). Further evaluations of lactate concentration and
organ function are needed to assess oxygen balance in the seriously ill patient
when the ScvO2 is normal.
 Figure 7-5. Determinants of Oxygen Balance

Abbreviations: Hgb, hemoglobin; SaO2, arterial oxyhemoglobin saturation

Oxygen balance depends on the oxygen delivered to the tissues and the metabolic needs
of those tissues. An estimate of the oxygen utilized by the tissues is provided by the
central venous oxyhemoglobin value (ScvO2 and mixed venous oxyhemoglobin saturation
(SvO2).

Elevated lactate concentrations correlate with a

worse prognosis in severely ill patients (Figure
7-6).

Lactate is another indicator of the overall oxygen balance. It is produced

during anaerobic metabolism when cellular hypoxia occurs. The elevation of
blood lactate in shock and hypoperfusion may be the result of an inadequate
oxygen supply to tissue but also may be affected by altered hepatic
metabolism, use of vasoactive drugs, and other factors. Lactate concentrations
do not have high sensitivity or specificity for inadequate tissue oxygenation,
but elevated concentrations often are associated with tissue hypoperfusion. A
decreasing lactate concentration may be a useful indicator of effective
interventions.

Figure 7-6. Lactate and Mortality

Capillary refill time is another useful tool. It is a simple clinical maneuver that
may assist with evaluation of oxygen delivery and hemodynamic resuscitation
in a critically ill septic patient.

Case Study (cont.)

A 67-year-old woman with a medical history of hypertension, diabetes
mellitus, and systolic heart failure (LVEF 20%) presented to the hospital with
altered mental status and shortness of breath. The patient’s pulse is 123
beats/min, blood pressure 84/54 mm Hg, respiratory rate 28 breaths/min and
oxygen saturation on pulse oximetry (SpO2) 89% while breathing room air.
She was found to have a lower gastrointestinal bleed.
 – What factors may lead to poor oxygen delivery?
– What monitoring strategies would be employed to assess the condition of
this patient?

IV. MONITORING DETERMINANTS OF OXYGEN

BALANCE

Trends in the values of measured variables are

usually more helpful than single values.

Precise monitoring of oxygen balance is not easily accomplished because

special expertise, invasive monitoring, and significant resources are required.
However, monitoring of variables, such as oxyhemoglobin saturation, blood
pressure, ScvO2, lactate concentration, and fluid responsiveness combined
with other clinical information, may provide guidance in evaluating the
adequacy of oxygen balance in seriously ill patients.

A. Monitoring of Oxyhemoglobin Saturation

1. Principles
The pulse oximeter is a simple, noninvasive device that estimates arterial
oxyhemoglobin saturation. The transmission of red and infrared light through
the capillary bed creates several signals throughout the pulsatile cardiac cycle.
These signals measure the absorption of the transmitted light by the tissue or
venous and arterial blood. Calculations made from the processed signals
provide estimates of the oxygen saturation of hemoglobin, expressed as a
percentage. This is not the same as the PaO2 in the blood, although PaO2 is
the primary determinant of the saturation of hemoglobin. It does not reflect
adequacy of oxygen delivery or ventilation. The value measured by the device
is commonly called the SpO2 to distinguish it as the oxyhemoglobin saturation
measurement by a pulse oximeter rather than the SaO2, which is determined
directly from an arterial blood sample by co-oximetry. Pulse oximetry is
useful in detecting hypoxemia and titrating the delivered oxygen concentration
in patients receiving supplemental oxygen.

2. Clinical Issues

Pulse oximetry measurements will be affected by

inflation of a blood pressure cuff on the same
extremity as the oximetry sensor because of
disappearance of the pulsatile waveform.

Studies have shown that to ensure a PaO2 of 60 mm Hg (8.0 k Pa), an SpO2

of 92% should be maintained in patients with light skin, whereas 94%
saturation may be needed in patients with dark skin. Oximetry sensors can be
applied to the finger, toe, earlobe, bridge of nose, forehead, or any skin
surface from which a reliable pulsatile signal can be obtained. Factors that
can affect signal detection or fidelity are listed in Table 7-3. Pulse oximeters
display a digital heart rate derived from the pulsatile signal detected by the
sensor. This rate should equal the patient’s heart rate as measured by another
method, so these two rates should be compared as the first step in the
analysis of an SpO2 measurement.

Table 7-3 Factors That Affect Accuracy of Pulse Oximetry

B. Blood Pressure Monitoring
Although blood pressure is not a direct determinant of oxygen balance, an
appropriate driving pressure is necessary for oxygen delivery at the tissue
level. Blood pressure is directly proportional to cardiac output and systemic
vascular resistance according to the following relationship:
Blood pressure = cardiac output × systemic vascular resistance
Blood pressure may be monitored invasively, with arterial cannulation, or
noninvasively with a cuff.

1. Automated Noninvasive Devices

a. Principles

Automated blood pressure devices are frequently used to obtain

intermittent blood pressure measurements. These devices use one of
several methods to measure systolic and diastolic pressures, but the
most common method is oscillometry. Systolic and diastolic pressures
and the mean arterial pressure are directly measured via appearance,
disappearance, and amplitude of oscillating waves. The arm is the
preferred measurement site in adults, but alternative sites include the
calf, forearm, or thigh, the latter being the least comfortable site for
patients. The cuff should not be placed on an extremity that is being
 used for intravenous infusion or in an area susceptible to circulatory
compromise. The appropriate cuff size is necessary for accurate
measurements. A cuff that is too large will underestimate the true
blood pressure, and a cuff that is too small will overestimate the true
blood pressure.

b. Clinical Issues
An adequate blood pressure measurement does not ensure adequate
tissue perfusion. Automated blood pressure devices are less accurate
in clinical situations commonly encountered with the critically ill
patient, such as shock, vasoconstriction, mechanical ventilation, and
arrhythmias. Shivering, muscle contraction, and movement of the
extremity can lead to erroneous measurements. Blood pressure
monitoring via an arterial catheter is preferable to the use of an
automated blood pressure device in hemodynamically unstable
patients.

2. Arterial Cannulation

a. Principles
An indwelling arterial catheter allows for continuous measurement of
blood pressure, pulse volume or pressure, and mean arterial pressure
(Figure 7-7) by transduction of pressure via a specialized monitoring
setup. Pulse pressure is the difference between the systolic and
diastolic pressure measurements. It may also be used for arterial
blood gas measurement. The primary indications for insertion of an
arterial cannula are the need for frequent arterial samples and
continuous assessment of arterial blood pressure. Use of an arterial
catheter should be considered for arterial blood sampling if more
than four samples are required in 24 hours. Arterial pressure
monitoring may also be used with minimally invasive hemodynamic
monitoring systems to evaluate cardiac output, stroke volume, or
pulse pressure variation.
Figure 7-7. Appearance of Arterial Pressure Wave with Invasive
Monitoring

When invasive monitoring is used, the calculation of the mean arterial pressure is based
on the area under the curve.

The dorsalis pedis artery is less reliable for

pressure monitoring in adults because of its size
and distance from the heart.

The most common insertion sites for arterial catheters are (in order of
preference for adults) the radial, femoral, axillary, and dorsalis pedis
arteries. Brachial artery cannulation is usually avoided if possible
because it is an end artery and hand ischemia is a potential
complication. Shorter catheters are used for radial and dorsalis pedis
artery insertion and longer catheters for insertion in femoral and
axillary sites. Preferred sites have alternative collateral circulations.
The choice of site is based on the presence of palpable pulses,
general hemodynamic state, and other anatomic or physiologic
factors unique to each patient.
b. Clinical Issues
The arterial catheter is never used for infusion of any medications or
fluids and must be monitored continuously. Concern about the
accuracy of the intra-arterial pressure measurements should lead to a
return-to-flow assessment with a manual blood pressure cuff.
Measurements should be made after calibration of the
catheter/transducer system at or near the level of the heart.
Several technical and anatomic factors may affect the accuracy of the
pressures obtained with the catheter system. Distortion of the arterial
waveform signal may occur because of vascular alterations, the
hydraulic coupling system of the transducer, the calibration of the
transducer, or the maintenance of the pressurized system tubing.
Inspection of the result may show an overdamped and domed
waveform or the high-spiking “overshoot or ringing” pattern of the
underdamped waveform. Both distortions have the greatest effect on
the systolic and diastolic pressures, whereas the mean arterial
pressure is less affected.

Pulse Pressure = Systolic Pressure – Diastolic

Pressure
Normal = 30–40 mm Hg

Hypotension is not always associated with the

presence of shock or tissue hypoperfusion.
As with noninvasive monitoring, intra-arterial blood pressure monitoring may
not be a sensitive indicator of hypoperfusion because of compensatory
vasoconstriction. Additional clinical information regarding volume status can
be obtained by visual inspection of the arterial blood pressure waveform in
mechanically ventilated patients (Figure 7-8). Positive pressure during
inspiration may decrease the stroke volume in patients with inadequate
intravascular volume because of decreased venous return. The decrease in
stroke volume leads to a decreased pressure that is visually represented as a
systolic variation of blood pressure and a decrease in the pulse pressure.

Figure 7-8. Variation of Blood Pressure in a Mechanically

Ventilated Patient with Hypovolemia

With positive pressure applied during inspiration, the decrease in systolic pressure is
greater than the decrease in diastolic pressure, resulting in a decrease in pulse pressure.

Possible complications associated with arterial catheter insertion are listed in

Table 7-4. These can be minimized by careful insertion technique,
appropriate catheter size for the artery, proper site care, and a continuous
flush system. The arterial waveform must be continuously monitored and
displayed, with alarm settings to prevent inadvertent blood loss through a
catheter that is accidentally opened to the atmosphere. The extremity with the
arterial catheter should be inspected frequently for evidence of ischemia or
infection. Any sign of ischemia distal to the catheter or infection at the site of
insertion requires immediate removal of the catheter. Arterial catheters
should be removed as soon as possible to minimize the risk of infection.

Table 7-4 Possible Complications of Arterial Catheters

C. Monitoring Right Ventricular Filling Pressures and SCVO2

A central venous catheter in the internal jugular or subclavian vein allows
measurement of CVP and ScvO2. Placement of a central venous catheter may
be indicated for other reasons as well (Table 7-5). Confirmation of catheter
placement in the internal jugular or subclavian vein and the tip in the superior
vena cava by chest radiography is recommended to ensure accurate
measurements of CVP and ScvO2 and to detect complications of the
procedure.

Table 7-5 Common Indications for Central Venous Cannulation

CVP, obtained from an appropriately positioned catheter, estimates the right
ventricular filling pressure as a reflection of preload (end-diastolic volume).
Normal values for CVP are 2 to 6 mm Hg, and measurements should be
made at the end of expiration. Significant variation of the CVP waveform may
occur during spontaneous breathing and mechanical ventilation, requiring
visual assessment of the waveform to identify the end of expiration (Figure 7-
9). In general, a low CVP indicates a low intravascular volume associated with
a low preload. Normal or high CVP measurements must be evaluated
cautiously because they may not predict adequate or increased preload
volume caused by changes in intrathoracic pressure or ventricular
compliance. Assessment of fluid responsiveness is necessary to estimate
adequacy of preload with normal or elevated CVP measurements. Right
ventricular preload estimates do not necessarily correlate with left ventricular
preload.
 Figure 7-9. Typical Cyclic Pattern for CVP Waveform

Typical cyclic pattern for continuous venous pressure (CVP) waveform that shows
inspiration (I) and expiration (E). A, Respiratory variation during spontaneous ventilation:
CVP decreases during spontaneous inspiration as intrapleural pressure decreases. B,
Respiratory variation during positive pressure mechanical ventilation: CVP increases
during delivery of the mechanical breath as positive pressure is transmitted from the
airway to the intrapleural space and great vessels. The vertical arrows denote the point of
end-expiration during spontaneous and mechanical ventilation.

ScvO2 can be monitored intermittently by withdrawal of blood for analysis or

continuously with a catheter containing an oximeter to evaluate oxygen
balance. Clinical protocols have used ScvO2 measurements along with other
parameters to determine adequacy of resuscitation. Normal ScvO2 values are
usually 70%.

D. Measuring Left Ventricular Filling Pressures

Left ventricular filling pressures are usually estimated from measurement of
the PAOP. A pulmonary artery catheter is necessary to obtain this information
but requires expertise in insertion, data collection, and data interpretation.
Static single measurements of left ventricular filling pressure can often be
provided by echocardiography.
E. Measuring Cardiac Output
Cardiac output plays a key role in determining oxygen delivery to the tissues.
Measurement methods, such as thermodilution with a pulmonary artery
catheter, esophageal Doppler ultrasonography, and arterial waveform pulse
pressure analysis, require varying degrees of invasiveness as well as special
expertise. In the absence of direct measurement of cardiac output, less-
specific indicators of tissue oxygenation, such as lactate concentration and
ScvO2, may guide specific interventions. A calculated value for cardiac output
can be achieved by using hemodynamic parameters along with laboratory
analysis of arterial blood gas, hemoglobin, and central venous blood gas. This
calculation is readily available online (search “FICK equation calculator”) and
gives an additional tool for resource-limited areas to monitor/trend cardiac
output.

V. TREATMENTS FOR A NEGATIVE OXYGEN BALANCE

After monitoring devices have been initiated and the patient has been
determined to be in a negative oxygen balance, resuscitation should be
continued until the balance has been restored. The first step in management
is to identify and reverse the underlying cause of the organ failure/shock.
Multiple disease processes reduce oxygen delivery or increase or alter oxygen
consumption (Table 7-6). In addition, resuscitation usually involves
increasing oxygen delivery because it is easier to alter than oxygen
consumption. At its core, resuscitation goals are to increase cardiac output,
hemoglobin, or oxygen saturation to improve oxygen delivery. Cardiac output
is dependent on preload, contractility, and afterload. A step-by-step process
for restoring oxygen delivery to the tissues will be discussed in the following
paragraphs.

Table 7-6 Disorders/Factors That Can Affect Oxygen Delivery

A. Cardiac Output
1. Fluid/Volume Responsiveness (Preload)
The practical question that clinicians often face in caring for critically ill
patients is whether further fluid administration will improve cardiac output
and oxygen delivery. This dilemma is not adequately addressed by single
measurements of heart rate, CVP, or blood pressure. It is important to
recognize that subpar fluid resuscitation can lead to inadequate perfusion. It
should be equally understood that overzealous administration of fluids can
have deleterious effects. In fact, only about 50% of unstable critically ill
patients respond to fluid administration.
Significant variation in the cardiac output, stroke volume, systolic blood
pressure, or pulse pressure in mechanically ventilated patients with evidence
of impaired oxygen delivery may suggest the need for additional fluids to
optimize cardiac output. With each positive pressure breath from the
ventilator, venous return and right ventricular preload is decreased. If the
right ventricle is dependent on preload, then positive pressure breaths will
result in a decrease in the right ventricular stroke volume, leading to a
decrease in left ventricular preload and left ventricular stroke volume (cardiac
output). A variety of devices are available that can monitor variation in
systolic blood pressure, pulse pressure, and/or stroke volume. All have
limitations in accuracy that must be considered, such as adequate tidal
volume, tachyarrhythmias, and adequate sedation.

A patient is deemed to be volume responsive if any of the following

hemodynamic parameters are demonstrated:
 Stroke volume increase of 10%–15%
Stroke volume variation/pulse pressure variation ≥12%
Cardiac output increase of 10%–15%
Passive leg raising (PLR) is another technique that may be used at the
bedside with less invasive monitoring techniques to determine whether
additional fluid is beneficial. This maneuver is performed by placing the head
of the bed flat from the semi-recumbent position and then raising both legs
simultaneously to a 45° angle (Figure 7-10). This action results in a
gravitational transfer of 250–350 mL of blood from the lower limbs and
splanchnic compartment toward the right heart. No fluid is infused and the
clinical effects are completely reversible. If a significant increase in cardiac
output or stroke volume is noted within 30 to 60 seconds of PLR, the patient
is determined to be fluid responsive. PLR has been noted to be reliable in
mechanically ventilated patients and patients with spontaneous respiratory
effort who are not mechanically ventilated. Although blood pressure and pulse
pressure have traditionally been used during PLR, cardiac output and stroke
volume changes are much more sensitive in assessing volume responsiveness.
No increase or an insignificant increase in blood pressure is less helpful in
this circumstance. PLR should not be performed in patients with increased
intracranial pressure and may not be reliable when intraabdominal pressures
are increased.
 Figure 7-10. Effects of Passive Leg Raising

Fluid boluses may also be used to determine whether a patient is fluid responsive. Boluses
of isotonic crystalloid (usually 250–500 mL) are administered over a short period (5–10
minutes) and subsequent cardiac output or stroke volume measurements are noted. If a
significant increase in cardiac output or stroke volume occurs following the bolus, the
patient is fluid responsive. This technique must be used carefully because additional fluid
may be detrimental to the patient’s cardiac or respiratory status.

2. Mean Arterial Pressure (Afterload)

If oxygen balance is not restored and the patient is found to be adequately
fluid resuscitated, the next parameter to regulate is the mean arterial
pressure. Addition of vasopressors or vasodilators leads to normalization of
afterload leading to an increase in cardiac output.

3. Contractility
Low cardiac output after normalization of preload and afterload requires the
addition of intravenous infusion of inotropes. Inotropes increase contractility,
thus leading to an increase in stroke volume. Prior to initiation of inotropic
agents, a healthcare practitioner should have monitoring of cardiac output
established to effectively titrate these medications.
B. Hemoglobin
The patient’s hemoglobin is monitored and if the level is <7g/dL (<8g/dL if
heart failure/ischemia), then the patient should be considered for a
transfusion. Transfusion may be required for hemoglobin levels >8g/dL if
the patient is symptomatic. Symptomatic anemia results in hypotension,
tachycardia, orthostatic hypotension, fatigue, dizziness with movement, and in
extreme cases, hypoxemia. As the transporter of oxygen to the tissues, loss of
hemoglobin significantly affects oxygen delivery. Blood transfusions have
significant risks on their own and should only be done if necessary.

C. Oxygenation
If the patient’s oxygen level is not adequate, supplemental oxygen can be
added to ensure appropriate saturation of hemoglobin. Supplemental oxygen
can range from a nasal cannula to endotracheal intubation. Treatment of the
underlying cause of hypoxemia is important to decrease the length of time
supplemental oxygen is required.

VI. ACID-BASE DISORDERS

Acid-base disorders are common in the critically ill patient, and assessment of
acid-base status may indicate a specific diagnosis and/or therapeutic
interventions. The presence of metabolic acidosis could suggest hypoperfusion
and prompt further assessment of the adequacy of the oxygen balance. An
appropriate evaluation of acid-base status requires accurate interpretation of
simultaneous measurements of electrolytes, albumin, and arterial blood gases,
as well as knowledge of compensatory physiologic responses. Appendix 2
includes acid-base case studies for practice in analyzing arterial blood gas and
electrolyte information and in determining appropriate interventions.

A. Evaluation of Acid-Base Disorders

Analysis of acid-base disorders in seriously ill patients requires a systematic
approach. Although several methods can be used (base excess, strong ion
difference), the approach discussed here relies on traditional analysis using
formulas based on hydrogen ion and bicarbonate (HCO3) concentrations that
can be applied at the bedside.
1. Determine the overall acid-base condition by measuring pH. Is
acidemia or alkalemia present?
2. If an abnormality is present, determine whether the primary process
is metabolic (change in [HCO3]) or respiratory (change in partial
pressure of arterial carbon dioxide [PaCO2]).

3. If a respiratory disturbance is present, determine whether it is an

acute or a chronic process.
4. If a metabolic disturbance is present, determine whether respiratory
compensation is adequate.
5. Always calculate the anion gap (AG); if needed, correct for albumin.
6. If an anion gap is present, is there another metabolic derangement
present?

B. Metabolic Acidosis
Metabolic acidosis results from an increase in endogenous acid production
that overwhelms renal excretion (eg, ketoacidosis, lactic acidosis), exogenous
acid input (eg, toxin ingestion), excessive loss of bicarbonate (eg, diarrhea), or
decreased renal excretion of endogenous acids (eg, renal failure).
Compensation is achieved primarily by increasing minute ventilation to
eliminate CO2. The adequacy of respiratory compensation can be estimated
by the following formulas:

Winter’s Formula/Expected PaCO2 = 1.5 × [HCO3] + 8 ± 2; or Δ PaCO2

= 1.2 × Δ [HCO3]

The lower limit of respiratory compensation is usually a PaCO2 of

approximately 10 mm Hg (1.3 k Pa). This means the PaCO2 will not go lower
than 10 mm Hg to compensate for a metabolic acidosis.

Metabolic acidosis is further characterized by a normal or increased anion

gap. Normally, unmeasured anions exceed unmeasured cations, and the
difference results in the anion gap (AG). A patient’s normal AG is made up of
albumin and phosphate, with a normal value of approximately 10 ± 4
mmol/L. An increased AG indicates an increase in unmeasured anions and/or
a decrease in unmeasured cations. The patient’s AG is calculated using the
following formula:

AG = Na+ – (Cl- + HCO3-)

If the patient’s calculated AG is higher than the patient’s expected normal

gap, the patient has an AG metabolic acidosis. An increased AG has
limitations as the sole indicator of a metabolic acidosis. In patients with severe
hypoalbuminemia, an AG acidosis can exist even when a normal AG is
measured. In such patients, the expected normal AG may be as low as 4 to 5
mmol/L. It is imperative to calculate a corrected AG for such patients. A
simple rule of thumb: for every albumin decrease of 1 g/dL, a decrease of
2.5 to 3 mmol in the expected normal AG will occur.
In seriously ill patients, the most common causes of metabolic acidosis with
an increased AG are lactic acidosis, renal failure, and diabetic ketoacidosis
(Table 7-7).

Table 7-7 MUDPILES Acronym for Increased Anion Gap Metabolic Acidosis
 Tachypnea is an early sign of critical illness. An
increased respiratory rate may be a
compensatory mechanism for metabolic acidosis.

Metabolic acidosis with a normal AG, often called hyperchloremic acidosis,

may result from gastrointestinal or renal loss of HCO3 or volume resuscitation
with normal saline (Table 7-8).

Table 7-8 HARD UP Acronym for Normal Anion Gap Metabolic Acidosis
C. Metabolic Alkalosis
Metabolic alkaloses are usually separated into chloride-responsive (most
common) and chloride-resistant. A urine chloride level is needed to
distinguish between these two categories. A urine chloride <20 mmol/L is
seen in chloride-responsive metabolic alkalosis and a urine chloride >20
mmol/L is seen in chloride-resistant metabolic alkalosis. Diuretic therapy is a
common cause of hypochloremic metabolic alkalosis in hospitalized patients.
Normal compensation for metabolic alkalosis is hypoventilation; PaCO2 may
rise 6 to 7 mm Hg (0.8–0.9 k Pa) for every increase of 10 mmol/L in HCO3.
Treatment includes chloride replacement for chloride-responsive states and
assessment of the renal-adrenal axis for chloride-resistant conditions.
Hypokalemia is common to both types and should be corrected. Severe
alkalemia is associated with high mortality and requires aggressive treatment.

D. Respiratory Acidosis
Respiratory acidosis is most commonly the result of ineffective alveolar
ventilation. If the respiratory acidosis is acute, the pH decreases by 0.08 units
for each increase of 10 mm Hg (1.3 k Pa) in PaCO2. A very small increase in
plasma HCO3 can be seen acutely because of titration of intracellular non-
bicarbonate buffers. For each acute increase of 10 mm Hg (1.3 k Pa) in
PaCO2, the HCO3 increases by 1 mmol/L to a maximum of 30 to 32
mmol/L. In chronic respiratory acidosis, the pH decreases 0.03 units and the
HCO3 increases 3.5 mmol/L for each increase of 10 mm Hg (1.3 k Pa) in
PaCO2. The limit of normal renal compensation in chronic respiratory
acidosis is an HCO3 of approximately 45 mmol/L. Higher values suggest an
associated metabolic alkalosis. Treatment of respiratory acidosis involves the
rapid identification of the etiology and implementation of corrective action. In
some circumstances, intubation and mechanical ventilation may be necessary
to support alveolar ventilation.

E. Respiratory Alkalosis
Respiratory alkalosis results from primary hyperventilation that is the result of
a variety of etiologies. Acute pulmonary processes or an acidosis should be
considered in the seriously ill patient. Similar to changes noted in respiratory
acidosis, pH increases 0.08 for every decrease of 10 mm Hg (1.3 k Pa) in
PaCO2 in acute respiratory alkalosis, and pH increases 0.03 for each
decrease of 10 mm Hg (1.3 k Pa) in PaCO2 in chronic respiratory alkalosis.
The [HCO3] decreases 2 mmol/L in acute respiratory alkalosis and 5 mmol/L
in chronic respiratory alkalosis for each decrease of 10 mm Hg (1.3 k Pa) in
PaCO2. Chronic respiratory alkalosis is unique among acid-base disorders in
that pH may return to normal if the condition is prolonged. Therapy is
directed to the underlying cause.

F. Complex Acid-Base Disorders

Simple acid-base disorders result from a single process such as metabolic
alkalosis. In many critically ill patients, multiple acid-base disturbances exist
concurrently and result in complex acid-base disorders. For example, sepsis
often presents with respiratory alkalosis and metabolic acidosis. A systematic
approach to acid-base analysis is needed to identify the ongoing disturbances
and determine appropriate diagnoses and interventions. Formulas that are
helpful in evaluating acid-base status are listed in Table 7-9.
 Table 7-9 Acid-Base Formulas

Reproduced with permission Killu K, Sarani B, eds. Fundamental Critical Care Support. 6th ed.
Mount Prospect, IL: Society of Critical Care Medicine; 2017.

Key Points
Monitoring Oxygen Balance and Acid-Base Status
Oxygen delivery is dependent on cardiac output (blood flow) and
the oxygen content of arterial blood (hemoglobin and oxygen
saturation).
Hemoglobin is the major contributor of oxygen for tissue demands.
 Normal ventricular filling pressure measurements may not indicate
adequate preload volume.
Measurements of global oxygen balance that may be useful to
monitor in the seriously ill patient include central venous
oxyhemoglobin saturation (ScvO2) and lactate concentrations.

Low ScvO2 values suggest an oxygen imbalance that may be the

result of decreases in cardiac output, hemoglobin concentrations,
or arterial oxyhemoglobin saturation, or increases in tissue oxygen
consumption.
The pulse oximeter estimates arterial oxyhemoglobin saturation but
does not reflect adequacy of oxygen delivery.
Blood pressure monitoring via an arterial catheter is preferable to
the use of an automated blood pressure device in unstable patients.
Determination of systolic blood pressure, pulse pressure, or stroke
volume variation and fluid responsiveness using special monitoring
devices may be helpful in optimizing cardiac output and oxygen
delivery.
Assessment of acid-base status may suggest specific diagnoses
and/or therapeutic interventions.

Suggested Readings
1. Cherpanath T, et al. Predicting fluid responsiveness by passive
leg raising: a systematic review and meta-analysis of 23 clinical
trials. Crit Care. 2016;44(5):981-991.
2. Gauthier PM, Szerlip HM. Metabolic acidosis in the intensive care
unit. Crit Care Clin. 2002;18:289-308.
3. Hartog C, Bloos F. Venous oxygen saturation. Best Prac Res Clin
Anaesthesiol. 2014;28:4194-4928.
 4. Hernandez G, Ospina-Tascón G, Damiani L, et al. Effect of a
resuscitation strategy targeting peripheral perfusion status vs
serum lactate levels on 28-day mortality among patients with
septic shock. JAMA. 2019;321(7):654-664.
5. Jubran A. Pulse oximetry. Crit Care. 2015;19:272.
6. Kellum JA. Disorders of acid-base balance. Crit Care Med.
2007;35:2630-2636.
7. Kraut JA, Madias NE. Lactic acidosis. N Engl J Med.
2014;371:2309-2319.
8. Magder S. Central venous pressure: a useful but not so simple
measurement. Crit Care Med. 2006;34:2224-2227.
9. Marik PE, Cavallazzi R, Vasu T, Hirani A. Dynamic changes in
arterial waveform derived variables and fluid responsiveness in
mechanically ventilated patients. A Systematic review of the
literature. Crit Care Med. 2009;37:2642-2647.
10. Marx G, Reinhart K. Venous oximetry. Curr Opin Crit Care.
2006;12:263-268.
11. Mohammed I, Phillips C. Techniques for determining cardiac
output in the intensive care unit. Crit Care Clin. 2010;26:355-
364.
12. Monnet X, Teboul JL. Assessment of volume responsiveness
during mechanical ventilation: recent advances. Crit Care.
2013;17:217.
13. Monnet X, Teboul JL. Minimally invasive monitoring. Crit Care
Clin. 2015;31:25-42.
14. Monnet X, Teboul JL. Passive leg raising. Intensive Care Med.
2008;34:659-663.
15. Ortega R, Hansen CJ, Elterman K, et al. Videos in clinical
medicine: pulse oximetry. N Engl J Med. 2011;3.
16. Whittier WL, Rutecki GW. Primer on clinical acid-base problem
solving. Dis Mon. 2004;50:122-162.
 Chapter 8
DIAGNOSIS AND MANAGEMENT OF
SHOCK

Objectives
Identify the four main categories of shock.
Discuss the goals of resuscitation in shock.
Summarize the general principles of shock management.
Describe the physiologic effects of vasoactive agents.
Discuss the diagnosis and management of oliguria and acute kidney injury.

Case Study
A 72-year-old man is admitted to the floor with difficulty breathing and a productive
cough. His medical history includes chronic obstructive pulmonary disease (COPD),
hypertension, and diabetes mellitus. He was prescribed oral antibiotics by his
primary care physician 3 days ago. He presented for care with worsening symptoms
and was admitted to a medical step-down unit. Now he is unable to speak in
complete sentences. Physical examination reveals coarse breath sounds on the left
side with scattered wheezes. His skin is cool and clammy. Vital signs include a
temperature of 38.8°C (101.8°F), heart rate of 136 beats/min, respiratory rate of
26 breaths/min, blood pressure of 112/40 mm Hg, and pulse oximetry of 84% on
2 L/min of oxygen.
– Is this patient in shock?
– What initial interventions will improve oxygen delivery to his tissues?
 – What initial investigations will identify the etiology?

I. INTRODUCTION
Shock is a life-threatening syndrome of impaired tissue oxygenation and perfusion
caused by a variety of different etiologies. The diagnosis of shock requires the
integration of patient information from the history and physical examination in
combination with results from diagnostic studies. Without recognition and
treatment, shock may progress to an irreversible state and death. Prompt
recognition and early, effective interventions are necessary to prevent organ
dysfunction and irreversible organ failure. Efforts to restore adequate perfusion and
investigate the cause of shock should occur simultaneously and without delay to
minimize morbidity and prevent mortality. Strong evidence supports timely
resuscitative efforts to restore perfusion through administration of fluids and
vasoactive medications while investigating and correcting the underlying causes of
shock.

Impaired tissue oxygenation and perfusion may result from one or more of the
following:
A decrease in systemic oxygen delivery (inadequate cardiac output, low
blood oxygen content)
Ineffective tissue perfusion (maldistribution of blood flow to tissues or
inadequate perfusion pressure)
Impaired use of delivered oxygen (cellular or mitochondrial dysfunction)

The metabolic consequences of cellular hypoxia can be manifested in laboratory

studies, such as serum lactate and pH.

II. CLINICAL ALTERATIONS IN SHOCK

The presentation of patients with shock may be subtle (eg, mild confusion, sinus
tachycardia) or easily identifiable (profound hypotension, anuria). Shock may be the
initial manifestation of an underlying condition or it may develop as the condition
progresses.
Providers must be vigilant and prepared to identify shock using clinical assessment
and trends in vital signs. Tachypnea is a readily apparent compensation and
early warning sign of shock. Clinical manifestations of shock result from
inadequate perfusion, compensatory responses, and the specific etiology of shock.
Shock that has overwhelmed compensatory mechanisms may present as
hypotension, altered mental status, oliguria/anuria, and dysfunction of other organs.
A systemic inflammatory response is often triggered by shock and contributes to
progression of organ dysfunction and failure.
Direct and indirect effects of hypoperfusion are apparent in laboratory findings,
such as abnormalities in blood pH, arterial oxygenation, blood urea nitrogen,
creatinine, bilirubin, hepatic transaminases, and coagulation parameters. An anion
gap metabolic acidosis is a common finding of hypoperfusion and is often
associated with an elevated lactate concentration. An elevated lactate level is
a surrogate for systemic hypoperfusion, the severity being reflected by the degree of
elevation. Trending lactate levels can be a means to monitor effectiveness of
resuscitation.
Compensatory mechanisms in shock involve complex neuroendocrine responses that
attempt to increase tissue perfusion and oxygenation. In many forms of shock,
sympathetic vasoconstriction redirects blood flow from organs requiring low levels of
oxygen (eg, skin) toward oxygen-dependent organs (eg, brain and heart).
Compensatory vasoconstriction can maintain blood pressure early in shock and lead
to an increase in the diastolic pressure and a narrowing of the pulse pressure.
Intense vasoconstriction correlates with cold, clammy extremities and contributes to
organ hypoperfusion. Hypothermia also may be a manifestation of severe
vasoconstriction. Patients with distributive shock (discussed later) often have
vasodilation and warm extremities, but other signs of hypoperfusion are usually
present. Tachycardia, mediated by the sympathetic response, reflects an attempt to
increase cardiac output in shock. Tachypnea may be a compensatory response to
metabolic acidosis, a response to lung injury, or a reaction to direct stimulation of
the respiratory center.

The increased systemic vascular resistance present in

cardiogenic, hemorrhagic, and obstructive shock
reflects compensation to maintain blood pressure
(perfusion pressure).
Additional changes in shock alter oxygenation at the tissue level. As discussed in
Chapter 7, hemoglobin releases more oxygen as it traverses the capillaries to meet
tissue demands. A rightward shift of the oxyhemoglobin saturation curve as a result
of acidosis or increased temperature facilitates release of hemoglobin-bound
oxygen. The greater extraction of oxygen is reflected in lower mixed venous
oxyhemoglobin saturation (SVO2) or central venous oxyhemoglobin saturation
(ScVO2) measurements in many forms of shock (Chapter 7). However, a normal
value for either of these measurements does not imply that tissue oxygenation is
adequate because some forms of shock (eg, septic shock) may lead to impaired
tissue or cellular use of oxygen.

III. CLASSIFICATION OF SHOCK

Undifferentiated Shock

Patients presenting in extremis with profound abnormalities in perfusion require

rapid interventions to begin correcting their shock state. Because of rapid
physiologic deterioration, providers often must begin resuscitative efforts with little
to no information as to the etiology of shock. Begin with a primary survey focused
on managing life-threatening airway, breathing, and circulation problems, including
acute hemorrhage. Effective delegation of tasks among available team members is
essential. Definitive interventions are not necessary at first; jaw thrusts and
oral/nasal airways can facilitate a patent airway resulting in effective gas exchange
and improved breathing. Direct pressure to the site of hemorrhage, use of a
tourniquet above the site of hemorrhage, and fluid resuscitation will reduce the loss
of hemoglobin and may improve cardiac output.

Obtaining frequent vital signs provides trend information to the resuscitating

provider. Initial diagnostics ideally have a short processing time and yield
information directly helpful in identifying the etiology of shock. Arterial blood gas
(ABG) data with lactate determination quickly provide insight into the perfusion and
oxygenation status of the patient. Chest radiographs will identify the presence of an
infiltrate, effusion, or pneumothorax contributing to inadequate oxygen delivery.
Electrocardiogram (ECG) and telemetry will demonstrate dysrhythmias and
morphology changes suggestive of acute ischemia earlier than troponin assays.
Point-of-care ultrasound (POCUS) has emerged as a beneficial tool for the
resuscitating provider to identify causes of shock and to assess response to
resuscitation efforts; however, specialized training is required for appropriate use.

Classification of Shock Causes

There are four main categories of shock based on causative factors: hypovolemic,
distributive, cardiogenic, and obstructive (Table 8-1). Each type of shock has
unique hemodynamic characteristics. Exacerbation of underlying chronic conditions
caused by shock may blur hemodynamic characteristics between the types of shock.
Septic shock is a form of distributive shock, but it may have a hypovolemic
component before fluid resuscitation. Myocardial dysfunction may be present in
septic shock and hypovolemic shock. A careful history and physical examination
and focused review of medical records often provide information that is helpful in
determining the likely cause of shock.

Table 8-1 Classification of Shock

Abbreviations: GI, gastrointestinal; STEMI, ST-elevation myocardial infarction.

Knowledge of the expected hemodynamic profiles associated with the different types
of shock is helpful in determining appropriate therapy, even when specific
measurements are not available. Table 8-2 presents the usual hemodynamic
profiles for more common forms of shock, but variations occur depending on
specific etiology, cardiac function, and resuscitation status.

Table 8-2 Hemodynamic Profiles of Shock

Abbreviations: SVO2, mixed venous oxyhemoglobin saturation; ScVO2, central venous oxyhemoglobin
saturation; N, normal
aMay be decreased before or early in resuscitation.
bLeft ventricular filling pressures may be normal or low in massive pulmonary embolism.
cCardiogenic shock may result from extremes of tachycardia or bradycardia.
Adapted with permission Killu K, Sarani B, eds. Fundamental Critical Care Support. 6th ed. Mount Prospect,
IL: Society of Critical Care Medicine; 2017.

A. Hypovolemic Shock
Hypovolemic shock occurs when intravascular volume is depleted because of
hemorrhage, gastrointestinal or urinary fluid losses, dehydration, or profound soft-
tissue edema. Internal fluid losses as a result of increased capillary permeability
may be prominent in burn injury, trauma, pancreatitis, and other forms of
inflammation-associated shock. The hemodynamic findings in hypovolemic shock
are decreased cardiac output, decreased right and left ventricular filling pressures
(preload), and an increased afterload (systemic vascular resistance [SVR]) caused
by compensatory vasoconstriction. The SVO2 or ScVO2 is decreased because of
decreased cardiac output. The value of hemoglobin and hematocrit measurements
in acute hemorrhage can be inaccurate because there may not be time for
equilibration between fluid compartments to dilute the remaining hemoglobin. An
above normal hemoglobin and hematocrit may reflect significant dehydration.
Physical examination and correlation with vital signs can direct the provider toward
a more complete understanding of hemoglobin and hematocrit measurements.
Tachycardia may reflect an attempt to increase cardiac output when stroke volume
cannot be increased because of hypovolemia. Capillary refill may be delayed, skin
turgor poor, and mucous membranes dry with hypovolemia. POCUS, used by a
trained provider, allows identification of hypovolemia by examining the size of the
inferior vena cava and response to inspiration. Coaptation of ventricular walls also
reflects significant hypovolemia. Internal jugular veins will not distend with the
Valsalva maneuver or may be flat on POCUS assessment.
B. Distributive Shock
Loss of peripheral vascular tone (vasodilation) is characteristic of distributive shock.
Fluid is sequestered in the venous spaces instead of being returned to the heart.
Characteristics of hypovolemic shock and cardiogenic shock are often seen with
distributive shock. The most common form of distributive shock is septic shock, with
neurogenic shock and anaphylactic shock being much less common. The
hemodynamic profile usually includes a normal or increased cardiac output, usually
related to low SVR and low to normal ventricular filling pressures. Decreased
cardiac output may result if intravascular volume is not optimized or there is co-
existing myocardial depression. SVO2 or SCVO2 may be normal or increased
because of shunting of blood in the microvasculature or the inability of tissue to use
oxygen (as in sepsis). In contrast to other forms of shock, the vasodilation of fluid-
resuscitated distributive shock results in warm extremities, decreased diastolic
pressure, and increased pulse pressure. Neurogenic shock caused by cervical or
upper thoracic spinal cord dysfunction or injury may be associated with bradycardia
rather than tachycardia. Fever may be present in septic shock and adrenal crisis.
Close monitoring of the patient with anaphylactic shock for airway compromise is
essential because of the risk of rapid development of airway edema.

Anterior myocardial infarction is a common source of

cardiogenic shock.

C. Cardiogenic Shock
Ineffective cardiac pump function causing hypoperfusion is the hallmark of
cardiogenic shock. Causes include acute valve dysfunction, tachy- and
bradydysrhythmias, and acute coronary syndrome. Most patients with cardiogenic
shock also have an acute coronary syndrome but other common causes include
decompensated heart failure and complications after cardiac surgery. The classic
and most common presentation is a low cardiac output or index, elevated SVR, and
a high pulmonary capillary wedge pressure, but ventricular preload measurements
and SVR can vary depending on the underlying cause. Clinical symptoms include
low blood pressure with evidence of end-organ hypoperfusion, such as low urine
output, mental status changes, cool extremities along with pulmonary congestion,
and a narrowed pulse pressure. POCUS is an excellent resource to identify
inadequate pump function, pericardial effusions, and acute valve dysfunction.
POCUS also evaluates the effectiveness of fluid resuscitation, vasopressors, and
inotropes. Measurement of serum Brain Natriuretic Peptide (BNP) or its fragment
molecule, NT-proBNP are useful as diagnostic markers of acute congestive heart
failure. Plasma BNP levels in excess of 100 pg/mL are indicative of acute
congestive heart failure with high sensitivity and specificity. An NT-proBNP level
greater than 900 pg/mL is similarly diagnostic with the same degree of accuracy.

D. Obstructive Shock
The common features in obstructive shock are limitation of cardiac filling because
of external compression and excessive afterload. Cardiac tamponade impairs
diastolic filling of the right ventricle, whereas tension pneumothorax limits right
ventricular filling by obstruction of venous return. Massive pulmonary emboli
increase right ventricular afterload and prevent blood from reaching the lungs to be
reoxygenated. Severe intra-abdominal hypertension as an element of abdominal
compartment syndrome impairs venous return to the heart. Decreased cardiac
output, increased afterload, and variable left ventricular filling pressures, depending
on the etiology, characterize the hemodynamic profile in obstructive shock. In
cardiac tamponade, the pressures of the right heart chambers, the pulmonary
artery, and the left heart chambers equilibrate in diastole. A drop of > 10 mm Hg
in systolic blood pressure during inspiration (pulsus paradoxus) is an important
clinical finding in patients with suspected cardiac tamponade. Distended jugular
veins may be seen, depending on the time course of development and intravascular
volume status. CT angiography of the chest remains the gold standard for diagnosis
of pulmonary embolism. The presence of pericardial effusion with impaired
ventricular function on bedside ultrasound is diagnostic for pericardial tamponade.
Chest radiography and ultrasound will both be diagnostic of pneumothorax. Tension
pneumothorax is diagnosed by a combination of severe hypoxia, absent breath
sounds, shock, and a pneumothorax on chest radiograph or absence of pleural slide
on bedside ultrasound.

IV. GENERAL PRINCIPLES OF SHOCK MANAGEMENT

 Restoration of hemodynamic stability should be a
priority while efforts to treat the cause of shock are
implemented.

The overall goal of shock management is to improve oxygen delivery and use to
prevent cellular and organ injury. Effective therapy requires treatment of the
underlying etiology, restoration of adequate perfusion, and comprehensive
supportive care. Monitoring should allow for trending and focus on assessing
effectiveness of interventions, commonly referred to as “end points of
resuscitation.” Interventions to restore perfusion center on achieving an adequate
blood pressure (typically a mean arterial pressure [MAP] > 65 mm Hg),
normalizing cardiac output, and optimizing oxygen delivery. In normal physiology,
oxygen delivery far exceeds oxygen consumption, allowing strenuous activity or
tolerance of physiologic stress. Oxygen delivery is improved by maximizing
saturation of hemoglobin, transfusing red blood cells, and increasing cardiac output
(stroke volume × heart rate). Oxygen consumption is increased in severe infection,
seizures, and fever. Source control of infections, administration of antipyretics, and
control of seizures are effective measures to reduce oxygen consumption. These
goals are usually accomplished with a combination of interventions, as summarized
in Table 8-3 and Figure 8-1.

Table 8-3 Interventions for Managing Shock

aVasodilator agents are used only when blood pressure is adequate.

 Figure 8-1. Approach to the Patient With Shock

Abbreviations: BP, blood pressure; MAP, mean arterial pressure

Key aspects of initial shock management include a blood pressure goal, with titration of fluids and
vasoactive drugs to ensure adequate intravascular volume and MAP > 65 mm Hg. After these
initial objectives are achieved, oxygen delivery and organ perfusion may be assessed by using
such monitors as lactate levels, central venous oxygen saturation (ScVO2), urine output, and
evidence of end organ performance. Fluid responsiveness may be determined by invasive
hemodynamic monitoring systems or simple tests such as straight leg raising.

Shock frequently occurs without hypotension. Providers should not await

hypotension to begin treating shock and improving perfusion. Hypotension is a clear
sign that compensatory mechanisms are failing and that organs are at risk of
progressive failure. The first goal in treating hypotensive shock is to achieve a
minimum MAP. This is needed to maintain blood flow to the heart and other organs
while optimizing other components of oxygen delivery. A MAP ≥ 65 mm Hg is
often recommended as an initial goal. A higher MAP may be needed in patients
with myocardial ischemia or chronic hypertension, but an increase in blood
pressure is beneficial only if it translates into improved perfusion. Achievement of
MAP targets is accomplished with fluid boluses and vasoactive drugs.
It is important to distinguish between achieving blood pressure goals and improving
perfusion, which may be exclusive of each other. Blood pressure measurement
using noninvasive and invasive methods is far more readily available than newer
technologies that measure tissue perfusion. Although normal blood pressure does
not necessarily correlate with adequate perfusion, targeting a goal MAP during the
early resuscitation of shock is a reasonable initial end point of resuscitation until
other markers can be assessed. Caution should be exercised with interventions to
improve blood pressure because an associated increase in cardiac output may
increase myocardial oxygen demand. Following initial resuscitation, the MAP goal
should be individualized based on further assessment of the adequacy of systemic
and organ perfusion.

Many patients with shock require intubation.

The next goal in the management of shock is to optimize oxygen delivery. As

outlined in Chapter 7, this can be enhanced by increasing cardiac output,
hemoglobin concentration, or oxyhemoglobin saturation. In the absence of specific
measurement of cardiac output or stroke volume, an assessment of adequate oxygen
delivery depends on the etiology of shock and the presence of perfusion
abnormalities (discussed later). Fluids and/or vasoactive agents are often needed to
optimize cardiac output. The determinants of the oxygen content of blood
(hemoglobin and oxyhemoglobin saturation) can be easily measured and optimized
when indicated. Increasing the hemoglobin concentration by transfusion is an
efficient way of improving oxygen delivery by increasing oxygen transport capacity.
For example, increasing the hemoglobin concentration from 7 g/dL to 9 g/dL
increases oxygen delivery by almost 30%, even if cardiac output remains constant.
The oxyhemoglobin saturation can be increased by raising the partial pressure of
arterial oxygen with oxygen supplementation and mechanical ventilation. However,
once the partial pressure of arterial oxygen has been increased to a range of 60 to
70 mm Hg (8–9.3 k Pa), little additional benefit is gained by increasing it further.
An oxyhemoglobin saturation of 95% and greater is recommended in patients with
shock.

A. Monitoring
Patients with shock require monitoring to determine appropriate interventions and
assess response to interventions (Chapter 7). Continuous electrocardiographic
monitoring is needed to assess changes in heart rate and rhythm. Blood pressure is
best monitored with an arterial catheter because of the inaccuracies of noninvasive
devices in patients with shock. Pulse oximetry should be monitored routinely to
facilitate assessment of oxyhemoglobin saturation. Hypoperfusion may be disclosed
by a poor pulse oximetry waveform. A low central venous pressure in the
appropriate clinical situation may suggest inadequate intravascular volume. New
technologies assess pulse pressure and stroke volume variation (PPV or SVV) to
monitor volume status with greater variability reflecting hypovolemia. Measurement
of ScVO2 via a central venous catheter may be useful as an indicator of oxygen
balance, but a normal ScVO2 value does not rule out hypoperfusion. Comparison of
oxyhemoglobin concentration (O2Hgb) between venous and arterial blood gases
provides insight regarding oxygen delivery and consumption. A urinary catheter
should be inserted to monitor urine output as an indicator of renal perfusion, with a
suggested goal of 0.5 to 1 mL/kg/h. Lactate concentration and acid-base status
should be assessed initially and at appropriate intervals. Normal or decreasing
lactate concentrations or improving acidosis suggest improved oxygen delivery and
tissue response. Other laboratory data should be considered to assess progression
or improvement of organ dysfunction.

The trend of measurements over time, especially in

response to interventions, is often more valuable than
a single measurement.

B. Fluid Therapy
Physical examination may provide valuable information about the intravascular
volume status. Diffuse or dependent crackles, as well as distended neck veins,
suggest high ventricular filling pressures unless acute respiratory distress syndrome
or diffuse pneumonia is present. Clear lung fields and flat neck veins suggest
inadequate preload in the hypotensive patient. Although orthostatic changes in
blood pressure and heart rate may be helpful in determining the degree of volume
depletion, the tachycardic hypotensive patient should not be subjected to these
positional changes. The nature and degree of fluid deficits should be determined to
identify the type and appropriate quantity of fluid replacement. Monitoring of fluid
responsiveness, as described in Chapter 7, may be helpful in determining the
appropriate volume of fluids.

The initial therapy for most forms of shock is expansion of intravascular volume.
Increasing preload creates more potential energy by distending the ventricles,
resulting in stroke volume increases. It is important to monitor volume status closely
to avoid excess preload which reduces cardiac output. Fluid resuscitation in the
patient with shock can be more complex in the context of acute and chronic medical
conditions. Guidance for fluid resuscitation in adults with septic shock is outlined in
Figure 8.2. Unless suspicious for hemorrhagic shock, initial fluid resuscitation is
begun with either crystalloid or colloid solutions. Crystalloids are less expensive
than colloids and typically accomplish the same goals, although a higher total
volume is needed because of their higher volume of distribution. Isotonic fluids
consisting of a balanced electrolyte solution which closely resemble normal
concentrations may avoid iatrogenic metabolic derangements. If 0.9% normal saline
is used for fluid resuscitation, providers should monitor electrolytes frequently to
avoid iatrogenic hyperchloremia and metabolic acidosis that can occur with infusion
of large volumes. Hypotonic fluids may create rapid fluid shifts between
intracellular, interstitial, and intravascular spaces as well as severe electrolyte
abnormalities. Hypertonic solutions (2%–23.4% saline) should be used with great
caution and frequent monitoring of electrolytes. Colloid solutions include hetastarch,
albumin, and gelatins. Use of albumin is limited by cost in some areas. Providers
should exercise caution in the use of hetastarch for resuscitation of patients in shock
because of the increased risk of renal injury and coagulopathy. Crystalloids in
titrated boluses of 500 to 1000 mL (up to 30 mL/kg) or colloids in titrated boluses
of 250 to 500 mL may be given initially to most adult patients and repeated as
necessary while appropriate parameters are closely monitored. Smaller bolus
amounts are indicated for patients with suspected or known cardiogenic shock. Use
of bedside assessment tools, such as ultrasound and the passive leg raise test, may
provide guidance on the benefits and risks of additional fluid. Providers should
establish which end points of resuscitation and measurements of volume status will
be monitored and evaluate data points regularly.

Initial administration of 30 mL/kg of crystalloid to

adults in septic shock should be followed by
reassessments of oxygenation.

Figure 8-2. Application of Fluid Resuscitation in Adult Septic Shock

 Abbreviations: ALI, acute lung injury; CHF, congestive heart failure; CMS, U.S. Centers for
Medicare and Medicaid Services; CVP, central venous pressure; ESRD, end-stage renal disease ;
SSC, Surviving Sepsis Campaign; SCVO2, central venous oxygen saturation
Reproduced with permission Dellinger RP, Schorr CA, Levy MM. A Users’ Guide to the 2016
Surviving Sepsis Guidelines. Crit Care Med. 2017; 45(3):381-385. Copyright © 2017 by the
Society of Critical Care Medicine and Wolters Kluwer Health, Inc. All Rights Reserved.

Only red blood cells have oxygen-carrying capacity. Transfusion is appropriate in

the setting of acute blood loss anemia (hemorrhagic shock) or among patients with
severe impairments in oxygen delivery. In the actively bleeding patient, hemostatic
resuscitation with whole blood or a mixture of plasma, platelets, and red blood cells
(balanced-ratio component transfusion) is necessary to restore oxygen delivery while
simultaneously controlling coagulopathy. Conservative transfusion thresholds (Hgb
of 7 g/dL) have been successful in reducing costs without compromising outcomes.
Among patients in shock, transfusion should be considered as a means of volume
expansion and to improve oxygen delivery. A more liberal approach to transfusion
may be relevant in patients with severe hypoxemia, myocardial ischemia, or co-
existent hemorrhage who could benefit from increased capacity for oxygen delivery.
Correction of coagulopathy among patients in septic shock should be reserved for
those with coincidental gastrointestinal bleeding or who are anticoagulated and
require reversal for an emergent invasive procedure. Fresh frozen plasma should be
used only for correction of a coagulopathy and not for volume replacement.
Priorities in the administration of fluids are resuscitation and replacement of
ongoing losses. As the clinical course continues, the solution that most closely
approximates the patient’s losses should be used, with serum electrolytes guiding
therapy.

The purpose of achieving euvolemia is to optimize cardiac output and restore

perfusion. Often, this correction manifests clinically as resolution of tachycardia,
hypotension, or oliguria. However, these end points may remain altered despite
euvolemia in states such as septic (distributive), neurogenic, or obstructive shock.
Vasoactive drug support is indicated in patients who continue to have a low blood
pressure or impaired cardiac output after euvolemia has been established, or who
no longer have a beneficial response to fluid challenge or passive leg raising. The
potential deleterious effects of overly aggressive fluid resuscitation include
deterioration of oxygenation because of pulmonary edema, ileus or bowel edema,
and compartment syndromes. Therefore, frequent auscultation of the chest for the
presence of crackles, determination of relevant compartment pressures, and
monitoring of partial pressure of arterial oxygen or oxyhemoglobin saturation by
pulse oximetry should be performed during fluid resuscitation.

No one vasoactive agent or combination of agents

has been demonstrated to be superior in managing
shock.

Intra-abdominal pressure monitoring should be considered in patients requiring

massive fluid resuscitation. In the absence of advanced hemodynamic monitoring,
volume therapy should be administered carefully in patients with persistent
hypotension and/or hypoperfusion until no further change is noted in the blood
pressure following a fluid bolus. This suggests that additional fluid no longer
improves the patient’s cardiac output and administration of more fluid can lead to
the deleterious effects noted previously. Further correction of hypotension or other
perfusion abnormalities may require pharmacologic support with vasoactive drugs.
This approach to volume therapy presents minimal risk in patients with adequate
oxygenation.

C. Vasoactive Agents
Vasoactive agents for the acute management of shock include medications with
vasopressor, inotropic, and chronotropic effects. A vasopressor is a medication that
results in arteriolar constriction, a rise in systemic vascular resistance, and a rise in
arterial blood pressure. An inotrope is a medication that augments cardiac
contractility. Many agents have more than one hemodynamic effect, and results may
vary among individual patients and with dosage. The goals of resuscitation are
usually more important than the specific agent chosen. Table 8-4 summarizes each
vasoactive drug and its mechanism of action. An intensivist should be consulted
when the decision to use vasoactive medications is made. Early initiation of
vasoactive medications is advised to decrease the duration of hypoperfusion.
Guidance for administering vasoactive agents in patient with septic shock is found in
Figure 8.3. Intraosseous access allows for early administration of vasoactive
medications without central venous access. In emergent circumstances, some ino-
tropes and vasopressors can be administered for a short duration through large-bore
peripheral IV catheters that are placed at the antecubital fossa or more proximally.

Vasoactive agents are important tools to achieve

adequate perfusion in shock patients. Steroid
administration to address relative or actual adrenal
insufficiency may contribute to improved perfusion.

Table 8-4 Vasoactive Agents

Abbreviations: BP, blood pressure; DA-R, dopamine receptor; HR, heart rate; UOP, urine output Potency scale
is from 1+ to 4+
aβ = adrenergic receptor that increases cardiac contractility and/or heart rate
1
bβ = adrenergic receptor that mediates bronchodilation and arteriole dilation
2
cα = adrenergic receptor that mediates arteriole constriction and increase in peripheral vascular resistance
1
dMilrinone = a phosphodiesterase inhibitor with indirect β and β effects V1 receptor= vasopressin binds to
1 2
G-protein-coupled V1 receptors on vascular smooth muscle that leads to increased intracellular calcium levels
and vasoconstriction
eAng II-type I = Binds angiotensin II receptor type 1 and stimulates aldosterone release yielding
vasoconstriction and increased afterload
 Figure 8-3. Vasopressor Use for Adult Septic Shock With Guidance for
Steroid Administration

Abbreviation: MAP, mean arterial pressure

Reproduced with permission Dellinger RP, Schorr CA, Levy MM. A Users’ Guide to the 2016
Surviving Sepsis Guidelines. Crit Care Med. 2017; 45(3):381-385. Copyright © 2017 by the
Society of Critical Care Medicine and Wolters Kluwer Health, Inc. All Rights Reserved.

1. Norepinephrine
Norepinephrine is the initial vasoactive drug recommended in the treatment of
septic shock. It is a more potent α-adrenergic vasoconstrictor than either dopamine
or phenylephrine, and it also has β1-mediated inotropic and chronotropic effects. In
adults, the infusion rate of norepinephrine starts at 0.05 µg/kg/min (µg/min) and is
titrated to desired effects. As with other vasoconstrictors, cardiac output may
decrease as afterload and blood pressure are increased. Norepinephrine may
increase renal blood flow in patients with adequate volume resuscitation. An
increase in heart rate is uncommon with use of norepinephrine.

2. Dopamine

Dopamine is a less frequently used vasoactive agent with dose-dependent inotropic

and vasopressor effects. It is no longer a drug of choice in the treatment of septic
shock. Although dose response varies greatly among patients, some generalizations
about dose and anticipated effect may be helpful. At low rates of infusion (1–5
µg/kg/min), dopamine has modest inotropic and chronotropic effects. In this dose
range, it acts on the dopaminergic receptors in the kidney and may increase urine
output; however, its use for renal effects is not recommended because it does not
prevent renal dysfunction or improve outcomes. At intermediate rates of infusion
(6–10 µg/kg/min), dopamine has primarily inotropic effects. At higher infusion rates
(≥ 10 µg/kg/min), it has significant α-agonist effects that produce dose-related
vasoconstriction. At infusion rates ≥ 20 µg/kg/min, dopamine usually offers no
advantage over norepinephrine, which may have greater vasopressor effect.
Potential adverse effects include arrhythmias (particularly atrial fibrillation) and
tachycardia.

3. Epinephrine
Epinephrine has both α-adrenergic and β-adrenergic effects, potent inotropic and
chronotropic effects, and at higher doses, vasopressor effects. Doses start at 0.05
µg/kg/min (µg/min) and can be titrated as desired. The epinephrine-induced
increase in myocardial oxygen consumption may limit the use of this agent in adults,
especially in the presence of coronary artery disease. Potential side effects of
epinephrine include tachyarrhythmias and increased lactic acid production. The
Surviving Sepsis Campaign recommends adding epinephrine as the second-line
agent after norepinephrine for patients in septic shock, with a recommended dose of
20–50 µg/min (Figure 8-3). Recent literature has also supported the use of “push-
dose” epinephrine in the resuscitation of patients with shock who do not have
central venous access. This can be especially useful among patients being
resuscitated outside of an intensive care unit. Epinephrine 1:10,000 diluted to an
epinephrine 10 µg/mL concentration given in 0.5- to 2-mL aliquots every 2 to 5
minutes can facilitate achieving MAP targets while infusions of other vasoactive
medications are prepared and intraosseous or central venous access is obtained.
Epinephrine is also part of Advanced Cardiac Life Support protocols.

4. Phenylephrine

Phenylephrine is a pure α-adrenergic vasoconstrictor. In adults, the infusion rate

starts at 25 µg/min and can be titrated to the desired blood pressure. Because its
mechanism of action involves solely arterial constriction, it is most useful in states
with arterial dilation without concomitant cardiac depression, such as neurogenic
shock or hypotension caused by an epidural anesthetic. Phenylephrine is not
recommended for use in septic shock unless in a salvage role when there is failure
to improve with multiple other vasoactive medications or significant dysrhythmias
occur with norepinephrine. In emergent circumstances, push-dose phenylephrine
may be administered via peripheral IV or intraosseous catheter to improve coronary
perfusion and cardiac output. Administration consists of 50–200 µg of
phenylephrine 100 µg/mL given every 2 to 5 minutes.

5. Vasopressin

Vasopressin is a potent vasopressor that acts through V1 receptors to produce

vasoconstriction. As blood pressure is increased, cardiac output may decrease,
similar to the effect of norepinephrine. The recommended dose in adults is 0.01 to
0.04 units/min. In septic shock, vasopressin is recommended by the Surviving
Sepsis Guidelines at a fixed dose (0.03 units/min) to augment MAP in patients
already on norepinephrine. The addition of vasopressin in septic shock may reduce
the dose of norepinephrine needed to achieve MAP targets. Higher doses (0.04
units/min) for prolonged periods of time may lead to ischemic events, especially
mesenteric ischemia. Vasopressin may be considered for use in hypotensive shock
refractory to other agents and fluid resuscitation, but it has not been found to
improve mortality.

6. Dobutamine

Dobutamine is a non-selective β-adrenergic agonist with inotropic effects. It is used

in doses of 5 to 20 µg/kg/min and is usually associated with an increase in cardiac
output, which is mediated mostly by an increase in stroke volume. Arterial blood
pressure may remain unchanged, decrease, or increase slightly. Dobutamine must
be introduced with care in the hypotensive patient; in the face of inadequate
intravascular volume replacement, blood pressure can drop precipitously and
tachycardia may be problematic. This agent has variable chronotropic effects.
Among patients in septic shock with concomitant acute heart failure, the inotropic
effects of dobutamine may be of value and supersede the use of norepinephrine to
achieve MAP targets and improve perfusion.

7. Milrinone

Milrinone is a phosphodiesterase inhibitor that inhibits the breakdown of cyclic

adenosine mono-phosphate, the second messenger for catecholamines. Therefore,
milrinone is a sympathomimetic agent with mostly β-adrenergic-like effects. It will
increase cardiac output mostly by increasing stroke volume and will decrease
afterload by causing arteriolar dilation. It should be used with caution in
hypovolemic patients because it can cause significant hypotension.

8. Angiotensin II

Angiotensin II is a potent vasoconstrictor and has been recently approved for use by
the Food and Drug Administration in high-output shock. Angiotensin II
accomplishes this through multiple mechanisms, including direct vasoconstriction of
peripheral vessels, water reabsorption through potentiation of antidiuretic hormone,
sodium retention via the synthesis of aldosterone, and through synergistic activity
with catecholamines. Although it is not a new drug, there is a renewed interest in its
use in treating refractory shock. Evidence suggests that angiotensin II may
preferentially be of benefit in acute kidney injury and acute respiratory distress
syndrome in which the renin-angiotensin system (RAS) is known to be disrupted.
During hypotension, the RAS is activated in response to decreased pressure and
solute content in the kidney. Acute kidney injury limits the response of the kidney
to hypotension. Acute respiratory distress syndrome disrupts the RAS as
angiotensin I is converted to angiotensin II in the lungs. Angiotensin II may have a
role in cardiogenic shock, angiotensin-converting enzyme inhibitor overdose,
cardiac arrest, liver failure, and in settings of extracorporeal circulation. Assessment
of a serum renin level may be helpful to determine whether a patient would benefit
from this medication.

D. End Points of Resuscitation

No single end point can be used to assess resolution of shock and return to normal
homeostasis. Furthermore, fluid and pharmacologic therapy should be titrated
based on the trend for the particular end point rather than its absolute value.
Blood pressure, pulse, and urine output are the most commonly used end points in
resuscitation of shock. When resuscitating patients with shock early in their course
or in facilities with limited resources, easily assessed end points should be used.
Achievement of euvolemia may reflect an ability to de-escalate vasopressors and
inotropes while maintaining a target MAP. Resolution of metabolic acidosis,
normalization of lactic acid levels, and resolution of altered mental status reflect
improved perfusion. Insertion of a urinary catheter to monitor urine output should
occur early to allow trending. In patients with prolonged hypoperfusion, urine
output may remain low despite achieving target blood pressures and improving
global perfusion. Urine output may not be a reliable end point in patients with
preexisting or new renal dysfunction. All parameters can be easily measured but
lack sensitivity and specificity for either detection of impending shock or its
resolution. As such, vital signs may be normal even if the patient is in a state of
compensated shock. Conversely, vital signs may remain abnormal despite
appropriate therapy (eg, low blood pressure and urine output despite reaching a
euvolemic state).
In addition to the clinical evaluation of vital signs and urine output, monitoring
techniques that assess cardiac output or stroke volume may be helpful in
determining when fluid resuscitation is optimized as an end point (Chapter 7).
Monitoring a PPV or SVV requires arterial catheterization and can be useful
beyond the initial resuscitation of patients outside of the intensive care unit. In
addition, use of POCUS to assess ventricular filling and inferior vena cava
dimensions may be helpful in the assessment of volume status. ScVO2 and lactate
concentrations as measurements of global oxygen balance may also be useful in
monitoring the patient in shock and assessing the impact of interventions. Neither
measurement assesses the need for fluid versus pharmacologic support of the
circulation. Normalization of organ function as assessed by laboratory values (such
as renal or liver chemistries) is another end point to assess, but these measurements
are not usually helpful in the first 24 hours.

V. MANAGEMENT OF SPECIFIC TYPES OF SHOCK

A. Hypovolemic Shock
The treatment goals in hypovolemic shock are restoration of intravascular volume
and prevention of further volume loss. Therapy for hypovolemic shock should be
targeted to reestablish normal blood pressure, pulse, and organ perfusion. For
initial resuscitation, either colloid or crystalloid fluids are effective if given in
sufficient volume. Subsequently, the fluid that is used should replace the fluid that
has been lost. For example, blood products may be needed to replace blood loss
(Chapter 12), and crystalloid should be used for vomiting and dehydration. For
hypotension, the crystalloid of choice is an isotonic solution because of the
osmolality needed to restore intravascular volume. In large volume resuscitation,
however, normal saline infusion may produce hyperchloremic metabolic acidosis.
Vasoactive medications should be considered only as a temporizing measure while
fluid resuscitation is ongoing or when hypotension persists despite adequate volume
resuscitation. POCUS allows for ongoing reassessment of volume status and
monitoring of response to fluid challenges. Passive leg raise provides an intrinsic
bolus equivalent to 300 mL and can demonstrate fluid responsiveness if blood
pressure increases by 10–20% after raising both legs to an elevation of 45°.
Central venous pressure monitoring may help to guide fluid resuscitation in patients
without significant heart or lung disease.

B. Distributive Shock
The initial approach to resuscitating the patient with septic shock, which is a
common form of distributive shock, is restoration and maintenance of adequate
intravascular volume. Patients with sepsis manifest life-threatening organ
dysfunction caused by a dysregulated host response to infection. Prompt recognition
is essential in patients with sepsis who have persistent hypotension requiring
vasopressors to maintain a MAP of ≥ 65 mm Hg and have a serum lactate level >
2 mmol/L (18 mg/dL) despite adequate volume resuscitation because they have
progressed to septic shock. Delays in recognition, resuscitation, antibiotic
administration, and achieving other source control are associated with increased
morbidity and mortality. Obtaining cultures and prompt administration of
appropriate antibiotics are essential, as are other interventions to control the
infection (eg, removal of contaminated catheters, surgical procedures including
drainage and debridement of infected collections). Culture-proven infection is not
necessary to initiate antibiotics; however, cultures are of value later in de-escalating
antibiotic therapy. Lactate concentration should be measured and repeated if
abnormal as one component of assessing the resuscitation efforts.
 Volume expansion is the initial treatment of septic
shock. Table 8-4 provides a summary of vasoactive
drugs that should be added if adequate perfusion is
not achieved despite administration of appropriate
intravascular volume.

Volume expansion should be initiated with isotonic crystalloid solutions with an

initial recommended bolus dose of 30 mL/kg and further boluses as needed based
on patient response to attain targeted resuscitation goals. Caution should be
exercised and lower bolus volumes may be indicated when resuscitating patients
with known cardiomyopathy or heart failure. Vasodilation and diffuse capillary
leakage are common in septic shock, and fluid requirements may be large. Colloid
solutions can be considered for patients who require substantial amounts of
crystalloids. If the patient with septic shock remains hypotensive despite adequate
fluid resuscitation, norepinephrine is recommended as the initial vasoactive drug.
Vasopressin or epinephrine can be considered for patients who fail to respond
adequately to norepinephrine. Dobutamine may be considered in those patients
with inadequate perfusion after adequate administration of fluids and vasopressors
and displaying concomitant heart failure. Reversible myocardial dysfunction with
ventricular dilation and a decrease in ejection fraction frequently occurs in shock,
especially septic shock. An initial MAP of < 65 mm Hg may require initiation of
vasoactive pharmacologic therapy until fluid resuscitation is optimized.
Corticosteroids, such as intravenous hydrocortisone in divided doses, may be
considered in patients with septic shock when adequate fluids and vasoactive
medications fail to restore hemodynamic stability.

Anaphylactic shock is often treated with volume resuscitation and subcutaneous

epinephrine. In circumstances of very low blood pressure and poor peripheral
perfusion, titrated intravenous vasopressors are indicated. Acute adrenal
insufficiency is treated with volume therapy, intravenous corticosteroids, and
vasoactive medications, if needed (Chapter 17). Chapter 9 contains information
about the management of neurogenic shock.

C. Cardiogenic Shock
The primary goal in treating cardiogenic shock is to improve myocardial function.
Arrhythmias should be treated promptly. Reperfusion by percutaneous intervention
is the treatment of choice in cardiogenic shock that is the result of myocardial
ischemia (Chapter 15). Diastolic dysfunction during myocardial ischemia may
decrease ventricular compliance and elevate the left ventricular filling pressures,
falsely indicating adequate preload. Therefore, a cautious trial of fluid
administration may be warranted (250-mL bolus amounts). When blood pressure is
decreased in cardiogenic shock, initial therapy with a single agent that has inotropic
and vasopressor effects (eg, norepinephrine or dopamine) is indicated. Severely
hypotensive patients (systolic arterial pressure < 70 mm Hg) should be treated
with norepinephrine to rapidly raise the systolic arterial pressure. The addition of
an intravenous inotrope, such as milrinone or dobutamine (or dopexamine, which is
available in some countries), may be considered to augment myocardial contractility
after blood pressure stabilizes, with the goal of decreasing vasopressor
requirements. If moderate hypotension is not responsive to initial therapy,
consultation should be sought for potential interventions, such as intra-aortic balloon
counterpulsation or left/right ventricular assist devices.

Afterload and preload reduction should be avoided in

cardiac failure when hypotension is present.

The elevated SVR may impair cardiac output if it is a primary hemodynamic

alteration, as occurs in chronic congestive heart failure. Often in acute cardiogenic
shock, the SVR is secondarily elevated to maintain vascular perfusion pressure.
Treatment aimed primarily at reducing afterload with a vasodilator should be
initiated very cautiously and only in patients with hypoperfusion accompanied by
adequate blood pressure.

When cardiac failure is characterized by low cardiac output, normal or elevated

blood pressure, and hypoxemia caused by high pulmonary capillary pressure,
reduction of preload and afterload is helpful in improving hypoxemia. High
pulmonary capillary pressure can be diagnosed clinically. Preload reduction is
accomplished with loop diuretics (furosemide or bumetanide) and venodilators
(nitroglycerin and morphine), whereas afterload reduction is accomplished with
arterial vasodilators (angiotensin-converting enzyme inhibitors or, occasionally,
nitroprusside). If the blood pressure can be increased to normal levels with
inotropes, the cautious addition of afterload and preload reduction is feasible in the
presence of low cardiac output or high pulmonary capillary pressure.

D. Obstructive Shock
In the patient with obstructive shock, relief of obstruction is the treatment of choice.
Maintenance of intravascular volume is vitally important. Increasing preload by fluid
resuscitation may improve the cardiac output and hypotension temporarily.
Inotropes or vasopressors have a minimal role in the management of obstructive
shock, and these agents provide only temporary improvement, if any. Massive
pulmonary embolus is a common cause of obstructive shock.

Treatment for obstructive shock caused by a pulmonary embolism is centered on

fluid resuscitation to maintain cardiac output and prompt anticoagulation to prevent
clot propagation. Thrombolytic therapy or thrombectomy is sometimes needed in
patients with refractory cardiac collapse caused by massive pulmonary emboli. If
cardiac tamponade is present, pericardiocentesis may be a lifesaving intervention.
Tension pneumothorax must be treated promptly by needle decompression and
subsequent tube thoracostomy. Abdominal compartment syndrome in the most
extreme cases may require decompressive laparotomy.

Diuretics and venodilators should be avoided in

obstructive shock.

VI. OLIGURIA AND ACUTE KIDNEY INJURY

The kidneys are frequently affected by hypotension and hypoperfusion in all forms
of shock. Oliguria, defined as urine output < 0.5 mL/kg/h in adults, is an
important manifestation of hypoperfusion or decreased glomerular filtration rate.
There have been several criteria proposed over the years for consistency in
classifying kidney injury. The Kidney Disease Improving Global Outcomes (KDIGO)
staging criteria provides a straightforward framework for providers to assess the
stage of acute kidney injury based on serum creatinine and urine output criteria. An
increase in serum creatinine by (0.3 mg/dL or 1.5-1.9 times baseline) or urine
output < 0.5 mL/kg/hr for 6-12 hours are indicative of Stage I Acute Kidney
Injury (AKI). Further increases in creatinine and prolonged oliguria or anuria
reflect worsening AKI. Additional details regarding advanced stages of AKI can be
accessed at https://kdigo.org. Patients with chronic kidney disease or who are
regularly dialyzed may be more challenging when assessing for AKI and may best
be co-managed with Nephrology. Oliguria may be an earlier indicator of renal
dysfunction than changes in laboratory parameters. Persistence of oliguria for at
least 6 hours is one criterion for acute kidney injury (AKI). Hypoperfusion may also
result in an increase of serum creatinine and blood urea nitrogen, which are the
most common laboratory measures of renal function. Acute changes in serum
creatinine and urine output are used to define AKI and classify severity across a
broad range of renal dysfunction. A key point is that small alterations in creatinine
(even a serum creatinine increase of 0.3 mg/dL [26.5 µmol/L] within 48 hours) or
urine output predict an increased risk of renal failure and require further
evaluation. The preponderance of AKI in the shock patient relates directly to
hypovolemia with renal hypoperfusion and development of acute tubular necrosis.
Early recognition of hypovolemia and inadequate renal perfusion is essential to
facilitate early fluid resuscitation and vasopressor administration to optimize renal
perfusion and maintain adequate renal function.

Along with other parameters mentioned previously, resolution of oliguria may be

considered a goal of resuscitation in shock. Oliguria also may be the result of
inherent renal injury or postrenal obstruction, a situation in which urine output
cannot be used as a goal of adequate resuscitation. The degree of oliguria correlates
with severity of AKI, with anuria reflecting the most severe cases. Worsening renal
laboratory studies should prompt concern and consideration of a nephrology
consultation. Maintenance of urine output of at least 0.3 mL/kg/h portends a better
prognosis. Causes of oliguria and AKI are categorized as prerenal, renal, and
postrenal, as outlined in Table 8-5.

Table 8-5 Differential Diagnosis of Oliguria and Acute Kidney Injury

Additional laboratory tests may help differentiate prerenal causes of oliguria and
AKI from other etiologies. Some laboratory tests of renal function are shown in
Table 8-6.

Laboratory Tests to Distinguish Prerenal Conditions from Acute Tubular

Table 8-6
Necrosis

aFractional excretion of sodium = ([urine sodium ÷ serum sodium] ÷ [urine creatinine ÷ serum creatinine]) ×
100.

Among patients who have received furosemide recently or chronically, fractional

excretion of urea can be measured in place of sodium excretion to assess for
prerenal etiologies of AKI and oliguria. Management of oliguria or AKI caused by
shock or other etiologies in the critically ill patient should follow an organized
approach. The patient should be evaluated promptly to determine the cause of renal
dysfunction. Reversible causes should always be rapidly identified and corrected.
Insertion of a urinary catheter and a renal ultrasound scan will exclude urinary
obstruction in most patients. The urinary catheter is also a useful device to monitor
urine output and should be used in patients with shock. More frequent
measurements of blood urea nitrogen, serum creatinine, and urine output are
needed in the setting of AKI. Volume status should be assessed using clinical
examination and the monitoring techniques outlined in Chapter 7. Intravascular
volume should be optimized with crystalloid and/or colloid solutions to improve
renal perfusion. Vasoactive drugs, along with fluids, may be needed in patients with
shock to achieve an adequate blood pressure. Loop diuretics may be considered (if
blood pressure is adequate) in the setting of volume overload. Although the
conversion to a non-oliguric state does not change outcome, fluid management is
usually easier with continued urine output, especially in patients with severe
hypoxemic respiratory failure. A single dose of furosemide (1–1.5 mg/kg ideal body
weight) may be administered as a physiologic stress test in patients without
hypotension or active resuscitation. A urine output < 200 mL over 2 hours is a
strong predictor of progression to stage III AKI, need for renal replacement
therapy, and mortality. No evidence supports the use of low-dose dopamine in
oliguric patients. Once oliguric or anuric AKI is confirmed and persistent, fluids
should be restricted to the replacement of ongoing losses (including insensible
losses). In disease states associated with ongoing loss of intravascular volume, fluid
administration is necessary to maintain adequate left ventricular preload. These
losses may be substantial, as in pancreatitis, severe sepsis, and large open wounds.

Because there is no specific treatment for most cases of AKI, expectant and
supportive care is maintained. Drug dosages need adjustment not only for the
severity of AKI but also for the type of renal replacement therapy that may be used.
Nephrotoxic drugs (such as intravenous contrast) should be avoided if possible.
Monitoring of drug concentrations should be used to guide therapy when possible.
Problems with extracellular fluid overload, hyperkalemia, and hypermagnesemia
should be anticipated and avoided if possible. Hyperkalemia usually can be
managed medically until dialysis is available (Chapter 17). Nutritional therapy
must be adjusted for renal function and renal replacement therapy.

Renal replacement therapy is necessary when uremic symptoms develop or

whenever extracellular volume excess, hyperkalemia (or other electrolyte
abnormalities), or metabolic acidosis is refractory to medical therapy. Various
intermittent or continuous therapies are available to accomplish fluid removal
(ultrafiltration) or solute removal (dialysis, hemofiltration, hemodiafiltration). An
appropriate selection depends on the circumstances of the individual patient
(especially hemodynamic status) and the resources available. Consultation with a
nephrologist is advised to assist with determining the most appropriate treatment.

Case Study Conclusion

A Rapid Response Team assessed the patient and spoke with the on-call hospitalist.
An arterial blood gas with lactic acid was obtained to assess adequacy of
oxygenation, ventilation, and perfusion. Inhaled bronchodilators were ordered and
BiPAP was initiated. A chest radiograph, ECG, and troponin were performed. No
evidence of acute coronary syndrome was evident; however, B-lines were present on
the chest radiograph and intravenous furosemide was administered. Blood cultures
were obtained while the antibiotic spectrum was broadened. Four hours later, the
patient was able to oxygenate adequately without BiPAP and was able to speak in
complete sentences. His skin is now warm and dry and his vital signs show the
following: temperature 37°C (98.6°F), heart rate of 90 beats/min, respiratory rate
of 18 breaths/min, blood pressure of 120/80 mm Hg, and SpO2 of 95% on 2
L/min of oxygen by nasal cannula.

Key Points
Diagnosis and Management of Shock
Shock is characterized by impaired tissue oxygenation and
hypoperfusion.
The four major categories of shock with characteristic hemodynamic
patterns are hypovolemic, distributive, cardiogenic, and obstructive.
The clinical manifestations of shock result from inadequate tissue
oxygenation and perfusion, compensatory responses, and the specific
etiology.
Interventions to restore perfusion center on achieving an adequate blood
pressure, increasing cardiac output, optimizing the oxygen content of
blood, and/or decreasing oxygen demand.
 The initial therapy for most forms of shock is replacement of
intravascular volume with crystalloid or colloid solutions.
The selection of a vasoactive agent to treat shock should be based on the
hemodynamic effect desired for an individual patient and knowledge of
the pharmacology of available agents.
Reversible causes of acute oliguria or AKI should always be excluded,
and intravascular volume should be optimized with crystalloid and/or
colloid solutions.

Suggested Readings
1. Cecconi M, De Backer D, Antonelli M, et al. Consensus on circulatory
shock and hemodynamic monitoring. Task Force of the European
Society of Intensive Care Medicine. Intensive Care Med.
2014;40(12):1795-1815.
2. Dabrowski GP, Steinberg SM, Ferrara JJ, et al. A critical assessment of
endpoints of shock resuscitation. Surg Clin North Am.
2000;80(3):825-844.
3. Gutierrez G, Reines HD, Wulf-Gutierrez ME. Clinical review:
Hemorrhagic shock. Crit Care. 2004;8(5):373-381.
4. Havel C, Arrich J, Losert H, et al. Vasopressors for hypotensive shock.
Cochrane Database Syst Rev. 2011;(5):CD003709.
doi:10.1002/14651858.CD003709.pub3.
5. Kidney Disease: Improving Global Outcomes (KDIGO) Acute Kidney
Injury Work Group. KDIGO: Clinical practice guideline for acute
kidney injury. Kidney Int Suppl. 2012;2:1-138.
6. Koyner JL, Davison DL, Brasha-Mitchell E, et al. Furosemide stress test
and biomarkers for the prediction of AKI severity. J Am Soc Nephrol.
2015;26(8):2023-2031.
7. Mehta RL, Pascual MT, Soroko S, et al. Spectrum of acute renal failure
in the intensive care unit: the PICARD experience. Kidney Int.
2004;66(4):1613-1621.
 8. Myburgh JA, Mythen MG. Resuscitation fluids. N Engl J Med.
2013;369:1243-1251.
9. Oh HJ, Shin DH, Lee MJ, et al. Urine output is associated with
prognosis in patients with acute kidney injury requiring continuous renal
replacement therapy. J Crit Care. 2013;28(4):379-388.
doi:10.1016/j.jcrc.2012.11.019
10. Radhakrishnan J, Cattran DC. The KDIGO practice guideline on
glomerulonephritis: reading between the (guide)lines--application to the
individual patient. Kidney Int. 2012;82(8):840-856.
doi:10.1038/ki.2012.280
11. Rhodes A, Evans L, Alhazzani W, et al. Surviving Sepsis Campaign:
International Guidelines for Management of Sepsis and Septic Shock:
2016. Crit Care Med. 2017;45: 1-67.
doi:10.1097/CCM.0000000000002255
12. van Diepan S, Katz J, Albert N, et al. Contemporary Management of
Cardiogenic Shock: A Scientific Statement. Circulation.
2017;136(16):e232-e268. doi:10.1161/CIR.0000000000000525
13. Vincent JL, De Backer D. Circulatory shock. N Engl J Med.
2013;369(18):1726-1734.

Suggested Websites
1. Kidney Disease: Improving Global Outcomes. www.kdigo.org.
2. Surviving Sepsis Campaign. www.survivingsepsis.org.
3. Society of Critical Care Medicine. www.SCCM.org.
 Chapter 9
NEUROLOGIC SUPPORT

Objectives
Review the principles of primary and secondary brain insults and the
common mechanisms of neuronal injury.
Apply the concepts of intracranial hypertension and brain oxygen
delivery and consumption to the management of the brain-injured
patient.
Review the clinical and diagnostic assessment of a brain-injured
patient.
List common treatments in brain injury.
Review specific management principles and options for selected
pathophysiologic conditions.

Case Study
A 62-year-old man is brought to the emergency department at 6:00 a.m. in
the morning after waking up with aphasia and right hemiplegia. He was last
seen well the evening before around 11:00 p.m. He has a history of
hypertension and type 2 diabetes mellitus. His current medications include
aspirin, hydrochlorothiazide, carvedilol, and glyburide. Examination reveals a
blood pressure of 160/100 mm Hg, heart rate of 90 beats/min and regular,
respiratory rate of 14 breaths/min, and temperature of 37.2°C (98.9°F). He
is alert but unable to speak or follow commands. His cranial nerve
examination shows a left conjugate gaze preference, absent movement of the
right lower face with sparing of the forehead, absence of response to noxious
stimuli on the right side of his face, and a diminished gag reflex on the right
side. He has a right hemiplegia and does not respond to noxious stimuli
applied to the right side of his body. The remainder of his physical
examination is unremarkable. An immediate computed tomography (CT) scan
of the head shows a small area of decreased grey matter/white matter
differentiation in the left insular cortex.
– What type of primary brain injury is likely to be present?
– What is the next important diagnostic test?
– What interventions and monitoring should be instituted in addition to
the CT scan?

I. INTRODUCTION
Primary injuries to the brain include ischemic events, trauma, hemorrhage,
and anoxia, which may occur either in isolation or in combination.
Mechanisms for these and other primary injuries are shown in Table 9-1.

Table 9-1 Common Mechanisms of Primary Brain Injuries

Often, little can be done to reverse the immediate and frequently devastating
effects of the primary cerebral insult that produces neuronal injury or death.
In some circumstances, the immediate effects of an injury may be reversed by
prompt surgical or medical intervention. Many types of brain insults produce
a region of maximum injury associated with a surrounding area of tissue, or
penumbra, that may survive and recover if further damage can be mitigated.
Common mechanisms of secondary injury are shown in Table 9-2. The
mechanisms of secondary brain injury may evolve over time from other
primary insults. For example, edema after head trauma commonly produces
secondary brain compression, vasospasm after subarachnoid hemorrhage
(SAH) may cause regional ischemia and stroke, or secondary hemorrhagic
conversion after an ischemic stroke may induce compression and further
ischemia.

Table 9-2 Common Mechanisms of Secondary Brain Injuries

II. BRAIN INJURY MANAGEMENT PRINCIPLES

Because the primary injury in the central nervous system is often not
reversible, the main goal for treatment is prevention of secondary injury.
The focus of treatment for a neurologically compromised patient is the same
as the one aimed for patients with other illnesses and injuries, that is, to
ensure adequate oxygen delivery to meet the needs of both the damaged and
the undamaged brain tissue. The initial care team must take early and
aggressive action to ensure that secondary brain injury is prevented,
minimized, or reversed with careful monitoring and management, particularly
the prevention and early treatment of hypoxia and hypotension. Optimizing
oxygen delivery to the brain requires attention to oxygenation, hemoglobin
concentration, cardiac output, and blood pressure (BP). Prevention and early
treatment of fever, pain, agitation, and anxiety can minimize oxygen
demands. A unique challenge in acute brain injury is the metabolic demand
caused by seizures which can potentiate secondary injury. Therefore,
monitoring and treatment of seizures is an important aspect of preventing
secondary injury.

A. Intracranial Hypertension
Intracranial pressure (ICP) reflects the balance of volume-control mechanisms
within the noncompliant cranial compartment. Because the brain is enclosed
within the rigid skull and relatively inflexible dura, with tissues and fluids that
are not compressible, control of the different intracranial components is
essential to maintain brain homeostasis, regulate ICP, and preserve cerebral
perfusion. The critical compartment relationship depends on the volume
occupied by each component. An increase in one component (eg, brain) must
be accompanied by a decrease in another component (eg, blood), also known
as the Monro-Kellie doctrine. When the compensatory mechanisms are
overwhelmed, ICP increases and injury may ensue. In addition to the
impaired cerebral perfusion, which may be a consequence of globally
increased ICP, small pressure gradients within the skull may cause herniation
of the brain around dural reflections (the falx and the tentorium), with shift of
the midline structures. These movements within the skull may compromise
function (eg, cause stupor or coma by disrupting the activity of the brainstem
reticular formation) or lead to vascular compression and stroke.
Understanding the vector of intercompartmental shifts in the cranium can
help predict which patients will experience life-threatening secondary injury
from compression.

Increased ICP has an important effect on the

regional and global supplies of oxygen to the
brain because it compresses arteries and
decreases cerebral blood flow.

An intensivist, neurointensivist, or a neurosurgeon should be consulted if

intracranial hypertension is suspected. The patient may need ICP monitoring
either through a catheter inserted into a lateral ventricle (allows both
monitoring and drainage of cerebrospinal fluid [CSF]), or a strain gauge (or
fiberoptic) pressure monitor inserted into the brain parenchyma (Table 9-3).
This monitoring includes ICP, temperature, and/or brain oxygen.
Measurements of cerebral oxygenation require special equipment and
expertise that are not available in most facilities. When direct measures are
not available, the initial care team must treat the patient based on the
principles of oxygen supply and demand.

Conditions Potentially Requiring Invasive Intracranial Pressure

Table 9-3
Monitoring

B. Impaired Substrate Delivery (Hypoperfusion and Hypoxia)

Cerebral autoregulation reflects an active and passive system of blood flow
physiology by which arteriolar dilation or constriction controls regional
cerebral blood flow (CBF) and links oxygen demand to its delivery. Thus,
global CBF normally remains constant over a defined range of mean arterial
pressures (MAP). Loss of autoregulation occurs in many pathologic conditions
and may lead to regional or global vasodilation and edema formation that can
further increase ICP. Increases in blood volume also profoundly affect the
pressure inside the noncompliant cranial vault (based on the Monro-Kellie
doctrine).
 Although related, changes in CPP may not
always result in similar changes in CBF.

CBF correlates with the cerebral perfusion pressure (CPP) in many pathologic
conditions in which autoregulation is impaired. CPP is defined as the MAP
minus the ICP (the pressure impeding blood flow):

CPP = MAP – ICP

The normal CPP is between 60 and 100 mm Hg. If the ICP increases without
a change in MAP, CPP decreases, and CBF will also decrease if
autoregulation has failed. The decrease in CBF increases the risk of brain
ischemia. Clinicians should pay particular attention to changes in mental
status because these may indicate inadequate perfusion (among many other
possibilities).

The MAP must be measured at the same location as the ICP to be accurate;
this is usually done by zeroing the arterial line transducer at the ear and
keeping it at the same height as the head when the head is elevated. It is
important to understand that the correlation between CBF and CPP assumes
normal cardiac output. Impaired cardiac output, particularly when associated
with strong vasoconstrictor medications (vasopressors), will dissociate CPP
and CBF.

C. Recommendations for Therapy

Therapy for acute brain injury is based on the two previously mentioned
physiologies: reduction of intracranial hypertension and optimization of
substrate delivery. Algorithmic management of ICP after brain injury is an
important mechanism to standardize care. The typical progression includes
the use of osmotic agents, such as mannitol and hypertonic fluids, to increase
the oncotic pressure in the blood and draw interstitial fluid out of the brain,
thereby decreasing “brain water.” Further management techniques include
diverting CSF through an external ventricular device, upright body positioning
to optimize CSF transit out of the calvarium, and prevention of events that
increase sympathetic tone, such as seizures.

In parallel to pressure-reducing therapies, strategies to minimize damage to

the brain in distress focus on therapies designed to balance oxygen demand
and substrate delivery (CBF and oxygen). Table 9-4 summarizes commonly
accepted principles and therapeutic guidelines for treating a variety of brain
insults and avoiding secondary brain injury. Note the focus on factors that
minimize oxygen consumption and maximize oxygen delivery.

Table 9-4 General Principles of Managing Brain Injury

III. ASSESSMENT

Early identification of patients with ischemic

stroke or potential surgical lesions provides the
 best opportunity to minimize secondary brain
injury.

After appropriate management of airway, breathing, and hemodynamic

concerns, the priority in neurologic assessment is to distinguish among
ischemic, structural, metabolic, and infectious injuries. Suspected ischemic
stroke requires an immediate decision regarding thrombolytic therapy or
intervention, and emergent neurologic consultation should be obtained. The
presence of an expanding mass lesion accompanied by significant brain shift
may indicate the need for immediate surgical evaluation and possible
intervention. The most common causes of such an event include epidural,
subdural, and intracerebral hematomas. Intracranial hematomas should be
suspected in the settings of head trauma, recent neurosurgery, anticoagulant
therapy, alcohol abuse, coagulopathies, and chronic or acute hypertension.
The diagnostic procedure of choice, CT scan of the brain, characterizes the
extent of structural injury. Medical treatment may be a temporizing option
until more definitive therapy is available and implemented.
Serial examinations are necessary to detect the possible sequelae of many
brain insults. Any change in the examination is an indicator of deterioration
and should prompt an immediate and thorough reevaluation. For example,
decreased consciousness without lateralizing findings may be the result of
elevated ICP, hydrocephalus, fever, toxic substances, or worsening of an
encephalopathy, etc.

The Glasgow Coma Scale (GCS) score is widely used in the initial and serial
assessment of patients with head trauma, and it may be useful in evaluating
patients with other brain insults. Importantly, it serves as a standardized
language by which the care team can communicate the level of responsiveness
of the patient. Table 9-5 lists its components.

When physical examination or CT scan suggests

significant brain compression, medical therapy to
 reduce ICP should be instituted immediately
while awaiting definitive treatment.

Serial examinations, including evaluation of brainstem and cranial nerve

function, should be performed. Pupillary asymmetry may be an important
sign of unilateral compression with midline shift, which commonly precedes
downward herniation in patients with supratentorial masses. Uncoordinated
eye movements, a change in respiratory pattern, or deterioration in motor
response may suggest an increase in intracranial mass effect and should be
investigated immediately.

Table 9-5 Components of Glasgow Coma Scale Score

Total Glasgow Coma Scale score = eye + verbal + motor scores; best possible score = 15, worst
possible score = 3
 The Cushing reflex of hypertension followed by
bradycardia and altered respiration may indicate
downward central brain herniation.

When clinical findings suggest downward central herniation, emergent

administration of mannitol or hypertonic saline should be initiated to lower
ICP, and emergent neurosurgical assistance should be obtained. A brief
period of hyperventilation may be considered with the understanding that
hyperventilation has been found to increase brain ischemia and should be
used only as a temporizing measure when the patient’s survival is in question.
Whether repetition of an imaging study or immediate surgical therapy is
required depends on the nature, location, and progression of the pathologic
process.
Neurosurgical consultation is advised for any patient who: (1) is at risk for
developing an expanding intracranial mass lesion; (2) has an open or
depressed skull fracture or acute ventricular obstruction; (3) demonstrates
blood in the fourth ventricle, cerebellar bleeding, or SAH; or (4) has CSF
leakage. Nontraumatic disease processes, such as spontaneous intracerebral
hematoma, large brain tumors, or brain abscesses, require urgent
neurosurgical consultation if clinical findings or an imaging study indicate
significant mass effect (midline deviation, ventricular obliteration, brainstem
or basal cistern compression).

Urgent neurosurgical consultation should be obtained for hemorrhages and

infarcts in the posterior fossa regardless of the level of consciousness.
Although such patients may have few findings on initial clinical examination,
progressive swelling around the lesion may necessitate emergent surgical
decompression. Typically, any cerebellar mass greater than 3 cm in diameter
with hydrocephalus or brainstem compression requires consideration of
evacuation.
IV. SPECIFIC DIAGNOSES AND CONSIDERATIONS
A. Traumatic Brain Injury
Approximately 25% of patients who experience blunt head trauma require
urgent evacuation of a subdural hematoma (Figure 9-1A) or an epidural
hematoma (Figure 9-1B) to relieve compression of the brain. Neurosurgical
consultation should be considered early. Because 20% of patients with severe
traumatic brain injury (TBI) will have concomitant cervical spinal cord
injuries, immobilization of the cervical spine until it can be appropriately
assessed is very important.

Figure 9-1A. Subdural Hematoma

 Figure 9-1B. Epidural Hematoma

Cerebellar hemorrhage with altered

consciousness is a surgical emergency.

Penetrating and nonpenetrating head injuries are often associated with the
formation of cerebral edema, brain contusions, or hemorrhage within the
parenchyma. Because the skull cannot expand to accommodate increased
intracranial volume and the compensatory space in the subarachnoid space of
the spinal canal is very limited, the ICP commonly becomes elevated.
Monitoring and treatment of increased ICP are considered important in such
patients.

Guidelines for the management of severe TBI have been developed by the
Brain Trauma Foundation on the basis of established evidence and expert
opinion. These principles are included in the recommendations in Table 9-6.
Table 9-6 General Principles for Treatment of Traumatic Brain Injury
Abbreviations: CPP, cerebral perfusion pressure; CSF, cerebral spinal fluid; CT, computed
tomography; DC, depressive craniectomy; EVD, external ventricular device; GCS, Glasgow Coma Scale;
ICP, intracranial pressure; PTS, posttraumatic seizures; TBI, traumatic brain injury.

B. Intracerebral Hemorrhage
Intracerebral hemorrhage (ICH) occurs in 12 to 31 per 100,000 people each
year in the United States, accounting for 10% of all strokes. Approximately
60% of patients with ICH have a history of hypertension. Other frequent
causes include cerebral amyloid angiopathy (CAA), coagulopathy, medication-
induced, vascular abnormalities, and sympathomimetic drugs.

Intracerebral hemorrhage (ICH) mortality

increases as ICH score increases. An ICH score 3
has a mortality of 72% and reaches 100% with
an ICH score 5 & 6.

ICH is a medical emergency. Rapid diagnosis and management are crucial

because early deterioration is common in the first few hours after the onset of
ICH. It is important for the clinician to assess the need for airway support, the
risk of herniation and brainstem compression, hematoma expansion, elevated
ICP, and strategies for prevention of secondary brain injury. A contrast-
enhanced CT scan can occasionally show a “spot sign” (a contrast spot in the
hemorrhage bed) that suggests continued bleeding. The clinician should also
calculate the ICH score, a grading scale composed of GCS score, age, and
initial neuroimaging. It predicts in-hospital mortality and is useful in
counseling families.

Rapid diagnosis and management is crucial

because early deterioration is common in the
first few hours after the onset of ICH.

Elevated BP may contribute to rebleeding and edema formation but may also
preserve regional CPP. Recent guidelines suggest target BP control (systolic
blood pressure [SBP] 140–180 mm Hg) with the understanding that patients
with long-standing hypertension and history of chronic kidney disease are at
higher risk of acute kidney injury. Basic principles of BP control include rapid
correction with titratable agents. If elevated ICP is suspected, expert
consultation is advised for assistance with BP management. Preferred agents
include labetalol, nicardipine, or clevidipine. Use of vasodilators remains
controversial, but medications that cause substantial intracranial vasodilation
(eg, nitroprusside, nitroglycerin) should be avoided.
Expansion of the hematoma occurs commonly, especially in patients taking
anticoagulants or antiplatelet agents, have liver disease, have platelet
dysfunction related to end-stage renal disease, or have a low platelet count.
Rapid reversal of coagulopathy with appropriate reversal agents should be
done as soon as possible. Neurosurgical consultation for evacuation of
hematoma should be considered in patients with a life-threatening
deteriorating neurologic examination, cerebellar location, intraventricular
hemorrhage causing hydrocephalus, and large mass effect. Some
neurosurgeons may consider removal of the hematoma, especially in a young,
clinically deteriorating patient with a large lobar hemorrhage or when the
hemorrhage is associated with a surgically treatable lesion, such as an
aneurysm, arteriovenous malformation, or cavernous angioma. Deep basal
ganglionic hemorrhages do not yet have a universally accepted surgical
therapy (Figure 9-2A). Small hemorrhages may not require specific surgical
therapy (Figure 9-2B).

Figure 9-2A. CT Scan Demonstrating Large Right Basal Ganglion

Intracerebral Hemorrhage with Midline Shift and Intraventricular
Extension
 Figure 9-2B. CT Scan Demonstrating Small Left Parietal Lobar
Intracerebral Hemorrhage

C. Subarachnoid Hemorrhage
Subarachnoid hemorrhage may be categorized as traumatic or nontraumatic.
Nontraumatic SAH, often aneurysmal in nature, accounts for 1% to 7% of all
strokes and is considered a neurovascular emergency. Overall, approximately
10% of patients die before arriving at the hospital and 65% of survivors are
left with some cognitive impairment. Therefore, prompt consultation with a
center experienced in the care of these patients is advised. Characteristics
from the patient history (“worst headache of their life”) and CT findings
usually confirm the diagnosis of SAH (Figure 9-3). Classification systems (eg,
the Hunt and Hess scale or the Fisher scale) have been used to categorize
findings and suggest prognosis but do not alter the care provided by the
primary team, as outlined in Table 9-7. The treatment plan should include
securing the aneurysm before the period of delayed deterioration (within first
24 hours has become a common standard) to prevent rebleeding, diagnose
and manage obstructive hydrocephalus, and monitor for and treat delayed
neurologic deterioration (cerebral vasospasm), including vasospasm
prophylaxis with nimodipine within 24 hours. Nimodipine is beneficial
because it can reduce the possibility of secondary cerebral hemorrhage, has
neuroprotective properties, and improves overall outcomes. Guidelines are
available from the American Heart Association/American Stroke Association
(AHA/ASA) and the Neurocritical Care Society. Almost all patients, regardless
of severity, should be stabilized and evaluated for rapid transfer to a
specialized center for management.

Figure 9-3. CT Scan Demonstrating Subarachnoid Hemorrhage

(FCCS 6th ed Figure 9-3)

Table 9-7 Treatment of Subarachnoid Hemorrhage

Abbreviations: CSF, cerebral spinal fluid; EVD, external ventricular drain; SIADH, syndrome of
inappropriate antidiuretic hormone

D. Ischemic Stroke
Stroke is a leading cause of disability. In the United States alone, there are
approximately 750,000 strokes each year. Of these patients, 15% to 30% are
disabled, 20% require long-term institutional care, and 50% are unable to
return to work. The estimated cost of stroke in the United States is $72
billion. Ischemic stroke usually occurs because of thromboembolic obstruction
of arteries. Administration of intravenous recombinant tissue plasminogen
activator (t Pa) during the first 3 to 4.5 hours following the known onset of
ischemic stroke substantially improves outcome in one-third of patients.
Recent studies have demonstrated a role for intra-arterial treatment with a clot
retrieval system (called a stent-retriever device) in selected patients with larger
artery occlusion if they present within the first 24 hours of symptoms (Figure
9-4). This aggressive intervention results in the impressive relative reduction
of disability in 73% of patients.

Figure 9-4. CT Angiogram Demonstrating Occlusion of Left Middle

Cerebral Artery (arrow)

The use of a stroke severity rating scale, such as

the National Institutes of Health Stroke Scale
(NIHSS), is recommended.

Onset of symptoms, or the last time the patient was known to be at baseline
(often called Last Known Well [LKW]), is the time used to determine whether
a patient is a candidate for thrombolytic therapy. The use of a stroke severity
rating scale, such as the National Institutes of Health Stroke Scale (NIHSS) is
recommended. Like the GCS, it forms a common language by which to risk-
stratify patients for treatment. After an initial CT scan rules out the presence
of hemorrhage, intravenous recombinant tPA should be administered in a
dosage of 0.9 mg/kg (10% as a bolus over 1 minute and 90% in a 1-hour
infusion) for patients in whom treatment can be started within 4.5 hours.
Protocols should be in place, including absolute and relative
contraindications, to ensure proper selection of candidates for thrombolytic
therapy. Personnel who are not familiar with the use of recombinant tPA for
the acute treatment of non-hemorrhagic stroke should seek immediate
neurologic consultation before administering therapy. Intra-arterial clot
retrieval is an important option for patients with large artery occlusion,
regardless of whether recombinant tPA has been administered. Guidelines are
available from the AHA/ASA.

In an otherwise eligible patient for acute

reperfusion patient whose BP is >185/110 mm
Hg, anti-hypertensive medications such as
labetalol, nicardipine, clevidipine, hydralazine
and enalaprilat can be used to lower and
maintain target BP. Please refer to AHA
guidelines for BP management protocol.

Supportive care includes management of hypertension. Although an elevated

BP is often present early, a decrease in pressure usually occurs in the first
hours after stroke without specific medical treatment. No evidence defines a
level of BP that requires emergent intervention. The AHA and ASA have
compiled consensus recommendations for patients who are candidates for
thrombolytic therapy. For those patients who are not candidates for
thrombolysis, emergency administration of antihypertensive agents is not
indicated unless the diastolic BP is > 120 mm Hg, SBP is > 220 mm Hg,
or there is evidence of end-organ injury (eg, pulmonary edema). If treatment
is indicated, the BP should be lowered cautiously with a reasonable goal of
lowering the pressure approximately 15% in the first 24 hours after stroke
onset.
If a patient deteriorates clinically during or after IV tPA, the clinician should
stop tPA infusion immediately, monitor vital signs, obtain head CT stat and if
confirmed hemorrhage, administer cryoprecipitate. Significant edema
formation, typically within the first 72 hours, or extensive hemorrhage within
the ischemic zone may indicate the need for emergent hemicraniectomy.
Younger patients with middle cerebral artery (MCA) or internal carotid artery
(ICA) infarction should be considered for decompressive hemicraniectomy
within 48 hours of the onset of symptoms. Medical management includes
osmotic therapy, sedation, prevention of secondary brain injury (avoid
hypotension and hypoxia), early nutrition, glucose control (range 140–180
mg/dL), temperature control, and venous thromboembolism (VTE)
prophylaxis.

Determination of when the initial stroke

symptoms appeared is critical.

VTE prophylaxis should be administered to immobilized patients. Low-

molecular-weight heparins are favored in relation to unfractionated heparin,
although both could be similarly effective. No data are available on the use of
new oral anticoagulants. Aspirin administration within 24 to 48 hours of the
onset of the stroke is recommended for most patients after hemorrhage is
excluded. In patients with minor strokes, treatment for 21 days with dual
antiplatelet therapy (aspirin and clopidogrel) started within 24 hours can be
beneficial for early secondary stroke prevention.

E. Anoxic Injury
Relative anoxia may be a part of other injuries and may be the result of
airway loss, systemic hypoxemia, hypoperfusion, and other causes. Anoxia
may also be the primary brain insult, as occurs during cardiac arrest.
Neuronal damage may occur as a direct result of the primary insult of
hypoxemia or hypoperfusion.
The initial team should maintain the usual standards of optimal oxygen
delivery. Despite extensive studies of many agents and therapy options, none
has proven selectively beneficial, nor has the poor prognosis from anoxic
brain injury improved over time. The International Liaison Committee on
Resuscitation (ILCOR) task force recommends targeted temperature
management for adults with out-of-hospital cardiac arrest with an initial
shockable rhythm at a constant temperature between 32°C to 36°C (89.6°F
to 96.8°F) for at least 24 hours. Guidelines are available from the AHA and
the ILCOR.

F. Metabolic Abnormalities, Infectious Emergencies, and Seizures

In the absence of papilledema or focal neurologic

signs, a lumbar puncture may be performed
without a prior CT scan for evaluation of
meningitis.

In adult patients with depressed consciousness after airway management and

initial resuscitation, the administration of 50% dextrose (50 mL intravenously)
and thiamine (100 mg intravenously) should be considered for the treatment
of potential hypoglycemia and the prevention of Wernicke encephalopathy if
an immediate determination of the blood glucose concentration is not
available. Intravenous naloxone should be administered if narcotic
intoxication is a possibility. Other metabolic abnormalities, such as electrolyte
disorders (ie, acute hyponatremia, hypercalcemia), liver failure, or uremia
may also cause coma. Because headache or altered state of consciousness
accompanied by fever, nuchal rigidity, and leukocytosis suggests meningitis or
encephalitis, the CSF should be submitted for physical, chemical, and
bacteriologic (culture and Gram stain) studies. If clinical examination suggests
a mass lesion or elevated ICP, a CT scan should be performed before lumbar
puncture. If the scan reveals evidence of mass effect or generalized cerebral
edema, a lumbar puncture may precipitate a herniation syndrome and should
be postponed. When infection is part of the differential diagnosis, appropriate
antibacterial and antiviral treatment should be initiated before performing the
imaging study or lumbar puncture because early therapy for bacterial
meningitis or encephalitis may be lifesaving. Blood cultures should be
obtained before antibiotic therapy unless this would delay treatment.
Antibiotics and resuscitation should not be delayed to obtain a lumbar
puncture or brain CT. Treatment recommendations are outlined in Chapter
11.

If possible, avoid the use of neuromuscular

blocking agents in patients at risk for seizure
because these agents obscure detection of seizure
activity.

G. Status Epilepticus
Status epilepticus (SE) is a life-threatening neurologic emergency that requires
prompt treatment and diagnosis. It is defined as 5 minutes or more of
continuous seizure activity or recurrent seizure activity without return to
baseline. It may be classified as convulsive and non-convulsive. The treatment
management plan should include work-up to determine possible etiologies and
rapid protocol for termination of seizures.

Possible etiologies of Status Epilepticus

Acute: CNS infection, metabolic, TBI, sepsis,
stroke, drugs, hypoxia, cardiac arrest,
hypertensive encephalopathy, autoimmune
encephalitis
 Chronic: Breakout seizures, CNS tumors, alcohol
withdrawal

Intravenous benzodiazepines are administered at the onset of prolonged or

repeated seizure activity. Status epilepticus requires emergent neurologic
consultation, and lorazepam 0.1 mg/kg should be administered intravenously.
Intramuscular midazolam, 0.15 mg/kg, is an alternative if intravenous access
is not immediately available. The addition of phenytoin/fosphenytoin,
valproate sodium, or levetiracetam has been shown to be useful. If seizures
continue, secure the airway and initiate advanced treatment for refractory SE.
Anticonvulsants used in refractory SE include propofol (3 mg/kg loading dose,
then infusion of 1–5 mg/kg/h) or midazolam (0.2 mg/kg loading dose, then
infusion of 1–20 µg/kg/min) with electroencephalography and other ICU
monitoring.
Seizure activity after an acute brain injury increases cerebral oxygen
requirements and typically elevates ICP. Appropriate therapy should be
administered to terminate seizure activity as soon as possible. The intravenous
administration of anticonvulsants, many of which have a potent sedative
effect, may depress respiratory function and requires appropriate supportive
therapy. In addition, hypotension may occur, requiring additional intravenous
fluids and/or vasopressors to preserve MAP and CPP.

H. Spinal Cord Injury

Cervical spine injury can usually be determined in awake patients because
they reflect neck pain and weakness. If awareness is impaired, cervical spinal
cord injury should be suspected in patients with respiratory weakness,
extremity weakness without facial weakness, hypotension with bradycardia,
priaprism in male patients, and difficulty maintaining normothermia. Patients
with lesions below the fourth cervical segment (C4) may breathe adequately
on presentation but could progress to respiratory failure with abrupt
decompensation and thus must never be left unmonitored.
Thoracolumbar spine injury spares the upper extremities but involves leg
weakness; depending on the spinal level, the patients may have hypotension
with tachycardia or unusual swings in BP.
Initial management includes spinal motion restriction (cervical collar,
backboard) while obtaining emergent spine surgery consultation. However,
patients should not be left on backboards after arrival in the emergency
department because of the risk of pressure ulcer development. A MAP of >
85 mm Hg for the first 7 days after injury is recommended by some clinicians
to improve perfusion to the injured area of cord. The American Association of
Neurological Surgeons/Congress of Neurological Surgeons do not recommend
the use of methylprednisolone in spinal cord injury.
CT scans of the spine can be obtained without removing immobilizing devices.

I. Other Neurologic Causes of Acute Respiratory Failure (Acute

Nontraumatic Weakness)
Patients with conditions causing global weakness, such as myasthenia gravis
and Guillain-Barré syndrome, may have problems maintaining upper airway
patency in addition to respiratory muscle weakness. In such patients,
endotracheal intubation may be warranted for airway protection before being
mandated by the falling tidal volume. Measurement of vital capacity and
negative inspiratory pressure is important. Patients with increased work of
breathing, hypoxemia, < 20 mL/kg vital capacity, or maximum inspiratory
pressure <-30 cm H20 should be moved to the ICU and will likely need
intubation soon. Intubation should be based on tachypnea and discomfort
without waiting for an elevation of PaCO2. Hypoxia as a result of atelectasis in
patients with adequate airway protection may be treated with continuous
positive airway pressure if airway protection is not a concern. A neurologist
should be consulted when the diagnosis is suspected because treatment with
intravenous immunoglobulin or plasma exchange may slow or halt disease
progression and speed recovery. Autonomic dysfunction is common in the
Guillain-Barré syndrome and may lead to large and rapid swings in BP and
heart rate requiring intravenous therapy.
J. Death by Neurologic Criteria (Brain Death) and Organ Donation
Despite the best efforts of medical and surgical teams, massive injury,
cerebral infarction, anoxia, or hemorrhage may result in a loss of all cerebral
and brainstem functions. Evaluation of brain death and the guidelines for
organ donation are variable, depending on the country, state, and facility. For
more information about brain death and organ donation, see Appendix 3 and
4.

Key Points
Neurologic Support
Brain injury occurs as a consequence of a primary insult and
secondary injury. The prevention of secondary brain injury is a
critical goal for the initial care team.
The most significant mechanisms for secondary injury in brain-
damaged patients are hypotension and hypoxia.
Optimizing oxygen delivery while controlling oxygen consumption is
a general treatment principle for all types of brain injury.
Important principles and guidelines for initial treatment apply to all
types of primary brain injury and help prevent harmful secondary
sequelae.
BP management is dependent on the initial brain injury. However,
excessive lowering of BP in any acute brain injury may induce
secondary ischemia.
Avoid prophylactic or routine hyperventilation in patients with
brain injuries. Mannitol should be administered for signs of
downward herniation or if neurologic deterioration is not
attributable to other factors. Hyperventilation may be initiated
cautiously as a temporizing measure.
 Ensure euvolemia using normal saline as the primary maintenance
fluid.
Seizure activity after acute brain injury should be terminated with
an intravenous dose of a benzodiazepine, followed by an
intravenous loading dose of an antiepileptic drug.

Suggested Readings
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at 6 to 16 hours with selection for perfusion imaging. DEFUSE 3
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2. Bleck TP. Bacterial meningitis and other nonviral infections of the
nervous system. Crit Care Clin. 2013;29(4):975-987.
3. Boland TA, Lee VH, Bleck TP. Stress-induced cardiomyopathy.
Crit Care Med. 2015;43(3):686-693.
4. Brain Trauma Foundation, American Association of Neurological
Surgeons, Congress of Neurological Surgeons, AANS/CNS Joint
Section on Neurotrauma and Critical Care. Guidelines for the
management of severe traumatic brain injury. 4th ed. 2016;1-:-
Retrieved from www.braintrauma.org.
5. Brophy GM, Bell R, Claassen J, et al. Guidelines for the
evaluation and management of status epilepticus. Neurocrit Care.
2012;17(1):3-23.
6. Busl KM, Bleck TP. Neurogenic pulmonary edema. Crit Care
Med. 2015;43(8):1710-1715.
7. Callaway CW, Donnino MW, Fink EL, et al. Part 8: Post–cardiac
arrest care: 2015 American Heart Association guidelines update
for cardiopulmonary resuscitation and emergency cardiovascular
care. Circulation. 2015;132(18 Suppl 2):S465–S482.
 8. Chesnut RM, Bleck TP, Citerio G, et al. A consensus-based
interpretation of the Benchmark Evidence from South American
Trials: Treatment of Intracranial Pressure Trial. J Neurotrauma.
2015;32(22):1722-1724.
9. Connolly ES, Rabenstein AA, Carhuapoma JR, et al. Guidelines
for the management of aneurysmal subarachnoid hemorrhage: a
guideline for healthcare professionals from the American Heart
Association/American Stroke Association. Stroke.
2012;43(6):1711-1737.
10. DeNett T, Feltner C. Hypertonic saline versus mannitol for the
treatment of increased intracranial pressure in traumatic brain
injury. J Am Assoc Nurse Pract. 2019;4:2327-6924.
11. Diringer MN, Bleck TP, Claude Hemphill J 3rd, et al. Critical
care management of patients following aneurysmal subarachnoid
hemorrhage: recommendations from the Neurocritical Care
Society’s Multidisciplinary Consensus Conference. Neurocrit
Care. 2011;15(2):211-240.
12. Donnino MW, Andersen LW, Berg KM, et al. ILCOR Advisory
Statement. Temperature Management After Cardiac Arrest.
Circulation. 2015;132(25):2448-2456.
13. Hawryluk GWJ, Aguilera S, Buki A, et al. A management
algorithm for patients with intracranial pressure monitoring: the
Seattle International Severe Traumatic Brain Injury Consensus
Conference (SIBICC). Intensive Care Med. 2019;45(12):1783-
1794.
14. Hemphill JC, Greenberg SM, Anderson CS, et al. Guidelines for
the management of spontaneous intracerebral hemorrhage: a
guideline for healthcare professionals from the American Heart
Association/American Stroke Association. Stroke.
2015;46(7):2032-2060.
15. Hutchinson PJ, Kolias AG, Timofeev IS, et al. Trial of
decompressive craniectomy for traumatic intracranial
hypertension. N Engl J Med. 2016;375(12):1119-1130.
16. Kapur J, Elm J, Chamberlain JM, et al. Randomized trial of three
anticonvulsant medications for status epilepticus. N Engl J Med.
2019;381(22):2103-2113. DOI:10.1056/NEJMoa1905795.
17. Kotloff RM, Blosser S, Fulda GJ, et al. Management of the
potential organ donor in the ICU: Society of Critical Care
Medicine/American College of Chest Physicians/Association of
Organ Procurement Organizations Consensus Statement. Crit
Care Med. 2015;43(6):1291-1325.
18. Liu Y, Qiu H, Su J, et al. Drug treatment of cerebral vasospasm
after subarachnoid hemorrhage following aneurysms. Chin
Neurosurg Jl. 2016;2(4).
19. Munoz J, Keough EA, Barrios JC, et al. Primary decompressive
craniectomy in neurocritical patients. A meta-analysis of
randomized controlled trials, cohort and case-control studies. J
Emerg Crit Care Med. 2018;2(9).
20. Nogueria RG, Ashutosh PJ, Haussem DC, et al. Thormbectomy 6
to 24 hours after stroke with a mismatch between deficit and
infarct. DAWN Trial Investigators. N Engl J Med.
2018:378(1):11-21.
21. Powers WJ, Rabinstein AA, Ackerson T, et al. 2018 American
Heart Association/American Stroke Association guidelines for the
early management of patients with acute ischemic stroke: a
guideline for healthcare professionals from the American Heart
Association/American Stroke Association. Stroke.
2018;49(3):e46-e110.
22. Rossetti AO, Bleck TP. What’s new in status epilepticus?
Intensive Care Med. 2014;40(9):1359-1362.
23. Shank CD, Walters BC, Hadley MN. Current topics in the
management of acute traumatic spinal cord injury. Neurocrit
Care. 2019;30:261-271.
24. Shemie SD, Hornby L, Baker A, et al. International guideline
development for the determination of death. Intensive Care Med.
2014;40(6):788-797.
25. Silbergleit R, Durkalski V, Lowenstein D, et al. Intramuscular
versus intravenous therapy for prehospital status epilepticus. N
Engl J Med. 2012;366:591-600.
26. Torbey MT, Bösel J, Rhoney DH, et al. Evidence-based
guidelines for the management of large hemispheric infarction: a
statement for health care professionals from the Neurocritical
Care Society and the German Society for Neurointensive Care and
Emergency Medicine. Neurocrit Care. 2015;22(1):146-164.
27. Vahedi K, Hofmeijer J, Juettler E, et al. Early decompressive
surgery in malignant infarction of the middle cerebral artery: a
pooled analysis of three randomised controlled trials. Lancet
Neurol. 2007;6(3):215-222.
28. Walters BC, Hadley MN, Hurlbert RJ, et al. Guidelines for the
management of acute cervical spine and spinal cord injuries:
2013 update. Neurosurgery. 2013;60(Suppl 1): 82-91.
29. Wilson MH. Monro-Kellie 2/0: The dynamic vascular and venous
pathophysiological components of intracranial pressure. J Cereb
Blood Flow Metab. 2016;36(8):1338-1350.

Suggested Websites
1. Society of Critical Care Medicine/Guidelines. www.SCCM.org.
2. Brain Trauma Foundation. http://www.braintrauma.org.
3. Brain Attack Coalition. http://www.brainattackcoalition.org.
4. Neurocritical Care Society. http://www.neurocriticalcare.org.
 Chapter 10
NEUROSURGICAL ICU

Objectives
Review the physiology of cerebrospinal fluid (CSF) composition,
production, circulation, and resorption.
Discuss the physiology of intracranial pressure (ICP) and cerebral
perfusion pressure (CPP).
Review the presentation, diagnosis, and management of acute
intracranial hypertension and hydrocephalus.
Describe the insertion, maintenance, and troubleshooting of external
ventricular drains (EVD).
Define and outline the management of syndrome of inappropriate
antidiuretic hormone secretion (SIADH), cerebral salt-wasting
syndrome (CSWS), and diabetes insipidus (DI) as they relate to
sodium abnormalities in patients with neurologic issues.
Discuss the recognition, management, and prevention in a patient with
cerebral vasospasm.
Identify the physiologic sequelae in spinal cord injury and neurogenic
shock.
Review steps to initiate management for the patient with neurogenic
shock.
 Case Study
A 42-year-old man with no significant medical history experiences sudden
onset of the worst headache of his life during strenuous exercise. The patient
is taken to the emergency department (ED) of the local hospital by his family.
The ED physician obtains a computed tomography scan (CT) of the head that
shows subarachnoid blood over the cerebral convexities and in the left Sylvian
fissure. A small amount of blood is seen in the dependent lateral ventricles
with prominence of the temporal horns. Early surgical and
neurointerventional consultations are obtained. The Glasgow Coma Scale
(GCS) score on admission is 11. The consulting neurosurgeon notes that the
patient is lethargic. The patient is admitted to the ICU. Measures are taken to
maintain adequate blood pressure control, pharmacologic vasospasm
prophylaxis, and a four-vessel cerebral angiogram is ordered. The patient has
embolization of a right anterior communicating artery aneurysm a few hours
after admission. Upon arrival back to the ICU, he is minimally responsive and
vomits. His GCS score is now 6.
– Why did the patient’s neurologic examination worsen?
– What immediate interventions are required?

I. INTRODUCTION
Neurosurgical patients can present unique challenges to the treating clinician.
Many symptoms are subtle combined with patient’s inability to express them
can lead to delay in diagnosis and unwanted complications. Many
neurocritical care emergencies can present special challenges and one must
have a high index of suspicion for the diagnosis and be able to provide timely
interventions to prevent catastrophic complications and consequences. In
managing certain neurocritical patients and conditions we need to follow
specific guidelines that sometimes don’t apply to the general surgical or
medical patient.
II. HYDROCEPHALUS
A. Introduction and Physiology

When CSF absorption decreases, unless another

intracranial volume (soft tissue or blood)
decreases to compensate, the rapid increase in
CSF volume will cause a rapid increase in ICP.

In healthy individuals, the production and reabsorption of the cerebrospinal

fluid (CSF) is maintained constant and in balance. Hydrocephalus occurs
when CSF accumulates in the brain, causing increased pressure within the
skull. CSF is a clear acellular saline solution with density and viscosity like
that of water, produced continuously in the subarachnoid space at a rate of
approximately 25–30 mL/hr (approximately 600–700 mL/day) as blood
flows through the choroid plexus located in the lateral ventricles and in the
subarachnoid space next to the cerebellopontine angles (Figure 10-1). The
total volume of CSF in the entire subarachnoid space is approximately 125–
150 mL, while the ventricles of the normal brain contain approximately 25–
30 mL. The volume of CSF in normal ventricles is only 1.5 to 2.0 times that
of the volume of CSF produced in an hour.

Normally CSF production and reabsorption are balanced so that the total
volume is constant. CSF moves from the subarachnoid space into the venous
circulation and ultimately to the kidneys where it is excreted in the urine.
 Figure 10-1. Cerebrospinal Fluid (CSF) Production and Flow

Reproduced with permission Open Stax [CC BY

(https://creativecommons.org/licenses/by/4.0)].

The Monro-Kellie hypothesis relates pressure in the non-expansible

intracranial compartment to the sum of the volumes of the tissues contained
therein (Figure 10-2).

Soft, semi-solid tissue, normal and pathologic (brain parenchyma,

hematoma, tumor)
CSF (intraventricular and subarachnoid)
Intradural blood vessels (arteries and veins) within and on the
surface of the brain
 According to the Monro-Kellie hypothesis, the
only way to decrease ICP is by decreasing the
volume of one or more intracranial
compartments:
1. Soft tissue (brain or mass lesion),
2. Blood (intravascular), and/or
3. CSF.

Because the cranium is non-compressible and has a fixed volume, the

compartments inside the cranium (brain tissue, blood, CSF) are in
equilibrium. Any increase in the volume of one compartment will have to be
balanced by a decrease in the volume of another; otherwise the intracranial
pressure (ICP) will increase and the CSF and blood will be displaced
downward through the path of least resistance.

Cerebral perfusion is a function of the forward-driving force of blood

imparted by the contractions of the heart that must overcome the resistance of
pressure inside the cranium. The calculation for cerebral perfusion pressure
(CPP) is mean arterial pressure (MAP) minus intracranial pressure (ICP):
 Figure 10-2. Monro-Kellie Hypothesis

Reproduced with permission Madden MA, ed. Pediatric Fundamental Critical Care
Support, 2nd ed. Mount Prospect IL: Society of Critical Care Medicine; 2013.

CPP = MAP − ICP

Neurons are physiologically stressed below a critical threshold of 60 mm Hg,

while a CPP of 70–80 mm Hg or greater is adequate for oxygen delivery to
sustain neuronal metabolism and electrical activity.

Symptomatic acute hydrocephalus is considered an emergency because CSF

continues to accumulate even when absorption slows or stops (this is called
communicating hydrocephalus) or when there is a blockage along the CSF
circulation pathway (this is called non-communicating hydrocephalus). Adding
25–30 mL/hr of CSF to ventricles with a normal volume of 35–50 mL and
limited compliance (ability to expand) will cause intraventricular pressure to
rise rapidly (Figure 10-3). The clinician should assume that decompensation
is imminent and that there will be a rapid increase in the slope of the
pressure-volume curve with each additional milliliter of CSF added to the
ventricular volume. When this occurs, CSF must be immediately drained to
prevent an acute, dramatic increase in ICP with decrease in CPP to the
ischemic or even anoxic range. Failure to do so will result in irreversible
neurologic deficit, coma, or death.

Figure 10-3. Pressure-Volume Curve

Reproduced with permission Pierre L, Pringle EJ, eds. Pediatric Fundamental Critical
Care Support, 3rd ed. Mount Prospect IL: Society of Critical Care Medicine; 2018.
Copyright © 2018 the Society of Critical Care Medicine.

B. Presentation, Signs, and Symptoms

The rapidity of onset of symptoms and signs of

increased ICP determines the urgency with which
ICP must be controlled and lowered.

Because presenting signs and symptoms of acute hydrocephalus are similar to

those of other intracranial pathology that increase ICP, a careful history and
neurologic examination of the patient are essential to diagnose hydrocephalus.
Headache (with or without vomiting) is the most common symptom in a
patient who is awake. Altered consciousness, irritability, sleepiness, lethargy,
and obtundation are the most common signs of ICP-related global neurologic
compromise.

The rapidity of onset of signs and symptoms is the most significant factor in
determining how urgently to treat acute hydrocephalus. A history of recent
and sudden change in ICP dynamics and failure to maintain ICP via the
Monro-Kellie compensatory mechanism suggests that, without immediate
intervention, CSF volume and ICP will continue to rise. This will put the
patient at risk for rapid deterioration and progression to coma and death. A
history of hemorrhage, infection, tumor, or ventriculoperitoneal shunt (or
other CSF shunt) with symptoms and/or signs consistent with acutely elevated
ICP is also an indication for imaging to rule out hydrocephalus.
Seizures are sometimes a result of the pathophysiologic process (such as
tumor or infection) that causes acute hydrocephalus, but isolated new onset or
increased frequency of seizures is seldom caused by hydrocephalus.
Regardless of how rapidly or slowly the pathophysiology progresses, clinical
progression to severe headache, lethargy, or cranial nerve palsy are indicators
for immediate intervention to lower ICP.
Other symptoms and signs include vomiting, snoring and gurgling, and fever.
Vomiting can be an indication that ICP is high and rising rapidly. Snoring and
gurgling breathing are alarming signs suggestive of worsening level of
consciousness. Fever can occur in association with acute shunt obstruction,
especially with infection.
Patients with elevated ICP, and especially nearing critical stages (nearing
herniation), might develop what is called the Cushing reflex, or Cushing’s
triad. Cushing’s triad consists of the following:
Abnormal breathing pattern
Hypertension
Bradycardia
Many patients with acute hydrocephalus do not present with Cushing’s triad.
However, the diagnosis should be considered, and emergency neurosurgical
consultation expedited when a patient presents with one or more of these vital
sign changes.

The thresholds for hypertension and bradycardia are different for small
children. In a baby, a heart rate of 80 beats/min may be bradycardic.
Symptoms and signs of acute hydrocephalus may be harder to pick up in
children who are uncooperative, irritable, and agitated. A pediatrician should
follow any child admitted with suspected acute hydrocephalus.

As noted previously, global neurologic findings such as alteration in the level

of consciousness, confusion, lethargy, and obtundation are most common with
acute hydrocephalus. On neurologic examination, a sixth nerve palsy is
indicative of an increase in ventricular size sufficient to stretch the cranial
nerve. Papilledema can be found if ICP has been elevated for several hours
or more.

C. Shunts
Shunts are the most common long-term treatment for hydrocephalus. Acute
hydrocephalus caused by shunt obstruction is near the top of the differential
of any rapid change in mental status in a patient with a ventriculoperitoneal
(VP), ventriculopleural, or other CSF shunt.

Because CSF is so rapidly produced, a sudden

complete obstruction of flow from the ventricles
into the peritoneal cavity is a neurosurgical
emergency. Without either an emergency shunt
revision or placement of an additional external
ventricular drain, ICP will rapidly rise and the
patient will become progressively lethargic,
obtunded, and ultimately comatose.
Shunts are placed in premature infants with intraventricular hemorrhage,
newborns with myelomeningocele and other neural tube anomalies, post-
meningitis, and for congenital stenosis of the Sylvian aqueduct. Shunts are so
effective at keeping ICP low and are inconspicuous under the scalp and skin
so that many adults who had one placed as a child forget they have one.
Examination for a shunt should be part of the physical examination of any
patient, child or adult with acute mental status changes.

Patients can usually recognize a shunt malfunction with symptoms such as a

headache or double vision. The parent of a developmentally delayed or
noncommunicative child who underwent placement of a shunt early in
childhood and has had VP shunt revisions will often recognize acute shunt
failure because the child’s symptoms and signs mirror those present before
the shunt revisions.

Shunt infections are more common in children but can also occur in adults.
Any patient with a VP shunt who presents with symptoms of acute
hydrocephalus should have CSF withdrawn and sent for analysis (WBC,
glucose, protein) and culture to rule out infection.

Patients with normal pressure hydrocephalus have the classic symptoms of

cognitive impairment, imbalanced gait, and urinary incontinence. They have a
VP shunt placed to control their symptoms. Acute onset of altered mental
status in a patient shunted for normal pressure hydrocephalus is almost never
due to shunt failure because the shunt was placed to lower already low ICP.
The altered mental status is usually due to infection or development of a
chronic subdural collection.

The design of VP shunts is simple, making it straightforward to identify the

reason for malfunction based on history and examination.

1. Partial Obstruction
 Increased ICP elevation due to partial shunt
obstructions may progress more slowly than
when due to completely obstructed flow but can
eventually result in dangerously elevated ICP.

Partial obstructions slow, but do not completely stop, CSF flow. The increase
in ventricular volume and CSF pressure and associated symptoms and signs is
more indolent but ultimately reaches the point of decompensation on the
pressure-volume curve. Sometimes a neurosurgeon can tell from the
resistance to withdrawing CSF or from the rate of flow into the abdomen
through the clear tubing attached to the butterfly shunt tap needle that
obstruction is only partial, but even a partial obstruction requires prompt
revision.

2. Proximal Obstruction
CSF enters the intraventricular portion of the shunt catheter through small
(approximately 1-mm diameter) holes. Because the diameter of the inflow
holes and ventricular catheter is small, clumps of particles small enough to
enter the holes can block flow if their diameter is close to that of the
ventricular catheter inner lumen or inflow holes. Even a partial VP shunt
obstruction can result in an increase in CSF accumulation that overwhelms
reabsorption, resulting in a rapid increase in intraventricular volume and ICP.
A proximal obstruction should be suspected whenever there is a history of
increased cellular or other biologic debris in the CSF. Inability to withdraw
CSF with suction on a needle placed into the reservoir in sequence with the
ventricular catheter suggests CSF inflow obstruction within the ventricles
(Figure 10-4).

3. Disconnection
Any of the connections—ventricular catheter to reservoir, reservoir to valve,
valve to peritoneal tubing—can become disconnected. A history of head,
neck, or generalized shaking or jerking preceding formation of a tumescent
swelling under the skin along the course of shunt tubing requires a radiograph
of the head, chest, and or abdomen to rule out a disconnection. It should be
assumed that there is minimal or no flow of CSF beyond the disconnection. If
a disconnection is discovered incidentally in a patient without symptoms or
signs of hydrocephalus, it may be that the patient no longer needs continuous
drainage of CSF for ICP control.

Figure 10-4. Tapping and Draining the Reservoir of a

Malfunctioning VP Shunt

Reproduced with permission Cancer Research UK, CC BY-SA 4.0

<https://creativecommons.org/licenses/by-sa/4.0>, via Wikimedia Commons.

4. Distal Obstruction

A history of recent or multiple abdominal surgeries with headache, mental

status changes, and ventricular volume increased from post-shunt baseline is
suggestive of blockage of outflow from the intraperitoneal portion of the
drainage tubing. Intraperitoneal bleeding or infection can also cause distal
obstruction. Distal obstruction suggested by surgery is confirmed on tapping
the shunt at the reservoir if the column of CSF sucked into the clear portion of
the butterfly needle placed into the reservoir does not flow quickly and
completely out of the tubing through the drainage tubing and into the
abdomen. Distal obstruction of ventriculopleural shunts should similarly be
suspected if there is new pathology in the pleural space and no CSF column
flow on tapping of the reservoir.

5. Abdominal Surgery

Contamination of the peritoneal tubing by spilled intestinal contents is a

concern, especially in patients who have had previous abdominal surgery.
Frequently a general surgeon will ask a neurosurgeon to scrub in and
examine shunt tubing intraoperatively during abdominal surgery, especially if
there is a possibility of intestinal violation with leakage into the peritoneal
space. If there is suspicion of contamination based on inspection or extent of
surgical manipulation in proximity, the neurosurgeon may elect presumptive
externalization with several days of external drainage and IV antibiotics with
subsequent internalization (perhaps draining into a pristine pleural cavity)
once CSF is confirmed to be sterile. (Possible contamination of
ventriculopleural shunts should similarly be suspected when the pleural space
is entered for surgical intervention.)

D. Ventriculostomy
An alternative to shunts that is increasingly popular over the past few years is
the ventriculostomy (making a hole in the floor of the ventricle) that treats
hydrocephalus by creating an alternative CSF circulation pathway that
bypasses a focal obstruction. If the scar tissue proliferates over time and the
ventriculostomy closes, CSF can accumulate above the floor of the third
ventricle with recurrent hydrocephalus. If patency is compromised over a
short period of time, hydrocephalus symptoms and signs can come on
relatively acutely.

1. Tumor
Tumor masses can focally block flow along the CSF circulation pathway.
Ventricles may dilate slowly over time if the mass obstructing flow is slow
growing. Sometimes ventricular dilatation due to CSF circulation blockage by
a slowly expanding tumor is asymptomatic. Asymptomatic ventriculomegaly
does not always require surgical treatment but should be followed over time
with serial imaging and neurologic examination surveillance.

2. Hemorrhage

Neurologic deterioration early after

subarachnoid hemorrhage is frequently related to
development of hydrocephalus.

Acute hydrocephalus following subarachnoid hemorrhage (SAH) is due to

accumulation of red cells and other particulate matter in the Pacchionian
(arachnoid) granulations of the sagittal sinus. Hydrocephalus can develop
quickly over a few hours after SAH but sometimes is seen shortly afterwards
on presentation. Neurologic deterioration early after subarachnoid
hemorrhage is more frequently related to development of hydrocephalus and
not to rebleeding of an aneurysm.
Expansion of bleeding into the lateral ventricles from parenchymal basal
ganglia bleeding (so-called hypertensive hemorrhage) introduces red blood
cell debris into the subarachnoid CSF space which can also block
reabsorption.

3. Infection
Meningitis is associated with an increase in the concentration of reactive
proteins as well as debris from the breakdown of inflammatory and immune
cells. A history of meningitis, especially if a shunt was placed for
hydrocephalus, should prompt imaging to evaluate for ventriculomegaly.
Shunt infections are more common in children but can also occur in adults.
CSF should be withdrawn and sent for analysis (WBC, glucose, protein) and
culture to rule out infection in any patient with a VP shunt who presents with
symptoms of acute hydrocephalus.

4. Postoperative

Brain surgery with bleeding into the subarachnoid space is sufficient to cause
blockage of reabsorption along the sagittal sinus. A patient with a SAH who
did not have hydrocephalus preoperatively and whose aneurysm ruptures
intraoperatively during clipping should be monitored carefully for
postoperative hydrocephalus.

E. Monitoring of Hydrocephalus
A CT scan of the head is adequate for assessment of ventricular size.
Decreased tissue density can be seen around the ventricles when CSF is
pushed across the ependymal wall into the surrounding brain parenchyma
when ICP is elevated. A head CT is also adequate for demonstration of
ventricular size and the presence of periventricular edema suggestive of
increased ICP. Rapid CSF production and increasing ICP can cause a
precipitous decline in mental status.
Large ventricles do not always correlate with symptomatic hydrocephalus.
Ventricular enlargement is normal as the brain ages. The clinical presentation
—history and physical examination—determine whether a patient’s
ventriculomegaly seen on head CT is acute or progressive hydrocephalus with
elevated ICP that requires treatment, or is asymptomatic, long-standing, low-
pressure ventriculomegaly.
MRI is not indicated for the workup of acute, life-threatening hydrocephalus.
If the onset of symptoms is slowly progressive over several hours and a
neurosurgeon is available to remove a lesion or bypass an obstruction of the
CSF circulation, such as Sylvian aqueductal stenosis, AND if the patient is
stable for transport AND can tolerate being still for 30 minutes in a narrow
tube, an MRI may provide surgical strategy information that justifies the risks
of taking the time to obtain the images.
Until the acutely elevated ICP is lowered with drainage of CSF, the patient is
at risk for a rapid, geometric rise in ICP. The time frame for resolution of
compromised consciousness and return of neurologic examination to baseline
after an acutely elevated CSF pressure and volume is similar to that of
deterioration at the inflection point of the pressure-volume curve in which
smaller and smaller increments in CSF volume led to larger and larger
increases in ICP and rapid progression toward coma.

F. Management of Hydrocephalus
1. Diuretics
Because the elevation in pressure is the result of additional fluid in the
ventricles and not in the brain parenchyma (cerebral edema), osmotic diuresis
to reduce interstitial fluid (and reduction of the Monro-Kellie soft-tissue
compartment) will not significantly reduce or slow an increase in ICP due to
acute hydrocephalus. Medications like acetazolamide that reduce the volume
of CSF produced at the choroid plexus take hours to work and do not
decrease production enough to restore the compromised CPP. A surgical
pathway for drainage of CSF must be created before pressure reaches the
dicrotic notch of the pressure-volume curve.

2. Analgesia and Sedation

Headache is the most common symptom of acute hydrocephalus. Untreated
headache contributes to agitation and makes the patient less cooperative with
imaging and monitoring. Heightened vigilance for acute loss of airway
protective reflexes is crucial when sedation and systemic pain relief is being
used on a patient with altered mental status caused by increased ICP. In most
instances, it is recommended to protect the airway by intubating the patient
who already has a marginal mental status that is going to get worse. Definitive
treatment of headache caused by acute hydrocephalus is reduction of CSF
volume.

3. Airway
 If a patient is no longer able to protect their
airway, becomes lethargic, or has evidence of
hypercarbia while waiting for neurosurgical
relief of intracranial hypertension, emergent
intubation for airway protection and ventilatory
assistance is indicated.

If a patient is no longer able to protect their airway, becomes lethargic, or has

evidence of hypercarbia while waiting for neurosurgical relief of intracranial
hypertension, emergent intubation for airway protection and ventilatory
assistance is indicated.

4. Cerebrospinal Fluid Volume Reduction

Drainage of CSF may have been initiated in the ED or the ICU team needs to
be prepared to quickly set up for rapid insertion of a surgical CSF drainage
system.

An emergent neurosurgical consult request should be placed for any patient

with rapidly progressing decrease in consciousness with a head CT showing
ventriculomegaly. All interventions for acute hydrocephalus should be
performed by a neurosurgeon or other appropriately trained physician able to
identify and manage any complications.

a. Lumbar Cerebrospinal Fluid Drainage

Lumbar drainage of CSF by tap is a reasonable temporizing measure
for acute reduction in CSF volume and ICP. The volume of CSF that
is removed by a lumbar puncture (10–20 mL) is rapidly replaced
(25 mL/hr through the choroid plexus) such that keeping ICP low
may require a lumbar drain that continuously drains CSF (usually
around 10–20 mL/hr). ICP can be measured at the time of lumbar
puncture but cannot be followed over time.
Lumbar drainage of CSF for control of ICP should only be done if
intracranial imaging confirms no brain swelling or focal lesion near
the foramen magnum where occlusion of flow could result in a
pressure gradient between intracranial and intrathecal CSF that could
lead to downward herniation and brainstem compression. If a
neurosurgeon and the required equipment are available, the safest
alternative to reducing CSF volume through a lumbar puncture is
placement of an external ventricular drain (EVD).

b. Ventriculoperitoneal Shunt Tap

Neurosurgeons are trained to place a needle into the reservoir of the

shunt (Figure 10-5) to withdraw CSF into a syringe. Withdrawal of a
large volume (20 mL or greater) of CSF can result in almost
immediate resolution of signs and symptoms in a patient with acute
shunt failure. If access to an operating room (OR) is limited and a
shunt revision is planned semi-electively, serial high-volume shunt
taps can be done while waiting.
If CSF is drawn into clear tubing held straight up, the fluid column
should decrease rapidly if there is free flow along the catheter into
the peritoneal (or pleural) cavity. If the fluid column remains high
there is most likely obstruction distally in the peritoneal tubing or
outflow openings.

c. Non-Communication Lesion Removal

Based on symptoms and signs, if the patient’s ICP clinically is low

enough and not increasing so rapidly that there is concern that the
patient will stop breathing or lapse into coma, emergency surgery can
be temporarily deferred and the patient admitted to the ICU with
frequent “neurologic checks” and expeditious identification and
workup of a resectable lesion that is causing non-communicating
hydrocephalus while setting up for an urgent craniotomy.
If there is any doubt that resecting a lesion that seems to be
obstructing CSF flow will result in immediate resolution of
 hydrocephalus, it is best to place an EVD in the ICU or OR before
the craniotomy, removing it only postoperatively after imaging
confirms that the obstruction is relieved, flow is restored,
transependymal edema is resolved, ICP is normal, and CSF drainage
is not required to control ICP.

Occasionally postoperative imaging shows persistent ventriculomegaly

even though the obstructing lesion has been completely removed. If
the ventricles remain enlarged and the patient becomes symptomatic
when the EVD is clamped, there is still hydrocephalus present and
the patient will need conversion of the preoperative EVD to a
permanent indwelling shunt.

G. External Ventricular Drain (EVD)

Although EVD insertion, maintenance, and troubleshooting are the purview of
the consulting neurosurgeon, the critical care providers frequently manage
patients with an EVD. An understanding of the principles of EVD design,
insertion, maintenance, and troubleshooting is important.

1. Insertion
EVD placement is a surgical procedure that requires informed consent
whenever possible. EVDs are placed under maximum sterile conditions.
During placement in the ICU an assistant should be present at all times to
hand the surgeon any instruments or other equipment that is not already on
the sterile field.
Lethargic, uncooperative patients may need to be sedated to minimize
movement during the procedure. Local anesthetic is used for potentially
painful scalp incision, tunneling, and suture placement. Vital signs, oxygen
saturation, and respiratory rate should be monitored during the insertion
procedure. Even when the patient appears to be adequately sedated and is
not moving as the procedure begins, the assistant should hold the patient’s
head and chin under the drapes during incision, drilling, dual puncture, and
catheter passage.
Essential elements of the procedure include:

Side of insertion
Number of attempted passes to successfully enter the ventricle
Color and clarity of CSF obtained
Identification of whether or not the fluid came out under pressure
ICP when the fluid column pressure is measured
Post-procedure imaging for confirmation of catheter placement is not
necessary as long as there is return of clear CSF after three or fewer passes. If
there is no CSF on the third pass or if the CSF is bloody, a CT scan for
catheter position and possible hematoma is indicated.
VP shunt obstruction due to infection requires conversion of the indwelling
shunt to an external ventricular CSF draining system. The infected VP shunt
should be removed and replaced with a sterile EVD, preferably placed on the
opposite side of the head contralateral to the ventricle from which the infected
catheter was removed.
If the acute obstruction is due to a process in the abdomen (or pleural space if
the shunt is ventriculopleural), the distal portion of the draining catheter can
be pulled upwards and out through an incision made just next to the catheter
where it lies over the clavicle. The end of the catheter can then be connected
to tubing draining into a bag so that CSF drainage continues until definitive
revision of the shunt system can be done in the OR.

2. Shunt Externalization

A neurosurgeon should be consulted for EVD:

1. Indications for placement,
2. Insertion,
3. Oversight of maintenance,
 4. CSF withdrawal,
5. Removal.

Externalization of a VP shunt creates an EVD. The subcutaneous peritoneal

(or pleural) tubing can be pulled up and out through an incision made next to
the tubing as it passes over the clavicle. The distal end of the externalized
tubing can then be connected to tubing and a drainage bag. ICP pressure
readings from partially externalized shunts are as reliable as with EVDs and
comparable volumes of CSF can be drained. Bedside externalization is a good
option for reducing acutely elevated ICP when VP shunt obstruction is distal
(intra-abdominal or intrapleural) and no OR option is available.

3. Maintenance

CSF output and ICP should be recorded hourly. ICP measurements should be
done with the head of the bed at 30 degrees and the pressure monitor zeroed
at the level of the foramen of Monro (Figure 10-5).
 Figure 10-5. External Ventricular Drain (EVD)

Reproduced with permission Sales J. external_ventricular_drainage.png [Operative

Neurosurgery]. https://operativeneurosurgery.com/lib/exe/detail.php?
id=external_ventricular_drainage_complications&amp;media=external_ventricular_drain
age.png. Accessed June 16, 2021.

The surgeon’s post-procedure orders should specify the continuous drainage

threshold, how many milliliters of CSF should be drained how quickly when
pressure is elevated, as well as a length of time that ICP is above a specified
number before draining CSF. Routine drainage options include:

Open to drainage at a set threshold pressure (continuous)

Opened in response to ICP elevation (intermittent)
Troubleshooting is required if the monitored ICP waveform changes or is lost
and if there is no movement or dripping into the bag of CSF when the tubing
is open to drainage. In this situation, surgical attention usually is needed for
the possibility of obstruction.
CSF samples should be taken from a port distal to the ventricular catheter.
Pushing fluid retrograde (against the direction of CSF flow) through the
catheter into the ventricle should only be done when antegrade suction (in the
direction of CSF flow) does not clear the line. Only a few milliliters of fluid
(1–3) should be flushed through the system into the ventricle to avoid
increasing the ICP, especially in cases in which ICP may already be near
decompensation on the pressure-volume curve.

EVD catheters that are placed under maximized sterile conditions, with their
draining end tunneled under the scalp for a few centimeters, are at low risk
for becoming infected and therefore routine sampling of CSF or replacement
is not indicated. An EVD should be tapped and CSF sent for protein, glucose,
cell count, and culture as part of a fever workup and/or if a patient with an
EVD has mental status changes (with or without a new abnormality on head
CT).
Antibiotics can be given as prophylaxis during the time the drainage catheter
is in the ventricle and brain parenchyma. Current recommendations suggest
one dose of periprocedural antibiotics can be considered, but prolonged
prophylaxis does not decrease ventriculitis but does contribute to resistant
organisms and Clostridioides difficile infections. Ventriculitis discovered
when tapping an EVD as part of a fever workup, or as part of the workup of
altered consciousness, should be treated as aggressively as meningitis is
treated.
Even with multiple scalp sutures along its length, ventricular catheters can be
pulled out. Patients agitated or too lethargic to cooperate may require
sedation and/or restraints to keep them from reaching up and grabbing the
EVD tubing. Transport out of the ICU for imaging or procedures in patients
with EVDs in place should be avoided unless absolutely necessary. Transfers
from the ICU bed to a CT scanner couch should be performed carefully with
constant attention to the EVD tubing, dressings, and stopcock.
Clots or air in the tubing can impede or stop flow. When flow stops, with no
slowdown in the continuous production of CSF, intraventricular CSF pressure
rises rapidly, and the patient begins the progression from alert to
unarousable. Daily checks should be done on every EVD and a 24-hour CSF
output and ICP mean and spikes should be monitored and tracked.
Accuracy of ICP readings can be problematic if there is significant drift over
time. In patients with symptomatic acute hydrocephalus with neurologic signs,
management is guided more by clinical response to CSF drainage than by
numbers on the monitor.

4. Removal

Once the patient’s acute hydrocephalus has been treated and symptoms and
signs are resolved, plans should be made to remove the EVD as quickly as
possible to prevent infection and transfer the patient out of the ICU.

Based on the etiology of the acute hydrocephalus, the amount of CSF drained
daily to keep the patient asymptomatic with an ICP of less than 20 mm Hg
without imaging evidence of dilation of ventricles or transependymal edema
should be decreasing before removal is considered. EVD occlusion or
clamping trials for several hours or days should be conducted. If the patient
remains asymptomatic and imaging is unchanged after the EVD clamping
trial, the EVD can be discontinued. If, however, with EVD clamping, the
patient’s symptoms recur or imaging reveals ventricular dilation, then
consideration for a permanent internalized drainage system
(ventriculoperitoneal or ventriculopleural) will be considered by the
neurosurgical team
After an aneurysm is clipped and there is no more bleeding, the red blood
cell breakdown debris becomes more dilute with continuing CSF production
and the initially red, opaque fluid becomes clear over several days. This
clearing of the CSF is frequently associated with a decrease in the amount of
fluid drainage required to keep ICP low. If after several days of low or no
drainage post-subarachnoid hemorrhage and a CT scan confirms that
ventriculomegaly is stable or resolved, the patient can have the EVD safely
removed without placement of a VP shunt.
5. Shunt Revision

Many patients with CSF shunts will require revision. A revision can be
replacement of one component of the VP shunt, such as the valve, tubing, or
ventricular catheter if a focal site of obstruction can be identified, but if the
CSF is infected, the entire system should be replaced.

III. INTRACRANIAL HYPERTENSION

Intracranial hypertension is a common neurologic condition in critically ill
patients. Increased ICP is a medical emergency due to uncompensated
compromise of cerebral perfusion that can result in reduction of oxygen
delivery to a critical level in which neuronal function fails and cells die. Rapid
intracranial CSF volume reduction is required to prevent irreversible
neurologic deficit secondary to injury or death of brain tissue. The physiologic
aspect effect is similar to that discussed earlier in the chapter.
The major causes of increased ICP include:

Obstructive hydrocephalus that commonly occurs after

subarachnoid hemorrhage
Intracranial mass lesions from tumor, hematoma
Cerebral edema from acute hypoxic ischemic encephalopathy,
large cerebral infarction, severe diffuse axonal injury
Cerebral edema from acute large cerebral infarction (ischemic
stroke)
Severe traumatic brain injury (TBI)/intracranial hemorrhage
(subdural, epidural, or intraparenchymal)
Increased CSF production or decreased production; idiopathic
intracranial hypertension as seen in pseudotumor cerebri
Central nervous system infections like meningitis or encephalitis
Malignant hypertension
 Obstruction of venous outflow that is seen after venous sinus
thrombosis, jugular vein compression, or neck surgery

A. Presentation and Diagnosis

Clinical presentation of patients with high ICP vary according to the
underlying cause and acuity of the illness. The global symptoms include
headache and decrease level of consciousness. Focal cranial nerve palsies,
such as cranial nerve VI and papilledema secondary to congestion, can occur.
The mechanism of the Cushing reflex or Cushing’s triad, discussed
previously, is controversial. However, when present it indicates the need for
possible urgent intervention to lower the ICP.
Diagnosis of elevated ICP is usually based on the history, clinical
examination, neurologic findings, and sometimes a CT scan of the head. A CT
scan of the head should not be used alone to diagnose elevated ICP.

B. Management

Case Study
Consider again the case study presented at the beginning of this chapter: A
42-year-old man with no significant medical history experiences sudden onset
of the worst headache of his life during strenuous exercise. The patient is
taken to the ED of the local hospital by his family. The ED physician obtains
a CT of the head that shows subarachnoid blood over the cerebral convexities
and in the left Sylvian fissure. There is a small amount of blood seen in the
dependent lateral ventricles with prominence of the temporal horns. Early
surgical and neurointerventional consultations are obtained. The GCS score
on admission is 11. The consulting neurosurgeon notes that the patient is
lethargic. The patient is admitted to the ICU. Measures are taken to maintain
adequate blood pressure control, pharmacologic vasospasm prophylaxis, and
a four-vessel cerebral angiogram is ordered. The patient has embolization of a
right anterior communicating artery aneurysm a few hours after admission.
Upon arrival back to the ICU, he is minimally responsive and vomits. His
GCS score is now 6.
– What is the likely diagnosis?
– What diagnostic test will provide further evaluation?
– What treatment is indicated?
The man in this case study likely has acute obstructive hydrocephalus that
can be diagnosed with a CT scan of the brain. Treatment will include
insertion of an external ventricular drain for ICP monitoring and therapeutic
drainage of CSF.
Intracranial hypertension can cause secondary injury in patients with acute
neurologic and neurosurgical disorders and may require special neurologic
monitoring, including ICP monitoring. A jugular bulb oximeter or brain tissue
PO2 monitor for cerebral oxygen extraction may also be indicated.
Monitoring should also include pulse oximetry and capnography to avoid
unrecognized hypoxemia and hypo- or hyperventilation.
A ventriculostomy catheter is the preferred device for monitoring ICP. A
ventriculostomy catheter can also be used for therapeutic drainage of CSF to
reduce ICP. Elevated arterial partial pressure of carbon dioxide (PCO2) and
hypoxemia with an arterial partial pressure of oxygen (PO2) of less than 50
mm Hg causes vasodilatation and may increase cerebral blood flow. A
decreased PaCO2 causes vasoconstriction and reduces cerebral blood flow.
An inadequate cerebral blood flow results in brain tissue ischemia and brain
tissue death.
If there is a presumed elevated ICP, an ICP monitor should be placed at least
for the initial period to monitor the treatments provided, which are not without
adverse effects. Indications for an ICP monitor include:
Glasgow coma scale (GCS) score of < 8
Diagnosis that needs aggressive management
Goals of therapy include maintaining ICP at less than 20 mm Hg, maintaining
CPP greater than 60 mm Hg, and avoiding factors such as anxiety/agitation
that precipitate an elevation in the ICP. The best therapy is resolution of the
problem that is causing the elevated ICP. Intracranial hypertension is a
medical emergency and should be treated as such.

Medical measures for management:

Elevate the head of bed to reduce ICP, promote adequate CPP,
and maximize venous outflow from the head.
Secure the head in a neutral straight position to reduce excessive
flexion or rotation of the neck that may decrease jugular venous
drainage.
Provide sedation and analgesia to reduce metabolic demand,
ventilator asynchrony, and sympathetic nervous system responses
of hypertension and tachycardia.
Avoid hyperthermia and maintain euthermia to reduce metabolic
demands in the brain.
Control hypertension to prevent an exacerbation of cerebral edema
and decrease the risk of postoperative intracranial hemorrhage.
Blood pressure should be sufficient to maintain a CPP > 60 mm
Hg.
Prevent seizures, which increase metabolic demands of the brain.
Medical management of refractory increased ICP:

Provide heavy sedation and paralysis to reduce ICP by the

avoidance of coughing.
Hyperosmolar therapy with hypertonic saline or mannitol. 1 g/kg of
mannitol should be given for an urgent reduction in ICP.
– Hypertonic saline has an advantage over mannitol in hypovolemic
and hypotensive patients.
 – Mannitol is relatively contraindicated in hypovolemic patients
because of the diuretic effects.
– Hypertonic saline augments intravascular volume and may
increase blood pressure in addition to decreasing ICP.
Mild hyperventilation can be used for short periods.
Hyperventilation has limited use in the prolonged management of
elevated ICP. It may produce a sufficient decrease in cerebral
blood flow to decrease ICP and cause brain ischemia by the exact
mechanism. It should only be used acutely when herniation is
impending to allow time for other treatments or get the patient to
surgical intervention.
Induce barbiturate coma which reduces brain metabolism and
cerebral blood flow. Continuous EEG monitoring is used to monitor
burst suppression which indicates maximal dosing. This treatment
can cause hypotension requiring vasopressor support.
Corticosteroids are not indicated and have been shown to have a
detrimental effect.
Surgical measures for management:
Perform surgical evacuation of the lesion.
Drain CSF slowly at a rate of 1 to 2 mL a minute for 2 to 3 minutes
at a time until a satisfactory ICP has been achieved. Care should
be taken to not over-drain the ventricular system.
Decompressive craniectomy removes the rigid confines of the skull
which circumvents the Monro-Kellie doctrine to improve brain
tissue oxygenation.
Please see previous information for further discussion of ICP monitoring,
management devices, and implementation.

IV. CEREBRAL VASOSPASM

 Case Study
A 65-year-old woman presented to the ED after experiencing the “worst
headache of her life.” She is diagnosed with a ruptured aneurysm and is
admitted to the neuro-intensive care unit by the neurology service. She
undergoes embolization of a right anterior communicating artery aneurysm a
few hours after her admission. Upon arrival back to the unit, she is minimally
responsive and has a large emesis. She undergoes a CT scan of her brain
which shows acute hydrocephalus. She undergoes placement of an external
ventricular drain and a short time after, her level of consciousness improves.
Three days later in her hospital course, however, she becomes less responsive
once again.
– What is the likely diagnosis?
– What diagnostic test should she have for further evaluation?
– What treatment is indicated?
The woman in this case study likely has cerebral vasospasm, which can be
tested using a transcranial Doppler or angiography. Treatment will include
hypertensive, euvolemic therapy and/or transluminal balloon angioplasty
and/or intra-arterial infusion of verapamil.

A. Definition and Risk Factors

Cerebral vasospasm is the narrowing of a cerebral blood vessel that results in
the reduction of distal blood flow leading to ischemia and cerebral infarction.
There are varying degrees of cerebral vasospasm, the worst of which causes a
blood vessel to be completely constricted resulting in damage to the brain
tissue in that area. It often is a complication of a ruptured brain aneurysm
resulting in a subarachnoid hemorrhage, occurring in up to 70% of cases
following a subarachnoid hemorrhage. The highest risk occurs 7–10 days
following the subarachnoid hemorrhage.
Risk factors include advanced age, poor neurologic function on admission,
smoking, hypertension, and genetic factors. There is no difference in the risk
of vasospasm between those who have had their aneurysm surgically clipped
or endovascularly coiled/embolized. The pathophysiology is not fully
understood but is thought to involve structural changes and biochemical
alterations of the vascular endothelium and smooth muscle cells. Blood in the
subarachnoid space is thought to trigger these changes that result in cerebral
vasospasm. Delayed ischemic neurologic deficits occur in about 50% of
patients with cerebral vasospasm. This may lead to stroke or death despite
aggressive treatment.

B. Clinical Presentation
The diagnosis of cerebral vasospasm is primarily a clinical finding and
symptoms typically develop several days to 2 weeks after the initial injury.
The frequent use of sedatives in these patients also makes it more difficult to
recognize changes in the neurologic examination. Patients at risk for cerebral
vasospasm should receive frequent evaluation by the medical and nursing
staff in an acute neurologic unit such as that found in a neuro-intensive care
unit. Signs and symptoms of cerebral vasospasm may be similar to those seen
in patients experiencing a cerebral vascular accident. These include an
altered level of consciousness, confusion, or loss of movement in the
extremities. Patient may also report a headache or have a fever.

C. Diagnosis
CT scanning is commonly used to evaluate patients who experience signs of
neurologic deterioration. A CT scan is also obtained to rule out the
development of rebleeding, infarction, or hydrocephalus. Communicating
hydrocephalus commonly occurs with subarachnoid hemorrhage, so this
needs to be ruled out. Infarcts may be seen on CT in patients that are having
cerebral vasospasm, but this is a later finding.
Transcranial Doppler (TCD) measures the velocity of blood flow in the
cerebral circulation. TCD detects elevation in the mean cerebral blood flow
velocities, primarily in the middle and internal cerebral arteries. The most
common locations to be affected by vasospasm include the middle cerebral
artery, bilateral anterior communicating arteries, and the terminal vertebral
artery or distal branches. Getting adequate windows in some patients can be
problematic. Cerebral angiography can be used to diagnose or confirm
cerebral vasospasm. Endovascular intervention can be done at the same time.

D. Prevention and Treatment

Cerebral vasospasm accounts for approximately 23% of severe disability and
death after a ruptured aneurysm. Nimodipine is a calcium channel antagonist
used to prevent cerebral ischemia and is administered at 60 mg oral every 4
hours (30 mg oral every 2 hours if significant hypotension) for 21 days after
the aneurysm rupture. This has been found to result in a significant reduction
in mortality. Current recommendations for initial management of cerebral
vasospasm include induced hypertension and ensuring euvolemia.
Hypervolemia and hemodilution, which are components of triple H therapy
(hypertension, hemodilution and hypervolemia), are no longer endorsed.
Complications of this therapy include volume overload, exacerbation of
cerebral edema, and potentially rupturing unsecured aneurysms. Nimodipine
is the only treatment that has been shown to provide benefit over multiple
studies. Studies using statins and other pharmacologic trials have failed to
show benefit.
Endovascular interventions are also likely responsible for the lower incidence
of delayed ischemic neurologic deficits. These include transluminal balloon
angioplasty and intra-arterial infusion of verapamil. Verapamil reduces the
angiographic spasm and has been shown to achieve clinical improvement in a
third of cases. Effects may be temporary and the treatment may need to be
repeated.

V.NEUROGENIC SHOCK

Case Study
A 27-year-old man is brought to the ED by emergency medical services after
diving head-first into a lake. He is awake and states he cannot feel anything
below his neck. His vital signs are 80/50 mm Hg, heart rate 66 beats/min,
and respirations 20 breaths/min. His breaths are shallow. Clinical
examination shows loss of motor and sensation at T4.
– What is the likely diagnosis?
– What diagnostic test should he have for further evaluation?
– What treatment is indicated?

A. Definition
The man in this case study has neurogenic shock syndrome. Neurogenic
shock syndrome is dilatory shock state, usually associated with cervical or
thoracic spinal cord injuries (above the T6 level). It is thought to be the end
result of the impaired autonomic control from loss of sympathetic tone with an
intact parasympathetic response. The loss of sympathetic regulation of the
vascular smooth muscles of peripheral vessels (vasodilation) results in
subsequent pooling of blood in the periphery and decreased contractility
leading to decreased cardiac output.
The vast majority of cases of neurogenic shock syndrome are posttraumatic,
but it can be associated with non-traumatic insults as well, such as spinal
epidurals, malignancies, and abscesses.

B. Clinical Manifestations
The patient presents warm and dry as opposed to the cool clammy
presentation of the classic shock patient. There is also an increase in the
unopposed vagal tone leading to a relative bradycardia. This affects the
patient’s ability to compensate for shock state with tachycardia. It can occur at
any time following an insult, but signs and symptoms are typically seen within
hours of injury. It is estimated that up to 77% of cervical spinal cord injuries
have a component of neurogenic shock (bradycardia), but less than 20% of
the injured have the classic presentation. The hemodynamic instability will
usually improve over 2 weeks.

C. Management
In the acute phase, judicious fluid resuscitation with crystalloid is suggested.
For the trauma patient there may be more than one cause of the patient’s
hypotension, and all possible causes should be investigated besides the
neurogenic source of shock and a careful search to eliminate other potential
causes. After the patient has been fluid resuscitated, vasopressors and/or
inotropes can be instituted. Care should be used to avoid over-resuscitation
with intravenous fluids because pulmonary edema, swelling of the cord, and
other untoward injury may occur.
Achieving a MAP of 85–90 mm Hg to maintain adequate perfusion pressure
to the spinal cord may be considered controversial by some but is
recommended by many guidelines and societies. Using vasopressors to
augment the blood pressure would be needed in many instances. For patients
with symptomatic bradycardia, atropine may be used. Particularly severe
bradycardia may require pacemaker placement.
The term neurogenic shock is often interchanged with spinal shock. However,
it should be noted that spinal shock is a completely separate clinical entity.
Neurogenic shock refers to the hemodynamic sequelae associated with spinal
cord injury. Spinal shock refers to the temporary stunning of the spinal cord
and can occur at any level of injury. Patients typically present with a flaccid
paralysis and areflexia below the level of injury. The true neurologic
examination can be affected. The duration varies from a few days to several
weeks. Spinal shock is diagnosed through observation of the bulbocavernous
or cremasteric reflexes. If these reflexes are absent, then the patient has
spinal shock.
Autonomic dysreflexia (hyperreflexia) is another hemodynamic syndrome
associated with spinal cord injury. It typically presents with sudden
hypertension. Flushing, headache, and sweating can also be seen. The
presentation can vary from an asymptomatic to a potentially lethal event. The
pathophysiology of autonomic dysreflexia has not been totally elucidated. It is
believed that the massive sympathetic discharge is from impairment of the
supraspinal inhibition. Automatic dysreflexia can occur at any time post-
injury. The diagnosis is typically made with a systolic blood pressure increase
greater than 20 mm Hg above the patient’s baseline and bradycardia may
also be seen. Autonomic dysreflexia has triggers such as urinary retention and
constipation which activate the sequence. It is recommended prior to initiating
pharmacologic modalities the following simple steps are performed: place the
patient upright, loosen any restrictive clothing or devices, investigate potential
bowel or bladder triggers, and search for any other triggers. If the above steps
fail to resolve the hypertension, antihypertensive medications may be needed.

VI. DISORDERS OF SODIUM BALANCE DURING BRAIN

INJURY

Case Study
A 40-year-old woman is admitted to the hospital with the worst headache of
her life. At the time of admission, her neurologic status deteriorates quickly
and she now only flexes to pain on the left side and withdraws to deep painful
stimuli. The CT scan of the head reveals a large amount of diffuse
subarachnoid blood. A cerebral angiogram shows a basilar artery aneurysm
that is subsequently successfully coiled. Although her sodium levels were
normal on admission, her sodium levels postoperatively gradually decreased
daily for the next week from a level of 145 mEq/L to 130 mEq/L.
– What is the likely diagnosis?
– What diagnostic test should she have for further evaluation?
– What treatment is indicated?

A. Secretion of Antidiuretic Hormone (ADH)

Antidiuretic hormone (ADH, also called arginine vasopressin or AVP) is
produced in the supraoptic nucleus of the hypothalamus which is then
transported and stored in the posterior pituitary and then secreted.
Osmoregulation is primarily mediated by osmoreceptors in the anteromedial
hypothalamus that are sensitive to small alterations in plasma osmolality. Ideal
plasma osmolality for adults is approximately 275–295 mOsm/kg. A decrease
in osmolality of 1–2% will suppress ADH levels to promote diuresis. An
increase in plasma osmolality will cause water retention. ADH is also released
in response to a decrease in circulating blood volume and a significant
increase in blood pressure. Syndrome of inappropriate antidiuretic hormone
(SIADH), cerebral salt wasting syndrome (CSWS), and diabetes insipidus (DI)
all affect the sodium and water balance, but each has a different
pathophysiology, diagnosis, and treatment. SIADH is caused by ADH-
induced dilutional euvolemic hyponatremia. Central DI results from
diminished ADH synthesis or secretion. The etiology of CSWS remains an
area of research. The exact mechanism remains open to debate.

B. Hyponatremia
Hyponatremia is a relatively common occurrence in patients with brain injury
and in postoperative neurosurgical patients. There are numerous causes of
hyponatremia including a variety of neurologic disorders. It is associated with
both SIADH and CSWS in neurosurgical patients (Table 10-1).

Table 10-1 Causes of SIADH and CSWS

Abbreviations: ICH, intracerebral hemorrhage; SAH, subarachnoid hemorrhage; SCI, spinal cord
injury; TBI, traumatic brain injury

Case Study
A 63-year-old man is admitted to the hospital for resection of a pituitary
adenoma. Postoperatively, his neurologic status is stable, but the serum
sodium levels continue to increase daily and his hourly average urine output
is approximately 500–600 mL/h.
– What is the likely diagnosis?
– What diagnostic test should he have for further evaluation?
– What treatment is indicated?

1. Clinical Presentation
The signs and symptoms resulting from hyponatremia secondary to SIADH or
CSWS are often nonspecific. The rate of decrease in the serum sodium
concentration is more important in terms of producing acute symptoms rather
than the actual sodium level. However, sodium concentrations <120 mEq/L
usually present with acute signs and symptoms such as ataxia, nausea,
malaise, muscle cramps, and vertigo. Changes in level of consciousness range
from minor changes to lethargy, coma, and seizures. Coma and seizures
usually reflect acute changes in the serum sodium level rather than with a
slow chronic decrease in sodium.

2. Diagnosis
It can be difficult to distinguish between SIADH and CSWS. Careful attention
must be given to the volume status of the patient. SIADH-induced
hyponatremia is associated with patients who are euvolemic in contrast to
those patients with CSWS who may have significant volume losses and are
usually volume depleted. In SIADH in the absence of hypovolemia,
hypotension, or adrenal insufficiency, there is impaired urine dilution with
urine osmolality values >100 mOsm/kg. A low serum uric acid concentration
is often seen in CSWS due to urate wasting in the urine.

3. Treatment
The treatment of choice for SIADH is careful volume restriction. Most patients
require fluid restriction to approximately 1 liter per day. In extreme cases of
SIADH with very low serum sodium levels and critical acute neurologic
changes, hypertonic saline (1.5%, 3%, 23.4% saline) should be used
judiciously. Infusion rates of hypertonic saline will depend on the
concentration of the hypertonic saline and the desired sodium level.
Furosemide and fludrocortisone can be used as adjunct therapy. Vasopressin
receptor antagonists (conivaptan and tolvaptan) have also been used in
SIADH with normal saline administration to replenish the sodium excreted
with diuresis (refer to Chapter 17, Management of Life-Threatening
Electrolyte and Metabolic Disturbances for more detailed information). The
treatment of CSWS is in contradistinction to SIADH and consists of fluid
resuscitation and keeping the patient well hydrated with a positive fluid
balance. Intravenous fluids with normal saline or hypertonic solutions may
also be used with NaCl oral administration and fludrocortisone as well.
It is important to recognize that too rapid iatrogenic increases or decreases of
the serum sodium level by aggressive treatment may result in central pontine
myelinolysis (CPM). CPM is a noninflammatory demyelination syndrome that
classically affects the central pons but can also affect the midbrain, thalamus,
and cerebellum. It is recommended that the sodium level be increased with
treatment at <0.5 mEq/L hourly if hyponatremia has been present for > 48
hours or the time of decrease is unknown. If the hyponatremia is chronic,
rapid correction of sodium (>1 mEq/L/h or 8–12 mEq/L/day) may result in
the demyelination syndrome.

C. Hypernatremia
In neurosurgical patients, hypernatremia can result from injudicious use of
hypertonic saline solutions but may also result from DI when there is
excessive diuresis from water excretion. DI is characterized by large volumes
of hypotonic dilute urine (polyuria and nocturia) and polydipsia. In the
neurosurgical patient, this is often associated with central DI.
The causes of central DI are a result from damage to the pituitary gland or
the hypothalamus. In the postoperative period, DI can be caused by
inflammation around the pituitary or the hypothalamus or from damage to
these areas intraoperatively. The causes of central DI postoperatively include:
Subarachnoid hemorrhage
Intracranial hemorrhage
Severe traumatic brain injury
Herniation
Resection of sellar and pituitary masses
DI associated with neurologic disorders increases both morbidity and
mortality. Central DI is secondary to a primary deficiency of ADH.
Nephrogenic DI results from an inappropriate response to ADH by the
kidneys. Acquired central DI can be seen in a variety of neurosurgical states,
such as head trauma, neoplasms, and meningeal and encephalitic infections.
DI has been reported to occur in about 75% of postoperative pituitary tumor
resections. Most postoperative DI resolves over time although there is a small
minority of patients who continue to have persistent DI.

1. Clinical Presentation of Diabetes Insipidus (DI)

Signs and symptoms of hypernatremia are usually nonspecific although
gastrointestinal symptoms can occur with nausea and vomiting. Severe signs
and symptoms are seen in patients who may be misdiagnosed or diagnosed
and treated late and present with signs of extreme volume depletion with
lethargy and subsequent coma. Polyuria, nocturia, and polydipsia are
commonly seen with central DI.

2. Diagnosis
The diagnosis of central DI should always be suspected in neurosurgical
patients, particularly in the postoperative period when diuresis is excessive in
relation to fluid intake. When the urine output is excessive, urine studies
should be ordered to monitor urine specific gravity, urine osmolarity, and
serum sodium levels. In DI, the urine osmolarity is low from 1.000 to 1.005;
the urine osmolarity is also low from 50–150 mOsm/L; and the serum sodium
is more often elevated in acute neurosurgical patients.

The various clinical parameters can help differentiate among the serum
sodium balance etiologies. In SIADH and cerebral salt-wasting etiologies, the
serum sodium parameter is low, but it is high in central DI. Urine output is
high in CSWS and central DI, but normal or low in SIADH. The intravascular
volume status is low in CSWS and central DI, but normal or high in SIADH.
CSWS and central DI have low vasopressin levels, but levels are high in
SIADH. The most striking difference is seen in the urine sodium parameter,
which is high in SIADH, very high in CSWS, but low in central DI.

3. Treatment
Treatment of DI is directed at decreasing urine output by increasing the
activity of ADH and replacement of previous and ongoing fluid losses. Fluid
replacement for hypernatremia secondary to DI is based on hourly urine
output, urine specific gravity, and by calculating the patient’s free water
deficit. In addition to oral fluids, additional fluid boluses and maintenance
intravenous fluids are often required. It is recommended to begin therapy if
the urine output is excessive at >300 mL/h for 2–3 hours or the patient
demonstrates any neurologic signs or symptoms (confusion, lethargy, coma).
A low-sodium, low-protein diet can be used in those patients with a milder
form of DI. Desmopressin (a synthetic analog of ADH) is recommended for
the early treatment of DI. Although oral and nasal spray preparations are
available, most neurosurgical patients are treated with doses of 1–2 mcg
intravenously or subcutaneously every 12 hours or on a prn basis depending
on the sodium level and the urine output.
While therapy is administered, careful monitoring of urine output and sodium
levels should be performed, and therapy should be titrated to normal urine
output and normal sodium levels. Excessive fluids and injudicious use of
desmopressin can lead to water retention and hyponatremia that can result in
brain injury and swelling. Although other drugs such as chlorpropamide,
carbamazepine, clofibrate, thiazide diuretics, and nonsteroidal anti-
inflammatory drugs are available for the treatment of DI, they are less
effective than desmopressin and are not often used in the ICU patient.

Key Points
Neurosurgical ICU
Increased intracranial pressure (ICP) is a medical emergency due
to uncompensated compromise of cerebral perfusion pressure
(CPP) that can result in reduction of oxygen delivery to a critical
level in which neuronal function fails and cells die.
Acute hydrocephalus is life-threatening and must be drained
immediately.
Cerebral vasospasm should be suspected in a patient with
significant subarachnoid blood with new neurologic changes within
the first 2 weeks after the initial bleed.
 Most cases of neurogenic shock are posttraumatic and are
associated with bradycardia, hypotension, and loss of sympathetic
tone.
Syndrome of inappropriate antidiuretic hormone secretion (SIADH)
and cerebral salt-wasting syndrome (CSWS) can be seen in brain-
injured patients and postoperatively.
Diagnosis can be confusing and should be based on urine studies
and volume status of the patient.
Central pontine myelinolysis (CPM) can result from iatrogenic rapid
increases or decreases in the sodium level.
Diabetes insipidus (DI) is often seen after pituitary surgery and the
primary goal is to maintain euvolemia and possibly include
treatment with desmopressin.

Suggested Readings
1. Carney N, Totten AM, O’Reilly C, et al. Guidelines for the
management of severe traumatic brain injury, Fourth Edition.
Neurosurgery. 2017:80(1): 6-15.
2. Chestnut R, Videtta W, Vespa P, et al. The participants in the
international multidisciplinary consensus conference on
multimodality monitoring. Intracranial pressure monitoring:
fundamental considerations and rationale for monitoring.
Neurocrit Care. 2014;21 Suppl 2:S64-S84.
3. Diringer, MN, Bleck TP, Hemphil JC et al. Critical care
management of patients following aneurysmal subarachnoid
hemorrhage: Recommendations from the Neurocritical Care
Society’s Multidisciplinary Conference, 15:211-240, 2013.
www.neurocriticalcare.org.
 4. Fried HI, Nwathan BR, Rowe AS, et al. The insertion and
management of external ventricular drains: an evidence-based
consensus statement: a statement for healthcare professionals
from the Neurocritical Care Society. Neurocrit Care.
2016;24(1):61-81.
5. Gaasch M, Schiefecker AJ, Kofler M, et al. Cerebral
autoregulation in the prediction of delayed cerebral ischemia and
clinical outcome in poor-grade aneurysmal subarachnoid
hemorrhage patients. Crit Care Med. 2018;46(5):774-780.
6. Herrera CAS, Su FB, Backer DD, et al. Treatment of
intraparenchymal hypertension with hyperosmotic therapy SH
7.45 vs. M20%. Crit Care Med. 2013;41(12):A44.
7. Hinson HE, Stein D, Sheth KN. Hypertonic saline and mannitol
therapy in critical care neurology. J Intensive Care Med.
2013;28(1):3-11.
8. Kristiansson H, Nissborg E, Bartek J Jr, et al. Measuring elevated
intracranial pressure through noninvasive methods: a review of
the literature. J Neurosurg Anesthesiol. 2013;25:372.
9. Livesay SL, McNett MM, Keller M, Olson DM. Challenges of
cerebral perfusion pressure measurement. J Neurosci Nurse.
2017;49(6):372-376.
10. Mastantuono JM, Combescure C, Elia N, Tramer MR, Lysakowski
C: Transcranial doppler in the diagnosis of cerebral vasospasm:
an updated meta-analysis. Crit Care Med. 2018;46(10):1665-
1672.
11. McMahon D, Tutt M, Cook AM. Pharmacological management of
hemodynamic complications following spinal cord injury.
Orthopedics. 2009;32(5):331.
12. Oiso Y, Robertson GL, Norgaard JP, Juul KV. Clinical review:
Treatment of neurohypophyseal diabetes insipidus. J Clin
Endocrinol Metab. 2013;98(10):3958-3967.
13. Popa C, Popa F, Grigorean VT, et al. Vascular dysfunction
following spinal cord injury. J Med Life. 2010;3(3):275-285.
14. Ruiz IA, Squair JW, Phillips AA, et al. Incidence and natural
progression of neurogenic shock after traumatic spinal cord
injury. J Neurotrauma. 2018;35(3):461-466.
15. Saindane AM: Recent advances in brain and spine imaging.
Radiol Clin North Am. 2015;53:477-496.
16. Sterns RH. Disorders of plasma sodium. N Engl J Med.
2015;372(13):1269.
17. Sterns RH, Silver SM. Cerebral salt wasting versus SIADH: what
difference? J Am Soc Nephrol. 2008;19(2):194-196.
18. Verbalis JG, Greenberg A, Burst V, et al. Diagnosing and treating
the syndrome of inappropriate antidiuretic hormone secretion. Am
J Med. 2016;129(5):537.
19. Webb A, Owens S: Subarachnoid hemorrhage. In Hemphill JC,
Rabenstein AA, Samuels OB, eds. The Practice of Neurocritical
Care. Minneapolis, 2016, Neurocritical Care Society.
20. Zoerle T, Lonbardo A, Colombo A, et al. Intracranial pressure
after subarachnoid hemorrhage. 2015;43(1):168-176.

Suggested Websites
1. Hydrocephalus Association. https://www.hydroassoc.org/about-
us/newsroom/facts-and-stats-2/
2. www.neurocriticalcare.org.
3. https://www.braintrauma.org/
 Chapter 11
LIFE-THREATENING
INFECTIONS: DIAGNOSIS AND
ANTIMICROBIAL THERAPY
SELECTION

Objectives
Understand and apply the terminology specific to life-threatening
infections.
List the risk factors for the development of infection.
Identify systemic and site-specific clinical manifestations of life-
threatening infections, and understand the diagnostic use of clinical
laboratory testing.
Describe the different clinical and epidemiologic variables used to
guide the selection of antimicrobial therapy.
Outline antimicrobial empiric therapy and treatment of specific
infections.

Case Study
A 55-year-old man with diabetes mellitus was transported to the emergency
department because of a change in mental status and right arm pain. The wife
reported that the patient has been having increasing arm pain with a
spreading reddish-colored rash over the arm in the last 24 hours. On
awakening, he was found to have a change in mental status with confusion
and lethargy. His vital signs at the emergency department show a blood
pressure of 90/60 mm Hg, heart rate of 120 beats/min, temperature of 39°C
(102.2°F), respiratory rate of 24 breaths/min, and pulse oximetry of 99% on
2-L nasal cannula. The arm is diffusely edematous and erythematous with
some areas appearing bruised. You are the responsible caregiver for the
patient, and you are admitting the patient to the hospital.
– Does this patient have sepsis?
– What level of care is needed for this patient?
– What initial immediate interventions should be instituted?

I. INTRODUCTION
Life-threatening infections are both a cause and a consequence of critical
illness. The incidence of life-threatening infections or sepsis is increasing as a
reflection of the growing population of patients at risk: the elderly,
immunocompromised patients, and those with malignancy, chronic illness, or
multiple trauma. Septic shock, the most severe form of systemic response to
infection, is a common cause of death in critically ill adults and children.
Early recognition and appropriate management of infections and their
sequelae can decrease the mortality rate.

Sepsis is defined as life-threatening organ dysfunction caused by a

dysregulated host response to infection. Abnormalities that suggest organ
dysfunction may include, but are not limited to, lactic acidosis, oliguria,
coagulation disorders, acute alteration in mental status, and an elevated
sequential organ failure assessment (SOFA) score. Septic shock is a subset of
sepsis with circulatory and metabolic/cellular dysfunction associated with a
higher risk of mortality. In the clinical setting, septic shock is characterized by
hypotension requiring vasoactive drugs to maintain a mean arterial pressure
of greater than 65 mm Hg along with a serum lactate level of greater than 2
mmol/L despite adequate fluid resuscitation. Patients with suspected infection
who are likely to have a prolonged ICU stay or die in the hospital can be
identified at the bedside using the quickSOFA (qSOFA) score which is
positive if a patient has two or more of the following: alteration in mental
status, systolic blood pressure of less than 100 mm Hg, and a respiratory rate
greater than 22 breaths/min.

Given heterogenicity in patient presentation,

formal definitions should not be the sole criteria
for diagnosis of sepsis and septic shock.

Sepsis definitions were primarily developed for research and quality

improvement purposes. Consequently, definitions of sepsis may be difficult to
apply to an individual patient. Attempts to use the definitions for individual
patients can result in a delayed or missed diagnosis and therapy. There can
be no substitute for clinical evaluation by a competent physician to diagnose
and initiate management of sepsis and septic shock.

Initial considerations in resuscitation and infection management are described

in Chapters 7 and 8.

II. DIAGNOSIS OF INFECTION

The diagnosis of serious or life-threatening infection is based on a careful and
complete assessment of the patient’s history, including risk factors, and the
presence of characteristic clinical manifestations. Atypical presentations that
may occur, particularly in the elderly and in immunocompromised patients,
must also be considered. Laboratory, microbiologic, and imaging results also
support the diagnosis of documented or suspected infection.

A. Evaluation of New Fever in Critically Ill Adult Patients

In an era when use of hospital and patient resources is under intensive
scrutiny, fevers should be evaluated in a prudent and cost-effective manner.
A new fever in a patient in the ICU should trigger a careful clinical
assessment rather than automatic orders for laboratory and radiologic tests.

Although some literature defines fever differently, the Surviving Sepsis

Campaign has recommend using a value of >38°C (>100.4°F). It is often
difficult to determine whether an abnormal temperature is a reflection of a
physiologic process, a drug, or an environmental influence. When evaluating
a new fever, an attempt should be made to rule out causes other than
infection before subjecting the patient to a barrage of investigations. A broad
range of medical conditions commonly seen in the ICU can cause fever
(usually low grade). These include but are not limited to alcohol or drug
withdrawal, transfusion reaction, postoperative fever, adrenal insufficiency,
pancreatitis, stroke, pulmonary emboli, and neoplasm. In addition, not all
infected patients are febrile. Evaluation should include a review of the
patient’s chart, a thorough examination and review of all environmental
factors as well as drugs (Table 11-1) that the patient has received recently,
and consideration of physiologic fever that can occur in patients in the ICU,
such as postoperative fever. The development of a temperature ≥ 38°C
(≥100.4°F) without a clear alternate cause or ≤ 36°C (≤96.8°F) in the
absence of a known cause of hypothermia (eg, hypothyroidism, cooling
blanket) is a reasonable trigger for a clinical assessment. Clinical evaluation of
the patient with fever should guide the requisition of additional laboratory or
radiologic studies.

Fever alone should not routinely trigger blood

cultures.

Table 11-1 Medications Associated With Fever

Reproduced with permission Cunha BA. Clinical approach to fever in the neurosurgical intensive care
unit: Focus on drug fever. Surg Neurol Int. 2013;4(Suppl 5):S318-S322. Copyright 2013 Cunha BA.

In the ICU, body temperature is most accurately measured by an

intravascular, esophageal, or bladder thermistor, followed by rectal, oral, and
tympanic membrane measurements. Axillary measurements, temporal artery
estimates, and chemical dot thermometers should not be used in the ICU.
Rectal thermometers should be avoided in neutropenic patients.
The diagnosis of drug-induced fever is usually established by the temporal
relationship of the fever to starting and stopping the drug. Patients can be
rechallenged with the drug to confirm the diagnosis, but this is rarely done
unless the drug in question is essential and alternatives are not available.
Patients developing anaphylaxis or toxic epidermal necrolysis as a result of
drug exposure should not be rechallenged.

Fever is a common phenomenon during the initial 48 hours after surgery.

Fever in this early postoperative period is usually noninfectious in origin,
presuming that unusual breaks in sterile technique or pulmonary aspiration
did not occur. However, 96 hours after surgery, fever is more likely to
represent infection.
Surgical site infections alone account for approximately 25% of overall costs
related to treatment of nosocomial infections. The rate of surgical site
infection is approximately 3%. This rate varies based on the degree of
contamination of the incision, the patient’s medical comorbidities (eg,
diabetes mellitus and obesity increase risk), whether surgery is prolonged or
an emergency, and whether any antimicrobial prophylaxis is administered
correctly (eg, appropriate narrow spectrum of activity, administration just
before incision, and discontinuation within 24 hours [48 hours for cardiac
surgery]).

B. Epidemiologic Factors
Serious or life-threatening infections may occur in patients from the
community, long-term care facilities (ie, nursing homes), or hospital settings.
Serious or life-threatening community-acquired infections include bacterial
pneumonia, central nervous system (CNS) infections or meningitis, urosepsis,
intra-abdominal sepsis caused by a ruptured or obstructed viscus, or sporadic
uncommon infections, such as necrotizing fasciitis. Patients from long-term
care facilities share this spectrum but often have infections with more resistant
pathogens. Patients from long-term care facilities have an increased risk of
developing device-related infections and/or infected decubitus ulcers. Finally,
hospitalized patients are exposed to antimicrobial-resistant flora and
numerous invasive devices, in addition to having more comorbidities and
greater severity of illness than the other populations, making them prone for
the development of sepsis.

Healthcare-associated infections are acquired while the patient is receiving

treatment for other conditions within a healthcare setting. They are of
particular importance because of the higher risk of resistant pathogens. It is
estimated that healthcare-associated infections result in almost 100,000
deaths annually in the United States. Infection can be acquired during the
current hospitalization or may be associated with an admission in the
preceding 60 days. In addition, other forms of healthcare-associated infection
include the development of infection in residents in a nursing home or
extended-care facility and patients receiving home intravenous antibiotic
therapy or chemotherapy, chronic dialysis, and/or home wound care.
C. Predisposing Conditions
The presence of predisposing conditions should alert the care team to patients
at higher risk of developing infections, including some infections that may be
associated with a particular predisposing condition (Table 11-2). Permanent
prosthetic implants, such as heart valves, intravascular grafts, or orthopedic
devices, may become infected in either the early or late postoperative period.
Invasive procedures (eg, surgery, vascular catheterization, placement of
urinary catheters, and endotracheal intubation) breech the normal mucosal
defense barriers and predispose patients to infection. Healthcare providers
need to remember that the lack of predisposing conditions does not eliminate
the possibility that a serious infection is present.

Table 11-2 Conditions Predisposing to Infection

D. Clinical Manifestations

Hypothermia predicts poor outcome in serious

infections.
The clinical manifestations of life-threatening infections are diverse, and they
may be subtle or overt, and localized or systemic. An awareness of the signs
and symptoms associated with specific infections allows early recognition and
prompt institution of appropriate empiric antimicrobial and supportive
management. However, most of the clinical manifestations are not specific.

1. Systemic Signs and Symptoms

Fever is the most frequent systemic manifestation of infection, but patients
with serious infections may be normothermic or even hypothermic.
Hypothermia is more frequently seen in the elderly; those with physical
debilitation/nutritional impairment, alcoholism, and hepatic or renal failure;
and with the use of antipyretic medications/steroids. Severe or prolonged
septic shock will often present with marked hypothermia. Temperature probes
on a urinary catheter, when available, are the most reliable methods to
measure the core temperature. Temperature measurement is most practically
obtained via the oral or rectal routes, although the limitations of each method
should be considered.

Other systemic manifestations include chills, rigors, hypotension, tachypnea,

dyspnea, tachycardia, and nausea and vomiting. Tachycardia is almost always
present but may be absent in the presence of cardiac conduction
disturbances, autonomic dysfunction, β-blockers or calcium channel blockers,
and drug fever. Hypotension may be the result of dehydration and
hypovolemia but may also indicate septic shock, particularly if the blood
pressure does not respond well to volume resuscitation. Hypoperfusion of the
kidneys may result in oliguria or anuria. Encephalopathy is a common clinical
manifestation and ranges from lethargy/irritability to delirium and coma.
Petechiae and/or ecchymosis may be present, particularly on distal
extremities.

2. Site-Specific Signs and Symptoms

Some signs and symptoms of infection could be associated with the specific
source of infection:
Infections of the CNS may be associated with headache, seizures,
meningismus, or focal neurologic findings. Altered mental status is
often present but not specific for CNS infections.
Diffuse or localized respiratory tract infections may be associated
with dyspnea, tachypnea, cough, sputum production, or (rarely)
hemoptysis. Chest auscultation findings, such as crackles, rhonchi,
or tubular breath sounds, indicate whether the process is localized
or diffuse. Diminished breath sounds and dullness on percussion
are suggestive of a pleural effusion.
Intra-abdominal infections may cause abdominal pain, abdominal
distension, nausea and/or vomiting, diarrhea, and anorexia.
Diaphragmatic irritation can be perceived as pain in the side of the
neck and proximal shoulder area or may cause hiccups. Findings
on examination may include diffuse or local tenderness, rebound
tenderness, ileus, or guaiac-positive stool. A wound infection with
evidence of fascial disruption may signal an intra-abdominal
infection below the fascia.
Urinary tract infections may produce flank pain or abdominal pain,
tenderness, dysuria, hematuria, and oliguria. Typically, a urinary
catheter–associated infection does not produce localized symptoms.
Cutaneous manifestations may result from a primary infection of
the skin or skin structures (eg, pain, erythema, and induration as a
result of cellulitis; wound margin erythema; tenderness or purulent
discharge; vesicular lesions caused by herpes infection) or be a
consequence of disseminated systemic infection (eg, erythematous
indurated papules or nodules of ecthyma gangrenosum caused by
bacteremia, septic emboli caused by infective endocarditis, diffuse
macular erythema caused by toxic shock syndrome, distal
symmetric purpura fulminans caused by meningococcemia).
Necrotizing soft-tissue infections can exhibit skin discoloration
(progressing from red to purple on to almost black), bullae with
hemorrhagic or dark fluid, and crepitus.
E. Laboratory Manifestations
Routine laboratory tests are not specific in the diagnosis of life-threatening
infections but may be suggestive and allow assessment of organ function. The
white blood cell (WBC) count is usually elevated with a shift of neutrophils to
more immature forms (called a left shift). Toxic granulation and Dohle bodies
are often observed in such neutrophils during severe infections, particularly
with septic shock. Leukocytosis is commonly seen in noninfectious processes,
such as the early postoperative period, corticosteroid therapy, massive
transfusions, and polytrauma. Conversely, a normal leukocyte count may be
observed despite active infection in the elderly and in patients with
hypersplenism or chronic myelosuppressive disorders. Neutropenia may result
from overwhelming bacterial or fungal infection and septic shock (especially
in the nutritionally deficient, alcoholics, and AIDS patients), severe viral
infection, typhoid fever, brucellosis, and other infections. Like an altered
WBC count, elevated procalcitonin and C-reactive protein typically indicate
ongoing inflammation/infection.

One of the most common coagulation abnormalities in sepsis is isolated

thrombocytopenia. A modest decline in platelet count may be a subtle, early
clue to the presence of infection. Platelet count nadir usually occurs within 4–
7 days of septic shock presentation. Prothrombin time is often elevated at
admission with severe infections, including septic shock. Overt disseminated
intravascular coagulation is a less common finding but is a poor prognostic
sign. It is characterized by elevations in prothrombin time, partial
thromboplastin time, fibrin split products, and/or D-dimer, and decreased
fibrinogen.

F. Clinical Manifestations
Sepsis is often associated with organ dysfunction at presentation. Apart from
cardiovascular collapse associated with septic shock, overt organ dysfunction
can involve the brain, kidneys, and liver among other organs. The
cardiovascular collapse results in an elevated serum lactate level as a
consequence of compromised oxygen delivery to the tissues. Tachycardia to
increase cardiac output is one of the first compensatory mechanisms noted in
clinical examination. Skin will be warm and flushed during early stages of
septic shock but can progress to cold/clammy if source control is not
obtained. Vasodilation, in addition to capillary leak from immunologic
response, results in intravascular volume depletion which contributes to
hypoperfusion associated with septic shock.
Hypoperfusion of the kidneys results in an elevated serum creatinine and urea
with decreased urine output. If perfusion is not restored in a timely manner,
the patient can progress to an acute tubular necrosis resulting in the need for
renal replacement therapy. Strict measurement of urine output with a goal of
0.5 mL/kg/h should be completed along with trending of serum
urea/creatinine levels.

Early liver injury caused by sepsis-associated hypoperfusion will typically

manifest as modest elevations of transaminases. Severe shock, however, is
often associated with markedly elevated transaminases and hepatic necrosis as
a result of shock liver or ischemic hepatitis. With respect to the liver,
persistence of sepsis will usually result in a cholestatic picture with elevated
bilirubin with or without a mild elevation of transaminases by the second
week.

Initial arterial blood gas measurements usually reflect a respiratory alkalosis

as a result of inflammatory stress-related tachypnea attempting to compensate
the metabolic acidosis produced by the elevated tissue lactate levels.
Persistence of sepsis can ultimately lead to adult respiratory distress
syndrome (ARDS).

A relatively underappreciated early marker of sepsis is hyperglycemia

resulting from inflammatory cytokine-driven insulin resistance. In contrast,
prolonged severe septic shock may demonstrate hypoglycemia because of
depletion of hepatic glycogen stores.

G. Microbiologic Studies
Microbiologic studies are divided into those with immediately available results
(minutes to a few hours) and those requiring a period for incubation or
laboratory determinations. Among the studies with quickly available results is
Gram stain of body fluids. Special stains (such as fungal and acid-fast stains),
immunoassays (such as urine Legionella antigen and Clostridioides difficile
toxins), and immunoelectrophoresis panels require time to process.

Empiric antimicrobial therapy for the patient

with a presumptive life-threatening infection
should be initiated based on clinical and
epidemiologic clues.

Ideally, all cultures should be obtained before initiation or modification of

antimicrobial therapy, but this may not be possible in a patient who is rapidly
deteriorating. The selection of culture site(s) should be guided by clinical
manifestations. Indiscriminate sampling from many sites not only may yield
misleading results because of culture contamination or site colonization, but is
also not cost-effective and may pose additional risks to the patient. Repeat
cultures may be appropriate to assess for changes in the type of organism or
resistance patterns.
At least two sets of peripheral blood cultures (aerobic and anaerobic bottles)
should be obtained from at least two, preferably three, different anatomic
sites. A blood volume of 10 to 15 mL per culture set is optimal in adults. The
volume of blood, number of cultures, and technique are more important
factors for detection of bacteremia than timing of culture collection. Fever at
the time of blood culture collection is neither sensitive nor specific for the
presence of bacteremia. Obtaining blood cultures from indwelling peripheral
or central intravascular catheters may yield false-positive results because of
microbial contamination of the catheter hub. Isolator blood cultures may
improve the diagnostic yield for some organisms (eg, Candida,
Mycobacterium) or in patients already receiving antimicrobial therapy; cost-
effectiveness, however, is unclear.
Respiratory tract cultures require expectorated sputum from the nonintubated
patient and tracheal suction or bronchoscopy specimens from an intubated
patient. Many microbiology laboratories will screen the specimen for the
number of epithelial cells and neutrophils to determine adequacy for culture.
Expectorated sputum samples can be unreliable for help in identifying
bacterial or fungal infections because oftentimes they are not a good sample.
Quantitative cultures of lower respiratory tract secretions obtained by
bronchoscopy can assist with discriminating between colonizing and
pathogenic bacteria.

Do not send endotracheal tube tip or Foley

catheter tip for culture.

In the absence of catheterization, urine cultures should be clean-catch voided

specimens; in catheterized patients, specimens should be aspirated from the
urinary catheter tubing. If the catheter has been in place for few days,
replacement is recommended and the culture should be obtained from the
new catheter. Thresholds for significance differ for clean-catch urine (>105
organisms/mL) and catheter-obtained urine (>103 organisms/mL). Urinalysis
for the detection of pyuria will help to discriminate bacteriuria from cystitis or
upper tract infection. It is not recommended to send endotracheal tube tip or
Foley catheter tip for culture.
If there is a suspicion of intravascular catheter infection, the catheter should
be removed in an aseptic fashion (by applying chlorhexidine to the
surrounding skin and external part of the catheter adjacent to the skin exit).
Do not routinely send catheter tip for culture. Clinical correlation between
blood culture(s) and appearance of the catheter exit site is required to
discriminate between catheter-related bacteremia and local catheter-related
infections. The most reliable method for diagnosis of intravascular catheter-
related bloodstream infections is the quantitative assay of paired cultures from
peripheral and catheter blood samples. Few institutions perform this routinely
because of resource requirements. An alternate approach is to examine the
difference in time to culture positivity between the paired cultures with a more
rapid positivity being seen in samples drawn from an infected catheter.

III. ANTIMICROBIAL THERAPY

Case Study
A 65-year-old man was admitted for altered mental status. He was found
down at home by his wife. He was in his normal state of health the day prior.
On physical examination, the physician noted a fever, nuchal rigidity, and
photophobia. A lumbar puncture is performed and his laboratory studies
confirm meningitis. You are asked to evaluate him.
– What is the likely source of this patient’s infection?
– What factors would influence your choice of antimicrobial agent?
A quick, highly targeted initial assessment, immediate resuscitation, and rapid
initiation of empiric antimicrobial therapy are co-priorities in the management
of hemodynamically unstable patients with a severe, life-threatening infection.
Refinements to therapy can be implemented following a more detailed
evaluation of the patient’s history, physical examination, and auxiliary test
results (laboratory and imaging studies).
Early source control (suspected source of infection) is paramount to favorable
outcomes and is an essential adjunct to adequate antimicrobial therapy.
Examples of source control include wound debridement, percutaneous or
surgical drainage of a closed-space infection, foreign body removal, and
surgery. The antimicrobial therapy recommendations found in this chapter
are general guidelines only. For each clinical scenario, antimicrobial choices
must be individualized to match the clinical manifestations, patient history of
previous antibiotic exposure, patient history of infection along with
organism/susceptibilities, and the available epidemiologic and microbiologic
information, including the patterns of microbial prevalence and resistance in
the institution or local community.

Early use of appropriate empiric antimicrobial

therapy reduces infection-associated mortality.

The selection of appropriate antimicrobial therapy depends on the following

factors:
1. The suspected microbial pathogen(s) and site of infection: The most
common sites for life-threatening infections in adult patients involve
the lower respiratory tract, the intra-abdominal cavity, and the
bloodstream. Rapidly progressive soft-tissue infections and CNS
infections should also be considered and are often clinically obvious.
Antimicrobial penetration to the site of infection should also be
considered. The CNS and lungs are two sites that allow limited
penetration of certain antimicrobials; therefore, the pharmacokinetic
characteristics of the selected agents must be understood to ensure
maximal antimicrobial activity at those sites.
2. Gram stain results of available specimens from the suspected site:
The description of early stain results may help direct the clinician to
the broad categories of organism(s) that should be covered. Examples
include gram-positive cocci in clusters (staphylococci) or pairs and
chains (enterococci, streptococci), lancet-shaped diplococci
(pneumococcus), gram-positive bacilli (Corynebacterium, Nocardia),
gram-negative bacilli (Enterobacteriaceae, Escherichia coli,
Klebsiella, Pseudomonas), small pleomorphic gram-negative bacilli
(Bacteroides spp), gram-negative coccobacilli (Haemophilus spp,
Moraxella, Acinetobacter), and yeast (Candida). However, the
clinician should wait for final culture and sensitivity results before de-
escalating to narrowly targeted antimicrobial therapy.
 If the source of infection is not obvious on
initial examination, reconsider the
possibility of the lungs or abdomen as the
source.

3. Assessment for antimicrobial resistance: Factors predicting that a

particular bacterial pathogen may be resistant to a wider range of
antimicrobials include the following:
– Prior isolation of resistant strains from the same patient
– Prior antimicrobial therapy (broad-spectrum antimicrobial
therapy such as antipseudomonal penicillin/β-lactamase
inhibitor combinations, third- and fourth-generation
cephalosporins, fluoroquinolones, carbapenems, vancomycin)
– Extended hospital or ICU stay
– High endemic rate of multidrug-resistant bacteria in the
institution or ICU (eg, methicillin-resistant Staphylococcus
aureus, vancomycin-resistant Enterococcus, multidrug-resistant
Pseudomonas, Stenotrophomonas, carbapenem-resistant
enterobacteriae (CRE), extended-spectrum β-lactamase (ESBL)
enterobacteriae)
– Ongoing epidemic outbreak in the hospital or ICU
– Long-term dialysis
– Residence in a nursing home or extended-care facility
– Immunosuppressive diseases or therapy

Certain common organisms have become increasingly resistant to

formerly effective antimicrobials. This category includes
 Streptococcus pneumoniae with intermediate- and high-level
resistance to penicillin and ceftriaxone, Enterococcus faecium strains
resistant to ampicillin and vancomycin, S aureus resistant to
oxacillin/methicillin (methicillin-resistant S aureus [MRSA]), gram-
negative bacilli (E coli, Klebsiella pneumoniae) with extended-
spectrum β-lactamase or chromosomal-mediated β-lactamase
production observed in strains of Pseudomonas aeruginosa,
carbapenemase-producing Enterobacteriaceae or other mechanisms
of multiple resistance to broad-spectrum antimicrobial therapy. It is
vital to know and update the resistance pattern of the different
bacterial pathogens in each institution and each ICU. Most
institutions will have an antibiogram that shows the resistance
patterns in the institution.
4. Comorbid conditions: Less nephrotoxic antimicrobials may be
preferable in patients with diminished renal function or patients at
risk for renal failure unless the benefit of use outweighs the risk of
renal dysfunction. Other comorbidities to consider include bone
marrow suppression, chronic or acute liver failure, prior hearing
deficits, pregnancy, and a history of major hypersensitivity or other
strong adverse reactions to a specific antimicrobial.

IV. RECOMMENDED ANTIMICROBIAL THERAPY

Prudent antimicrobial therapy involves early

initiation as well as suitable de-escalation.

The use of the antimicrobial therapies recommended here is based on the

suspected site of infection in the absence of culture results. The clinician
should always consider the dose, dose adjustments, possible interactions, and
adverse effects of selected agents. Antimicrobial therapy should be given in
maximum appropriate therapeutic doses. The celerity on the administration of
the appropriate antimicrobials following clinical diagnosis has been shown to
be a critical determinant of outcome in a variety of severe infections including
meningitis, community-acquired pneumonia, and septic shock. In critically ill
patients, intravenous administration is preferred to intramuscular or oral
routes. Oral dosing of antimicrobials with similar bioequivalence (eg,
fluoroquinolones) and adequate gastrointestinal absorption may be substituted
after the patient stabilizes and is able to take medication by mouth or via
feeding tube. Dosage adjustments must be made for the elderly, neonates,
children, and patients with renal or hepatic dysfunction. Antimicrobial de-
escalation should be implemented in appropriate clinical situations once
cultures are negative or a specific organism and antibiotic susceptibilities are
identified. In the treatment of infection, antimicrobial agents must be used
appropriately and responsibly. A list of selected site infections with empiric
antibiotic therapy is found in Table 11-3. Source control is a critical element
of treatment for a variety of severe infections found in the ICU, including
empyema, abdominal sepsis (eg, ischemic bowel, bowel perforation, volvulus,
ascending cholangitis, and cholecystitis), pyelonephritis associated with
ureteral obstruction, necrotizing soft-tissue infections, wound infections,
decubitus ulcers, and vascular central line-associated blood stream infections
(CLABSI).

Table 11-3 Site Infections and Empiric Antibiotic Therapies

Abbrevitions: GNB, gram-negative bacilli; GPC, gram-positive cocci; MRSA, methicillin-resistant S
aureus. PO, by mouth.
Data taken from Lexi-Comp. Wolters Kluwer. 2020.

A. Central Nervous System

1. Meningitis
Bacterial meningitis causes one of the crucial emergencies. When it is
suspected clinically, antimicrobial therapy should be instituted immediately,
within 60 minutes, without waiting for the results of a lumbar puncture.
Community-acquired acute bacterial meningitis in adults is most commonly
caused by S pneumoniae or Neisseria meningitidis, and initial empiric
therapy with a third-generation cephalosporin (ceftriaxone or cefotaxime)
provides adequate empiric coverage, with vancomycin added if penicillin-
resistant S pneumoniae is suspected or confirmed. If S pneumoniae is
isolated, a third-generation cephalosporin should be continued until penicillin
sensitivity is confirmed, at which point the patient should be switched to high-
dose penicillin G. N meningitidis in cerebrospinal fluid (CSF) or blood
culture should be treated with high-dose parenteral penicillin G. If N
meningitidis is isolated, healthcare workers with significant exposure require
antimicrobial prophylaxis. In addition to antimicrobial therapy, adjunctive
dexamethasone (0.15 mg/kg intravenously every 6 hours for 2–4 days) is also
recommended to decrease the risk of morbidity and mortality, particularly in
pneumococcal meningitis.

Special circumstances require different empiric antimicrobial coverage.

Listeria monocytogenes may be a cause of bacterial meningitis in extremes of
age (neonates, infants, and the elderly) and in patients with T-lymphocyte
defects, usually associated with diabetes mellitus, corticosteroid use, and
immunosuppressive therapy (eg, organ recipients and patients with
autoimmune disease). Patients with suspected Listeria meningitis should
receive ampicillin (trimethoprim-sulfamethoxazole in the patient with penicillin
allergy). Those patients who have undergone recent neurosurgical procedures
or placement of CSF shunts are at increased risk for S aureus, coagulase-
negative staphylococci, and gram-negative bacilli (Pseudomonas, Klebsiella).
Therefore, such patients require initial empiric antimicrobial coverage with
high-dose vancomycin and a third- or fourth-generation cephalosporin. If
methicillin-susceptible S aureus (MSSA) is confirmed, nafcillin is the drug of
choice.

Meningitis presenting in a subacute fashion over several weeks or longer, with

predominance of CSF lymphocytes, is more likely to occur in
immunocompromised patients. Pathogens such as Mycobacterium
tuberculosis, Toxoplasma gondii, and Cryptococcus neoformans should be
considered in this setting.

2. Encephalitis or Meningoencephalitis
Many viral agents can cause encephalitis or meningoencephalitis, but only
herpes simplex (HSV) and cytomegalovirus (CMV) encephalitis are amenable
to therapy. Herpes simplex encephalitis usually occurs in immunocompetent
individuals presenting from the community. This is considered an emergency.
Fever, lethargy, confusion, and seizures are the most common presenting
signs and symptoms. Hemorrhagic CSF and temporal lobe involvement on
imaging studies (computed tomography or magnetic resonance imaging) or
electroencephalography are suggestive of HSV encephalitis. Polymerase chain
reaction testing of CSF is sensitive for diagnosis of this infection. If HSV
encephalitis is suspected or confirmed, a 14- to 21-day course of parenteral
acyclovir should be initiated promptly, pending further studies. CMV
encephalitis usually occurs in patients with suppressed immune status (HIV
and transplant patients) and could have the same clinical manifestations as
HSV encephalitis. Polymerase chain reaction testing of CSF for CMV is also
highly sensitive, and therapy should include ganciclovir or foscarnet.

3. Brain Abscess
Brain abscess is an uncommon infection but should be suspected in patients
with chronic infections of parameningeal structures, left-sided endocarditis, or
congenital cyanotic heart disease. Brain abscesses also have been associated
with immunosuppression, as in patients with AIDS, intravenous drug abusers,
or transplant recipients. Infections are often polymicrobial, and etiologic
organisms include aerobic and anaerobic streptococci, staphylococci, gram-
negative bacteria, and anaerobes. Initial antimicrobial therapy should include
vancomycin, high-dose metronidazole, and a third-generation cephalosporin
(ceftriaxone). In patients at high risk for toxoplasmosis (eg, those with AIDS,
cardiac transplant recipients), pyrimethamine/sulfadiazine should be part of
the initial antimicrobial regimen. Less common causes of brain abscess
include tuberculosis, nocardiosis, syphilis, amoeba, and other parasites. The
diagnostic yield of CSF cultures for brain abscess is extremely low, and brain
biopsy may be needed in patients who fail to respond to empiric therapy.

B. Respiratory Tract
1. Severe Community-Acquired Pneumonia (Immunocompetent Host)
The most common organism resulting in hospitalization for community-
acquired pneumonia is S pneumoniae, but other causative organisms include
Legionella, Mycoplasma, and Chlamydia. Haemophilus influenzae is an
uncommon pathogen in the United States because of the introduction of the
vaccine against H influenzae type B in children. A β-lactam (ceftriaxone,
cefotaxime, ampicillin-sulbactam) plus either a macrolide (azithromycin) or a
respiratory fluoroquinolone (moxifloxacin, gemifloxacin, or levofloxacin) are
recommended in patients admitted to the ICU. The CURB-65 Score can be
used to determine the need for hospitalization as well as placement in the
ICU. If the patient is allergic to penicillin, a respiratory fluoroquinolone and
aztreonam are recommended. If aspiration pneumonia is suspected (alcoholic
patients, presence of poor dentition), the addition of clindamycin is warranted
unless a β-lactam/β-lactamase inhibitor combination is used. If Pseudomonas
is a consideration, an antipseudomonal β-lactam (piperacillin-tazobactam,
cefepime, imipenem, or meropenem) should be used. Vancomycin or
linezolid may be added if community-acquired MRSA is suspected.

2. Community-Acquired Pneumonia (Immunocompromised Host)

Immunocompromised patients with pneumonia may have the same pathogens
as an immunocompetent host but with more severe infection. Radiographic
evidence of interstitial pneumonia or a normal chest radiograph in a patient
with prominent respiratory symptoms who has T-cell deficiency (AIDS,
chronic steroid use) should prompt the addition of trimethoprim-
sulfamethoxazole in appropriate doses for possible Pneumocystis jirovecii
(formerly carinii). Consider the addition of steroids in P jirovecii pneumonia
associated with significant hypoxemia. Focal lesions (eg, abscess, nodules) are
suggestive of fungal infections, M tuberculosis, or Nocardia; empiric
coverage with antifungal agents, anti-mycobacterial agents, and trimethoprim-
sulfamethoxazole may be warranted in these circumstances. Patients with
suspected M tuberculosis infection also require respiratory isolation. CMV or
other viral infection also should be considered in the differential of an
interstitial pneumonitis.

3. Nosocomial and Ventilator-Associated Pneumonia

 Use short courses of antimicrobial therapy when
appropriate.

Gram-negative organisms and S aureus are frequent causes of pneumonia in

hospitalized patients or those who require mechanical ventilation. Nosocomial
organisms tend to be more resistant and are more likely to be present in
patients with extended hospital stays, prior antimicrobial therapy, and
comorbidities. If possible, attempts should be made to obtain lower
respiratory tract samples for quantitative microbiologic evaluation in
mechanically ventilated patients. Adequate antimicrobial coverage can usually
be provided with a third- or fourth-generation cephalosporin, β-lactam/β-
lactamase inhibitor combinations, or a carbapenem, plus an anti-pseudomonal
fluoroquinolone (ciprofloxacin, moxifloxacin, or levofloxacin) or an
aminoglycoside. If Pseudomonas is a consideration, an antipseudomonal β-
lactam (piperacillin-tazobactam, cefepime, imipenem, or meropenem) should
be used. Therapy with trimethoprim-sulfamethoxazole should be included if
the possibility of Stenotrophomonas maltophilia is suspected or confirmed.
Vancomycin should be considered if methicillin-resistant S aureus is a
possible pathogen. Pneumonia caused by methicillin-sensitive strains of S
aureus should be treated with an anti-staphylococcal penicillin because these
agents are superior to vancomycin. Patients with methicillin-resistant S aureus
who are vancomycin-intolerant or are not responding to vancomycin may be
treated with linezolid. If vancomycin is used, serum trough levels should be
maintained no lower than 15 to 20 µg/mL because lung penetration of this
agent is limited. Shorter courses (8 days) of therapy may be appropriate as
long as non-lactose fermenting organisms are not isolated. Consideration may
be given to stop the antibiotic therapy if the lower respiratory tract cultures
are negative.

C. Heart
Infections of the heart are usually severe and life-threatening and require
coordinated medical care with a cardiologist and sometimes with a
cardiovascular surgeon. Microbiologic studies and echocardiography
(transthoracic or transesophageal) are the cornerstones for the diagnosis and
management of any infection in the heart.
Infective endocarditis, or infection of the endocardial surface of the heart,
most frequently involves the heart valves. Intravenous drug abuse, prosthetic
valves, sclerosing of natural valves as a result of aging, hospital-acquired
infections, and newly identified pathogens (Bartonella spp, Coxiella burnetii,
Tropheryma whipplei, fungi) are the main risk factors for this condition.
Demonstration of bloodstream infection and positive echocardiographic
evidence of valvular vegetations are key to making the diagnosis, although
peripheral embolic phenomena and other findings are strongly suggestive.
Gram-positive cocci, mainly Staphylococcus and Streptococcus, but also
Enterococcus, are the most common microorganisms isolated in infective
endocarditis in the general population and in specific risk groups (intravenous
drug users and prosthetic valve endocarditis), but gram-negative,
polymicrobial, fungal, and culture-negative cases of endocarditis are
becoming more common. Bactericidal antimicrobial therapy (eg,
penicillins/third-generation cephalosporins, daptomycin with or without an
aminoglycoside, glycopeptides, linezolid), high drug concentrations,
knowledge of resistance pattern of the microorganism, and long-term therapy
are the cornerstones of treatment.

D. Intravascular Catheters

Because of the increasing incidence of

vancomycin-resistant organisms, attempt to limit
the indiscriminate use of vancomycin.
In patients with confirmed or suspected intravascular catheter infection
associated with organ dysfunction, systemic emboli, or cardiovascular
instability, the intravascular catheter should be removed promptly. In
addition, local changes at the catheter site (purulence, erythema) mandate
catheter removal. Coagulase-negative Staphylococcus and S aureus are the
most common pathogens in catheter-related bloodstream infections. In the
immunocompetent patient who has a coagulase-negative staphylococcal line
infection but no systemic symptoms, the removal of the infected catheter line
may be sufficient. Vancomycin is recommended in immunocompromised
patients with coagulase-negative staphylococcal line infections, patients with
systemic manifestations, or those with prosthetic devices at risk for becoming
secondarily infected. If S aureus is the infecting organism, nafcillin is
recommended; however, if there is a high rate of MRSA in the hospital or
MRSA is confirmed, vancomycin should be used. Daptomycin can also be
used; linezolid is less likely to be helpful but is sometimes used as part of a
combination therapy or salvage therapy. A third- or fourth-generation
cephalosporin or fluoroquinolone should be added if a nosocomial gram-
negative organism is suspected.

Candida is occasionally isolated from catheter tips and should increase the
suspicion that occult candidemia may have been recently present. The
treatment of choice is fluconazole; if there is a possibility of resistant
Candida, such as Candida glabrata or Candida krusei, an echinocandin
(caspofungin/micafungin/anidulafungin) should be used. When a fungal
microorganism is identified in an intravascular catheter-related bloodstream
infection, a non-tunneled catheter always should be removed, whereas the
removal of a tunneled catheter should be based on the likelihood of catheter-
related candidemia rather than candidemia from another source.
Antimicrobial-impregnated catheters appear to have a lower rate of
bloodstream infection, but the maximum longevity of such catheters is still
under investigation.

E. Abdomen
When an intra-abdominal infection is suspected, a surgeon must be involved
in the evaluation of the patient. Definitive source control of intra-abdominal
process may require surgical intervention or interventional radiology drainage.
Both the infecting flora and the antimicrobial therapy are related to whether
the infection was acquired in the community or healthcare setting. For
community-acquired infections, location of a possible perforation determines
the probable organism, with gram-positive, facultative, and aerobic gram-
negative bacteria beyond the proximal small bowel and anaerobes beyond the
proximal ileum. Recommended therapies include β-lactam/β-lactamase
inhibitor combinations and carbapenems as monotherapy or
cephalosporins/fluoroquinolones with metronidazole. Antimicrobial therapy
should be continued until clinical resolution, which typically occurs in 5 to 7
days. Further diagnostic workup should be pursued in patients with persistent
or recurrent symptoms. Flora isolated from healthcare-associated intra-
abdominal infections resembles that of other nosocomial infections.
Antimicrobial therapy should be based on knowledge of the flora and
antimicrobial susceptibilities of the institution. Anti-enterococcal therapy is
indicated only when enterococci are isolated from patients with healthcare-
associated infections. Antifungal therapy is indicated only in those who have
isolated fungi and comorbid conditions, such as recent immunosuppressive
therapy for neoplasms, transplantation, and inflammatory disease, or who
have postoperative or recurrent infections.

F. Urinary Tract
The most common pathogens in urinary tract infections are gram-negative
enteric bacteria. Hospitalized patients with urinary catheters in place
commonly have bacteriuria yet exhibit no pyuria or localized symptoms,
classified as asymptomatic bacteriuria (ASB). Such patients (in the absence of
urologic obstruction) rarely develop sepsis or bacteremia arising from the
urinary tract, and removal of the catheter may allow resolution of the
bacteriuria. For this reason, in patients with a short-term indwelling urethral
catheter (less than 30 days), it is recommended to avoid screening or treating
ASB. The Infectious Disease Society of America (IDSA) now only
recommends screening for and treating ASB in pregnant women and those
patients undergoing invasive urologic procedures. Patients who develop upper
urinary tract infection always merit antimicrobial therapy. More serious
complications may be seen in patients with diabetes mellitus or patients who
are immunocompromised, including those with emphysematous
pyelonephritis, papillary necrosis, or perinephric abscess, which may require
surgical intervention. Empiric antimicrobial options for gram-negative urinary
tract infections are dictated by susceptibility testing and include the following:
Third-generation cephalosporins
Aminoglycosides
Piperacillin-tazobactam
Trimethoprim-sulfamethoxazole
Enterococcal infection in the urinary system should be suspected in patients
who have had urinary catheters in place for long periods or who have had
recent manipulation of the urinary tract. Therapy should include ampicillin,
piperacillin, or vancomycin. Narrowing of antibiotic therapy should be
dictated by susceptibility testing.
Candiduria is not uncommon and usually occurs in patients who have long
periods of urinary catheterization and are receiving broad-spectrum
antimicrobial therapy or patients with glycosuria. For asymptomatic
candiduria, therapy is not usually indicated unless the patient is at high risk
(eg, neonates, unstable or neutropenic adults) or is undergoing urologic
procedures. Therapeutic options include a short course of fluconazole (not
effective against C glabrata or C krusei) or continuous amphotericin bladder
irrigation; however, relapse rates are significant with either treatment. If
candiduria is treated in a patient with an indwelling catheter, the catheter
should be changed or removed during the treatment course.

G. Cutaneous Infection
S aureus or group A β-hemolytic streptococci are the most likely etiologic
organisms in cellulitis or cutaneous abscess. H influenzae must also be
considered in facial or orbital cellulitis. Onset of postoperative wound
infections usually occurs 5 to 7 days after surgery. However, rapidly
progressive wound infections occurring within 24 to 48 hours after surgery
should prompt the consideration of Clostridium perfringens or group A β-
hemolytic streptococci (Streptococcus pyogenes). This type of infection
warrants surgical debridement and prompt antimicrobial therapy directed by
Gram stain and culture results. Antimicrobial choices include the following:

Cefazolin or nafcillin if methicillin-resistant S aureus is unlikely

Vancomycin or linezolid if there is a possibility of methicillin-
resistant S aureus
Daptomycin because of its bactericidal properties
Penicillin G with or without clindamycin for wound infections
developing within 48 hours of surgery to cover C perfringens and
β-hemolytic streptococci
Wound toxic shock syndrome is a rare condition that can occur within 48
hours of a wound or surgical incision. The causes are toxin-producing S
aureus or β-hemolytic streptococci. Often, the wound does not appear
infected because of a diminished inflammatory response. Diagnosis can be
made based on presenting symptoms such as fever, diarrhea, vomiting,
hypotension, and uremia. Erythroderma and subsequent desquamation are
characteristic signs but may be delayed for several days. Treatment involves
debridement, drainage, and prompt use of specific antimicrobial therapy.

H. Necrotizing Soft-Tissue Infection

Antibiotics are adjuvant therapy to early and

repeated debridement in necrotizing soft-tissue
infection.

Infection of the subcutaneous tissue, fascia, and muscle can occur in any
patient but may be more common in immunocompromised patients,
particularly individuals with diabetes mellitus. If gas is present in the tissue,
cutaneous gangrene or bullae are noted, or infection progresses rapidly, a
necrotizing soft-tissue infection must be considered. This condition requires
prompt surgical debridement in addition to broad-spectrum antimicrobial
therapy. These infections are usually polymicrobial, involving aerobic and
anaerobic gram-positive and gram-negative organisms.
Adequate empiric therapy should include vancomycin and a β-lactam/β-
lactamase inhibitor, a carbapenem and a fluoroquinolone, or an
aminoglycoside and clindamycin (the latter to reduce the amount of toxins).
Antimicrobial administration should be continued until no further
debridement is needed and the patient’s clinical status has improved.
Prolonged courses of antibiotics can lead to wound colonization with drug-
resistant organisms.

I. Immunocompromised or Neutropenic Patients

In the absence of a specific source, pending culture results, broad-spectrum
antimicrobial therapy is indicated in the immunocompromised or neutropenic
patient with fever. Initiation of monotherapy with an antipseudomonal beta-
lactam agent, such as cefepime, a carbapenem, or piperacillin-tazobactam, is
initially recommended. Additional agents such as aminoglycosides,
fluoroquinolones, and/or vancomycin can be added to this regimen in patients
with complicated presentations. Initial antibiotic therapy should be based on
colonization or prior infection with a multidrug-resistant organism, site of
infection, local antibiotic susceptibility patterns, presence of organ
dysfunction, and previous antibiotic therapy.
The use of white cell growth factors (ie, granulocyte colony-stimulating factor,
granulocytemacrophage colony-stimulating factor) may improve the outcome
by shortening the duration of neutropenia. These progenitor cell stimulants
should be targeted for patients with an anticipated duration of neutropenia of
5 to 7 days and a high risk for serious infection.

J. Clostridioides difficile (Cdiff) Infection

Antibiotic-associated diarrhea and colitis resulting from Clostridioides
(formerly Clostridium) difficile infection can complicate the course of
treatment for many patients. The antimicrobials most commonly involved
include clindamycin, penicillins, cephalosporins, and fluoroquinolones,
although C difficile has been described in association with almost all
antimicrobials. Patients do not need to receive antimicrobial therapy to
develop this condition.

C difficile is also recognized as an important nosocomial pathogen capable of

cross transmission to patients in adjacent areas. Diagnosis is usually based on
identification of C difficile toxins and detection of cytotoxic activity in tissue
culture. Toxin testing is hampered by lack of sensitivity, and the polymerase
chain reaction testing appears to be rapid, sensitive, and specific, and
ultimately addresses testing errors. Repeat testing is not recommended within
7 days during the same episode of diarrhea. In those patients recently treated
for C difficile, testing can remain positive even if symptoms have resolved.
Treatment begins with discontinuation of the implicated antimicrobial therapy
(if possible) and initiation of specific antimicrobial therapy against C difficile
if symptoms are moderate, severe, or persistent. The preferred regimen is
oral vancomycin, 125 mg four times daily for 10 to 14 days or fidaxomicin
for an initial episode. Metronidazole can be used for a non-severe initial
episode if access to both vancomycin and fidaxomicin is limited or the patient
is intolerant to these first-line options. For patients who are unable to take oral
medications, intraluminal vancomycin with or without intravenous
metronidazole is recommended. Fidaxomicin is a first-in-class, narrow-
spectrum macrocyclic antibiotic that acts by eradicating C difficile with
minimal disruption of the normal intestinal flora. High cost limits its use and
in practice, fidaxomicin is used for recurrent C difficile infections or as a
bridge to fecal microbiota transplant (FMT). A trial of treatment with either a
vancomycin or fidaxomicin taper is recommended before pursuing FMT.
Fidaxomicin is recommended along with oral vancomycin as a first-line option
for treatment of an initial C difficile episode. Fulminant C difficile infection is
present if the patient has any of the following: hypotension, ileus, or shock,
and it is recommended to add IV metronidazole and increase the dose of
vancomycin to 500 mg four times daily. Fulminant colitis unresponsive to
these measures or progressing to toxic megacolon may require total
colectomy.

Proper infection control is important in the

management of C difficile infections, including
the use of soap and water for hand washing and
not alcohol-based hand sanitizers.

K. Fungal Diseases
Life-threatening infections caused by fungi may be extremely difficult to
diagnose by routine physical examination or routine cultures. Candida
albicans is the most common etiologic organism in critically ill patients. Non-
albicans species of Candida and other fungi have increased significantly in
recent years. Fungal infection should be considered in certain geographic
regions and in the presence of predisposing factors, such as HIV, malignancy,
neutropenia, long-term use of steroids, broad-spectrum antimicrobial therapy,
parenteral nutrition, severe burns, organ transplantation, or central venous
vascular catheters.
The polyenes (amphotericin B and lipid preparations of amphotericin B) have
been the most commonly used antifungal agents for serious infections. Newer
agents (echinocandins, voriconazole) have shown comparable or superior
clinical outcomes compared with the polyenes and have much less toxicity
than usually associated with amphotericin B. All lipid formulations have less
nephrotoxicity, and their efficacy against Candida is equivalent to
conventional amphotericin B. Fluconazole is still active against most Candida
species and Cryptococcus, and itraconazole may be used for some of the
mold infections. Both agents have an important role in primary or secondary
prophylaxis. The newer agents, such as voriconazole, posaconazole, and
echinocandins, have activity against resistant Candida strains and some of the
mold infections resistant to other regimens. Voriconazole is the drug of choice
for Aspergillus infection.

L. Other Therapy
In addition to antimicrobial therapy, surgical intervention must be considered
in patients with life-threatening infections. Any abscess must be drained and
injured or ischemic organs must be repaired or removed. Vascular catheters
that may be a source of infection should be removed.
Early surgical consultation should be sought when the abdomen may be a
source of infection in the critically ill patient. Guidelines for tetanus
prophylaxis are found in Chapter 12. Further management of the patient
with septic shock is discussed in Chapter 8.

M. Healthcare-Associated Infection Control

Patients can acquire healthcare-associated infections (HAIs) during the course
of receiving treatment for other conditions within a healthcare setting. For
example, pneumonia would meet the healthcare-associated criteria if the
patient was hospitalized for at least 2 of the preceding 90 days, was a resident
in a nursing home or extended-care facility, received home intravenous
(antibiotics or chemotherapy) therapy, or received chronic dialysis or home
wound care (or both) during the preceding 30 days.
Recent data estimate that one in every 25 hospitalized patients experience a
HAI each year. Pneumonia and surgical site infection from any inpatient
surgery were the most common HAIs. Many studies show that HAI increases
hospital length of stay and morbidity and mortality rates. Strategies have been
proposed to prevent HAI. Most important is proper hand hygiene and use of
personal protective equipment (PPE). More details are available in the
websites listed at the conclusion of this chapter. Guidelines cannot always
account for variations among patients and are not intended to supplant
physician judgment with respect to individual patients or special clinical
situations.
Key Points
Life-Threatening Infections
Fever is the most frequent systemic manifestation that raises the
suspicion of infection.
Ideally, appropriate cultures should be obtained before initiation of
antibiotics in patients with suspected infection.
Selection of appropriate empiric antimicrobial therapy depends on
the suspected pathogen(s) and site of infection, Gram stain results
of available specimens from the suspected site, assessment for
antimicrobial resistance, and comorbid conditions.
Rapid administration of appropriate antimicrobials has been shown
to be a critical determinant of outcome in a variety of severe
infections including meningitis, community-acquired pneumonia,
and septic shock.
When bacterial meningitis is suspected clinically, antimicrobial
therapy should be instituted immediately, without waiting for the
results of lumbar puncture.
For suspected septic shock, available evidence suggests that
administration of appropriate antimicrobials within an hour is
recommended because it has been associated with improved
survival.
The most common organism resulting in community-acquired, life-
threatening pneumonia is Streptococcus pneumoniae.
Resistant gram-negative organisms and Staphylococcus aureus are
frequent causes of pneumonia in hospitalized patients or in those
who require mechanical ventilation.
Bactericidal antimicrobial therapy, high concentrations of the
antimicrobial agent, the resistance pattern of the microorganism,
 and long-term therapy are the cornerstones of therapy for infective
endocarditis.
When source control is an option for infection management, it
should be implemented early, particularly for septic shock.
Suspicion of intra-abdominal infection requires the prompt
involvement of a surgeon.
Necrotizing soft-tissue infection requires prompt surgical
debridement in addition to broad-spectrum antimicrobial therapy.
In the absence of a specific source and pending culture results,
broad-spectrum antimicrobial therapy is indicated in the
immunocompromised or neutropenic patient with fever.
Fungal infection should be considered in the presence of
predisposing factors, such as malignancy, neutropenia, broad-
spectrum antimicrobial therapy, parenteral nutrition, severe burns,
or organ transplantation, or if central venous vascular catheters are
in place.

Suggested Readings
1. Ferrer R, Martin-Lochese I, Phillips G, et al. Empiric antibiotic
treatment reduces mortality in severe sepsis and septic shock for
the first hour: results from a guideline based performance
improvement program. Crit Care Med. 2014;42(8):1749-1755.
2. Funk D, Kethireddy S, Kumar A. Improving outcomes in sepsis
and septic shock: Getting it right the first time. In: Rello J,
Lipman J, Lisboa T, eds. Sepsis Management: PIRO and
MODS. Springer-Verlag; 2010.
3. Kalil AC, Metersky ML, Klompas M, et al. Management of adults
with hospital-acquired and ventilator-associated pneumonia: 2016
clinical practice guidelines by the Infectious Diseases Society of
 America and the American Thoracic Society. Clin Infect Dis.
2016:63(5):e61-111.
4. Kumar A, Ellis P, Arabi Y, et al. Initiation of inappropriate
antimicrobial therapy results in a 5-fold reduction of survival in
human septic shock. Chest. 2009;136(5):1237-1248.
5. Kumar A, Roberts D, Wood KE, et al. Duration of hypotension
before initiation of effective antimicrobial therapy is the critical
determinant of survival in human septic shock. Crit Care Med.
2006;34(6):1589-1596.
6. Lim WS, van der Eerden MM, Laing R, et al. Defining
community acquired pneumonia severity on presentation to
hospital: an international derivation and validation study. Thorax
2003;58:377-382.
7. McDonald LC, Gerding DN, Johnson S, et al. Clinical practice
guidelines for the Clostridium difficile infection in adults and
children: 2017 update by the IDSA and SHEA. Clin Infect Dis.
2018;66(7):e1-e48.
8. Mermel LA, Allon M, Bouza E, et al. Clinical practice guidelines
for the diagnosis and management of intravascular catheter-
related infection: 2009 update by the Infectious Diseases Society
of America. Clin Infect Dis. 2009;49(1):1-45.
9. Metlay JP, Waterer GW, Long AC, et al. Diagnosis and treatment
of adults with community-acquired pneumonia: An official clinical
practice guideline of the American Thoracic Society and
Infectious Diseases Society of America. Am J Respir Crit Care
Med. 2019;200(7):e45–e67.
10. Nicole LE, Gupta K, Bradlye SF, et al. Clinical practice guideline
for the management of asymptomatic bacteriuria: 2019 update by
the Infectious Diseases Society of America. Clin Infect Dis.
2019;68(10):e83-e110.
11. O’Grady NP, Barie PS, Bartlett JG, et al. Guidelines for
evaluation of new fever in critically ill adult patients: 2008 update
from the American College of Critical Care Medicine and the
Infectious Diseases Society of America. Crit Care Med.
2008;36(4):1330-1349.
12. Pappas PG, Kaufman C, Andes D, et al. Clinical practice
guidelines for the management of candidiasis: 2016 update by
the Infectious Diseases Society of America. Clin Infect Dis.
2016;62(4):e1-e50.
13. Rhodes A, Evans LE, Alhazzani W, et al. Surviving Sepsis
Campaign: International Guidelines for Management of Sepsis and
Septic Shock: 2016. Intensive Care Medicine. 2017;43(3):304-
377.
14. Seymour CW, Liu VX, Iwashyna TJ, et al. Assessment of clinical
criteria for sepsis: For the Third International Consensus
Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA.
2016;315(8):762-774.
15. Shankar-Hari M, Phillips GS, Levy ML, et al. Developing a new
definition and assessing new clinical criteria for septic shock: For
the Third International Consensus Definitions for Sepsis and
Septic Shock (Sepsis-3). JAMA. 2016;315(8):775-787.
16. Singer M, Deutschman CS, Seymour CW, et al. The Third
International Consensus Definitions for Sepsis and Septic Shock
(Sepsis-3). JAMA. 2016;315(8):801-910.
17. Solomkin JS, Mazuski JE, Bradley J, et al. Diagnosis and
management of intraabdominal infection in adults and children:
guidelines by the Surgical Infection Society and the Infectious
Diseases Society of America. Clin Infect Dis. 2010;50(2): 133-
164.
18. Timsit JF, Bassetti M, Cremer O, et al. Rationalizing antimicrobial
therapy in the ICU: a narrative review. Intensive Care Med.
 2019;45(2):172-189.
19. Tunkel AR, Hartman BJ, Kaplan SL, et al. Practice guidelines for
the management of bacterial meningitis. Clin Infect Dis.
2004;39(9):1267-1284.
20. Yokoe DS, Anderson DJ, Berenholtz SM, et al. A compendium of
strategies to prevent healthcare-associated infections in acute care
hospitals: 2014 update. Infect Control Hosp Epidemiol.
2014;35(5):455-459.

Suggested Websites
1. Society of Critical Care Medicine. http://sccm.org.
2. Surviving Sepsis Campaign.
https://www.sccm.org/SurvivingSepsisCampaign/Guidelines/Adult-
Patients
3. Centers for Disease Control. http://www.cdc.gov.
4. Infectious Diseases Society of America. http://www.idsociety.org.
 Chapter 12
BASIC TRAUMA AND BURN
SUPPORT

Objectives
Prioritize and initiate a timely assessment of the traumatized patient.
Initiate treatment of life-threatening traumatic injury.
Use radiography in identifying significant traumatic injury.
Identify and respond to significant changes in the patient’s status after
traumatic injury.
Initiate early burn management.
Review indications for initiating surgical consultation and/or
transferring the patient to a higher level of care.

Case Study
A 37-year-old man was working at a construction site when he fell
approximately 20 feet off of scaffolding. He was wearing his hard hat, but it
had come off during the fall. He is difficult to arouse and only groaning. He
has an open wrist fracture and bruising on his back and left flank. His vital
signs include a blood pressure of 86/68 mm Hg, heart rate of 100 beats/min,
and a respiratory rate of 32 breaths/min.
The patient is lethargic and only moves his upper extremities. His skin is cool
and clammy.
– What are the goals of the primary survey?
– What are the most urgent initial interventions?

I. INTRODUCTION
It is not the intention of the FCCS program to replace the Advanced Trauma
Life Support (ATLS) course provided by the American College of Surgeons
Committee on Trauma. Critical care is a component of caring for the injured
person. The material presented here is intended to highlight evaluation and
treatment issues for the provider confronted with a critically injured patient.
Those providers who regularly encounter patients with traumatic injuries are
encouraged to enroll in more formal trauma-specific training, such as the
ATLS course.
In the United States, traumatic injuries remain the leading cause of death in
individuals aged 1 to 44 years. Death as the result of injury occurs in one of
three periods. The first period is within seconds to minutes of injury, when
deaths generally result from severe brain or high spinal cord injury, loss of
the airway, or rupture of the heart, aorta, or other large blood vessels. Few of
these patients can be salvaged because of the severity of injury, and
prevention is the only way to reduce such trauma-related deaths. The second
period occurs within minutes to hours following injury; these deaths are
usually the result of subdural and epidural hematomas, hemopneumothorax,
solid organ rupture (spleen or liver), pelvic fractures, or other injuries
associated with blood loss. The “golden hour” after trauma is characterized
by the need for rapid assessment and resolution of these injuries. The third
period occurs days to weeks after the initial injury and is most often caused
by sepsis with associated multiple organ failure (Figure 12-1). Advances in
critical care and multi-organ support have blunted the late peak that occurred
at the 3–4 week interval, creating a bimodal distribution of mortality
(immediate and early deaths). This is described in the work by Gunst et al
(see Suggested Readings). This flattening of the curve emphasizes the
importance of critical care in caring for the critically injured.

Figure 12-1. The Trimodal Distribution of Trauma Deaths

Reproduced with permission Feliciano D, Mattox K, Moore E. Trauma. 6th ed. New
York: McGraw-Hill; 2008.

II. TRAUMA MANAGEMENT

The approach to the trauma patient follows a three-tiered approach:
1. Primary survey with simultaneous resuscitation – identify and
treat life-threatening injuries
2. Secondary survey – head-to-toe evaluation and treatment, and
patient history
 3. Tertiary survey – all injuries are identified, catalogued, and
treatment plans initiated
This three-tiered approach is guided by the following principles:
1. Treat the greatest threat to life first.
2. It is not necessary to establish a definitive diagnosis before
initiating lifesaving treatment.
3. A detailed history is not essential to begin care.
Early management of the seriously injured patient requires simultaneous
evaluation and treatment. The first goal is to ensure adequate oxygen delivery
to vital organs by following an established sequence of priorities that allows
identification and treatment of injuries causing immediate threats to life
(primary assessment). Patient management should begin with the rapid
primary evaluation and simultaneous resuscitation of vital functions, followed
by a more detailed secondary assessment (head-to-toe examination), and
finally, the initiation of definitive care. This process begins with the ABCDE of
trauma care, which guides the identification of life-threatening conditions
through the initial assessment sequence of airway, breathing, circulation,
disability, and exposure (Table 12-1).

Table 12-1 Initial Assessment of Trauma

A surgeon skilled in trauma management should be consulted early in the

course for all serious trauma patients. Routing trauma patients to a center
with trauma surgeons is crucial in the survival of these patients. When a
surgeon is not immediately available or when the patient’s injuries exceed the
capabilities of the institution, the transfer process to a definitive care facility
should be initiated without delay. While waiting for transfer to a definitive
care facility, life-threatening injuries should be addressed and the patient’s
response to these interventions should be monitored and reassessed.

A. Primary Survey with Simultaneous Resuscitation

1. Airway

If the patient is able to communicate verbally, the airway is unlikely to be in

immediate jeopardy. In this situation, a definitive airway is unlikely to be
needed. A definitive airway is defined as a cuffed tube secured in the airway
with the cuff inflated below the vocal cords. During evaluation of the airway,
cervical spine motion should be restricted. Assessment of the airway includes
inspection for foreign bodies and facial, mandibular, or tracheal/laryngeal
fractures that may result in airway obstruction. Patients can develop signs of
airway obstruction after a benign initial presentation; therefore, reassessment
is paramount. Profuse bleeding from an oropharyngeal injury may warrant
placement of a definitive airway.

Airway patency should be reassessed frequently,

particularly in patients with head injury, shock,
facial fractures, facial burns, and potential
inhalation injury.

The patient’s neurologic status (disability) is related to the airway. Patients

with a severe head injury, a Glasgow Coma Scale (GCS) score of 8 or less,
usually require placement of a definitive airway. Nonpurposeful motor
responses support the need for immediate airway management (Table 9-5).
Reassessment of airway patency and neurologic status throughout the
resuscitation is essential, and supplemental oxygen should be administered to
all severely injured trauma patients.
After blunt trauma, airway control should proceed on the assumption that an
unstable fracture or ligamentous injury of the cervical spine (C-spine) exists. If
active airway intervention is needed before evaluation for possible C-spine
fracture, the technique chosen for airway control (intubation, adjunctive
device, or surgical airway) should take into account the expertise of available
personnel, type of equipment available, patient factors, and injuries. If the
patient is apneic or deteriorating rapidly, effective bag-mask ventilation can
be lifesaving. Standard orotracheal intubation should be attempted with the
use of cervical spine motion restriction. Proper cervical spine motion
restriction may be accomplished from the front or the side of the patient. One
care provider supports the occiput and mandible with both hands to maintain
neck alignment without applying traction or distraction. With secure
stabilization, the anterior portion of the cervical collar may be removed to
allow airway interventions. Cervical spine motion restriction is continued until
the cervical collar is replaced and the definitive airway device is secured.

If the patient is combative and needs an airway, a

drug-assisted intubation should be performed.

If a definitive airway cannot otherwise be secured, adjunctive devices (eg,

laryngeal mask airway, esophageal-tracheal double lumen airway) can be
considered, but a surgical airway is indicated.
Other key issues in airway control deals with concomitant facial fractures.
Facial fractures are not an immediate priority unless heavy bleeding or
uncontrollable secretions are present. Similarly, facial fractures usually do not
require that the patient be intubated. Mandibular fractures, however, are
more likely to be associated with soft-tissue injury that may compromise the
airway. Orotracheal intubation or surgical airway should be performed if a
definitive airway is needed.
 If unable to achieve orotracheal intubation or
adequately oxygenate/ventilate a patient, an
emergent cricothyroidotomy is indicated or
tracheostomy, when tracheal/laryngeal injury is
suspected.

2. Breathing

Whereas many injuries can eventually affect the ability to ventilate and
oxygenate, several important injuries need to be identified and managed
urgently. These include: tension pneumothorax, open pneumothorax, and
massive hemothorax.
Tension pneumothorax – this is a clinical diagnosis resulting from air in the
pleural space affecting the patient’s physiology. Treatment (chest tube) should
be performed prior to obtaining a chest radiograph. Patients who are
breathing spontaneously have signs of tachypnea, air hunger, and absent
breath sounds on the affected side. Although hemodynamic collapse can
develop in any patient, it may be the presenting signs in patients receiving
positive pressure ventilation. Other findings include tracheal deviation away
from the side of injury and distended neck veins. See Chapter 6 for more
detailed information.

Open pneumothorax – is generally associated with chest wall soft-tissue loss

creating a “sucking chest wound”. Prehospital providers commonly treat this
injury at the scene with air-occlusive dressing secured on three sides. Once at
the hospital, a chest tube should be placed and definitive wound closure
should be performed in the operating room. Prior to definitive wound closure,
a sterile dressing should be applied to the wound.

Massive hemothorax – is suggested by the patient’s physiology, physical

examination, and chest radiograph. It is often defined as > 1,500 mL of
blood (which corresponds to Class III hemorrhagic shock) in the pleural
space, or ongoing blood loss of > 200 mL per hour for subsequent 2 to 4
hours. This amount of blood in the pleural space can compromise oxygenation
and ventilation. A chest tube should be placed and surgical consultation
obtained for possible thoracotomy. Auto-transfusion of the scavenged blood
from the pleural space can aid in the patient’s resuscitation.

Other injuries associated with breathing problems include a simple

pneumothorax and rib fractures. Usually, a simple pneumothorax is
associated with rib fractures and may require chest tube placement. These
patients often present with chest wall tenderness. Subcutaneous emphysema
may be palpable. A chest radiograph with subcutaneous air is highly
suspicious for a pneumothorax and a chest tube should be placed. High
consideration should be given to placement of a chest tube in any patient who
has a pneumothorax on a chest radiograph and is receiving general anesthesia
and positive pressure ventilation.
Rib fractures are often missed on a chest radiograph; however, a fracture may
be suspected and documented when tenderness over the fracture is identified
during physical examination. Pain control may be required to ensure
adequate spontaneous ventilation. These patients can develop hypercapnic
respiratory failure from inadequate ventilation; therefore, their ventilation and
oxygenation should be continually monitored. Flail chest is defined as two or
more fractures in two or more consecutive ribs. This may result in paradoxical
chest movement (ie, inward movement of the flail segment during inhalation).
Flail chest is also associated with contusion of the underlying lung, pain, and
hypoxemia. These patients require aggressive pain control and continuous
monitoring of oxygenation and ventilation. They may need to be intubated
because of severe respiratory compromise.

Case Follow-up: A 37-year-old man was working at a construction site when

he fell approximately 20 feet off of scaffolding. He sustained a high-grade
splenic injury requiring splenectomy and a spinal cord contusion at T10.

3. Circulation
 Case Study
A 22-year-old woman presents to the emergency department with a gunshot
wound to the right thigh. Her initial blood pressure is 92/78 mm Hg and
heart rate is 130 beats/min. She has received 1 L of crystalloid fluid by EMS
with some improvement in blood pressure to 108/70 but returns to the
previous blood pressure reading. She is confused and thrashing about.
– Is this patient in shock?
– What is the primary concern?
– What therapy is recommended?

If the initial fluid bolus produces only transient

improvement or no response, immediate surgical
consultation is required. Transfusion of blood
products should be initiated as well.

The leading cause of shock in a trauma patient is hemorrhage. The primary

goal is to identify and stop the hemorrhage and restore tissue oxygenation as
soon as possible. Initial empiric treatment in adults consists of warmed
isotonic crystalloid infusion (1 L of lactated Ringer or normal saline solution)
via two large-bore (minimum 18-gauge) peripheral intravenous catheters and
control of external hemorrhage by means of manual compression. Targets for
empiric fluid therapy are normalization of blood pressure, reversal of
tachycardia, and maintenance of adequate organ perfusion (Chapter 8).
Patients with no traumatic brain injury, but extensive hemorrhage that may
require surgical intervention, are better managed by resuscitation with
permissive hypotension to a systolic blood pressure of 90 to 100 mm Hg until
surgical control of the hemorrhage can be accomplished. This action supports
control of vessels that may have thrombosed and are not presently bleeding,
but may rebleed if the blood pressure is normalized. When hypoperfusion
and vascular compensation limit peripheral access, cannulation of a central
vein (ideally with a 7F, 8.5F, or 9F introducer) is an alternative, as is
intraosseous access. Concomitant diagnostic studies for the source of bleeding
can include chest radiographs (hemothorax), pelvic radiograph (pelvic
fracture, open-book or vertical pelvic shear injury), focused assessment
sonography in trauma (FAST), or diagnostic peritoneal aspirate (DPA) or
lavage (DPL) [intraperitoneal hemorrhage]. If the patient is hemodynamically
stable, a computed tomography (CT) scan of the abdomen and pelvis ideally
with intravenous contrast may be performed to better delineate the injuries
and evaluate the retroperitoneum, unless a definitive indication to operate is
present. A patient who is hemodynamically unstable should not be moved for
CT scanning. Immediate control of external hemorrhage should proceed
simultaneously with rapid resuscitation. When trauma is present in an
extremity, direct pressure is recommended. This can be accompanied by a
hemostatic gauze dressing. If bleeding persists, a tourniquet should be
applied on the extremity above the injury. Blind clamping in a bleeding
wound is discouraged to avoid potential injury to adjacent structures.

It is critical not to equate the absence of

hypotension with the absence of shock. Patients
may have significant blood loss (Class I or II
shock) without a change in blood pressure.

As shown in Table 12-2, a patient’s systolic blood pressure, heart rate,

respiratory rate, and mental status can be used to assess blood loss. The
American College of Surgeons also validates a decrease in pulse pressure as a
sign of occult hypoperfusion. Circulating blood volume corresponds to 7% of
normal body weight (70 mL/kg) in an adult. Blood loss up to 1,200 mL may
occur in a normotensive adult (70 kg [154 lb]) with minimal tachycardia.
Class II hemorrhage is uncomplicated shock, but crystalloid resuscitation may
be sufficient. Class III hemorrhage requires crystalloid resuscitation and often
blood replacement. Class IV hemorrhage can be considered preterminal and
requires aggressive measures to restore intravascular volume, oxygen-carrying
capacity, and to control bleeding. Treatment should be directed by the initial
response to therapy rather than by a classification scheme. Patients will
respond to fluid resuscitation in one of three ways. One group of patients,
known as rapid responders, will regain normal vital signs with small volumes
of fluid. A second group of patients, known as transient responders, will
initially respond to the fluid resuscitation, but then demonstrate signs of
hemodynamic deterioration with time or a decrease in the fluid resuscitation.
These patients will require additional fluids and focused evaluation of the
etiology and treatment of the injuries. This transient response is suggestive of
ongoing hemorrhage. The third group of patients, known as non-responders,
will not show signs of physiologic improvement despite volume resuscitation;
these patients often need immediate surgical intervention. They likely have
ongoing major hemorrhage. Without rapid and aggressive intervention, their
mortality will be high and they may ultimately receive massive transfusions
(> 10 units of packed red blood cells [PRBCs] in the first 24 hours of
admission or more than 4 units in 1 hour).

Ionized calcium may need to be followed and

repleted ascitrate in PRBCs may chelate calcium,
promoting a coagulation defect in patients
receiving massive transfusions.

When beginning resuscitation for patients in shock, isotonic crystalloid can be

used. However, the volume should be controlled and minimized to no more
than 1 L. If there is an inadequate physiologic response, this therapy should
be followed by the early administration of blood products. Fully crossmatched
blood is rarely available for emergency trauma resuscitation. Uncrossmatched
type-specific blood can be safely administered and is available in many
hospitals within 15 to 20 minutes after a request is received. If type-specific
blood is not available and the patient is unstable, O-negative PRBCs should
be used. In most trauma centers, uncrossmatched blood is almost
immediately available in the trauma resuscitation area for use in the unstable
trauma patient. O-positive PRBCs are an option for men and women beyond
childbearing age.

Table 12-2 Hemorrhage Classification Signs and Symptoms

aBase excess is the quantity of base (HCO -, in mEq/L) that is above or below the normal range in the
3
body. A negative number is called a base deficit and indicates metabolic acidosis.
Reproduced with permission Mutschler M, Nienaber U, Brockamp T, et al. A critical reappraisal of the
ATLS classification of hypovolaemic shock: does it really reflect clinical reality? Resuscitation.
2013;84(3):309-313.

In situations in which massive transfusion is anticipated or probably likely, the

early use of a balanced resuscitation using a combination of PRBCs, fresh
frozen plasma, platelets, and cryoprecipitate should be strongly considered.
In these situations, the most urgent priority is control of ongoing hemorrhage.
Typically, this involves surgical intervention. However, with certain injuries,
especially severe pelvic fractures with active bleeding into a pelvic hematoma,
other interventions, such as angiography with embolization, can be lifesaving.
Many trauma centers have a massive transfusion protocol in place to allow the
rapid procurement of blood products for administration in the critically
injured, unstable, massively bleeding patient. Developing evidence suggests
that the administration of crystalloid solutions should be minimized, especially
in this population. There is also increasing evidence that the use of ratio-
based blood product resuscitation (PRBCs, fresh frozen plasma, and platelets
close to a 1:1:1 ratio) improves outcomes and may decrease the physiologic
insult to these critically ill patients. Ratio-based resuscitation likely provides
some of the same benefits as the use of fresh whole blood and may be helpful
in minimizing the coagulopathy that can develop in patients who have massive
injuries. Whole blood is available in some facilities and part of the massive
transfusion protocol for patients in hemorrhagic shock. Investigations into the
benefits of whole blood are still ongoing.

Patients with massive blood loss require an early

and aggressive balanced resuscitation with
PRBCs, fresh frozen plasma, and platelets, along
with aggressive hemorrhage control.

Tranexamic acid (TXA) may also be considered as part of the resuscitation of

these patients but some evidence has shown increased thrombotic
complications. Thromboelastography (TEG) or rotational thromboelastometry
(ROTEM) may also be used to guide more precise replacement of product
deficiency during the resuscitation.

4. Disability (Neurologic Evaluation)

Rapid neurologic evaluation is performed as part of the primary survey and

includes determination of level of consciousness/GCS, pupillary size and
reactivity, lateralizing signs, and gross level of spinal cord injury, if present.
The GCS score is a quick, simple method for determining the level of
consciousness and is predictive of outcome (specifically the best motor
response). A decrease in the level of consciousness may reflect decreased
cerebral perfusion or may be the result of direct brain injury. Hypoglycemia,
ethanol, narcotics, and other drugs may also be involved. An altered level of
consciousness indicates the need for immediate reevaluation of oxygenation,
ventilation, and tissue perfusion. Changes in consciousness should be
assumed to be caused by intracerebral conditions until proven otherwise. To
improve patient outcomes, every effort should be made to prevent secondary
brain injury and to ensure adequate oxygenation, ventilation, and blood
pressure. If the patient’s condition permits, a thorough examination prior to
sedation and intubation may be performed to determine the presence of any
localizing intracranial or spinal cord injury. Establishment of a definitive
airway to control the airway and/or breathing and ventilation should not be
postponed for a detailed neurologic examination. Once a neurologic injury is
diagnosed, or even suspected, a referral should be made to a definitive care
facility prior to additional imaging.

5. Exposure and Environmental Control

Throughout the initial resuscitation period, efforts should be made to control

and prevent hypothermia. Patients are often hypothermic after environmental
exposure, and the body temperature may fall further after administration of
room temperature resuscitation fluids and cold blood, removal of clothing for
examination purposes, loss of normal temperature-regulating reflexes in
shock, or the use of some medications.
Patients may lose heat through any of multiple mechanisms including
radiation, conduction (direct transfer), convection (air current), and
evaporation. It is imperative to remove wet clothing. For example, patients
with wet clothing lose heat faster because the thermal conductivity of water is
far greater than that of air. In addition, because hypothermia contributes to
coagulation abnormalities, cardiovascular collapse, and poor outcome, it
should be avoided and treated.
The most common treatment strategies can be characterized as passive
external rewarming and active rewarming (external and internal). Passive
external warming measures include warming the environment, removing wet
clothing, and providing insulating materials (eg, blankets). Additional
maneuvers, such as active external rewarming measures, include warming
blankets, heating pads, radiant energy, and force heated air systems. Active
internal methods include warmed intravenous fluid to approximately 39°C
(102°F) via a high-flow fluid warmer and warmed (40–45°C [104°F–
113°F]) humidified air via an endotracheal tube. More invasive interventions
include internal cavity lavage or extracorporeal blood warming.
6. Monitoring
Parameters such as heart rate, blood pressure, pulse pressure, respiratory
rate, acid-base status, body temperature, and urinary output are used to
guide adequacy of resuscitation. Evaluation begins during the initial survey
and should be repeated frequently. Pulse oximetry is a valuable adjunct for
monitoring hemoglobin saturation with oxygen in injured patients, but it is not
useful for evaluating the adequacy of ventilation. Blood pressure, as the sole
marker of resuscitation, may be a poor measure of actual tissue perfusion.
Additional metabolic markers, such as serum lactate, base deficit, and pH,
will assist in the determination of the adequacy of resuscitation. Perfusion of
extremities may be evaluated by examining capillary refill as well as the
presence of the peripheral pulses.
A urinary catheter should be inserted as soon as is practical to monitor urine
output as a gauge of renal perfusion, although it must be used with caution in
male patients when urethral injury is suspected (eg, blood at the urethral
meatus, scrotal hematoma, or abnormal prostate on rectal examination). In
these patients, a retrograde urethrogram can be used to rapidly evaluate for
urethral injury.

7. Hemorrhagic Shock

As resuscitation proceeds, it is crucial to identify potential causes of

hypotension. A search for occult blood loss should be undertaken after any
external hemorrhage is controlled. The most frequent sites for such blood loss
are the chest, abdomen, pelvis/retroperitoneum, and the soft tissues adjacent
to long bone fractures.
a. Hemothorax

A chest radiograph (ideally with the patient in an upright or reverse

Trendelenburg position if hemodynamically stable) is a reliable
screen for intrathoracic bleeding. Ultrasonography of the chest also
may reliably detect a hemothorax or pericardial fluid.
A hemothorax should be drained promptly by chest tube placement,
with a subsequent radiograph to verify the location of the chest tube,
blood evacuation, and lung expansion. As noted earlier, rapid loss of
1,500 mL of blood on chest tube insertion or continued losses of >
200 mL/h for 2 to 4 hours may necessitate a thoracotomy. If
available, autotransfusion devices should be attached to any chest
tube drainage canister placed for massive hemothorax.
b. Intra-abdominal Hemorrhage
Abdominal examination is often misleading in the detection of acute
bleeding, especially in patients with lower chest trauma, rib fractures,
spinal cord injury, intoxication, or altered level of consciousness. Any
patient who has sustained significant blunt torso injury from a direct
blow or deceleration, or a penetrating torso injury must be
considered to have an abdominal visceral or vascular injury. Focused
ultrasound for trauma and DPA or DPL are the most expedient
methods of identifying significant intraperitoneal hemorrhage,
although the FAST examination has largely replaced the use of DPL
in most institutions. When readily available and used by trained
individuals, FAST has the sensitivity, specificity, and accuracy of
DPL in detecting hemoperitoneum requiring immediate surgical
evaluation to determine the need for a surgical intervention. In stable
patients with a positive FAST result, abdominal and pelvis CT scan
with intravenous contrast may be appropriate to identify the source of
bleeding and determine the need for any further intervention (eg,
angiography for blunt solid organ injury). Abdominal hemorrhage
frequently comes from splenic or liver laceration, other visceral
injury, or retroperitoneal hematoma. Patients who are in shock are
not candidates for CT scanning and require surgery to control
bleeding.
c. Pelvic Hemorrhage
Assessment of bony stability by means of physical examination and
plain radiographs of the pelvis is crucial for early identification of
major pelvic fractures. Patients with pelvic fractures (particularly
high-grade anterior-posterior compression or vertical shear) are at
high risk for major bleeding, which is usually venous. Initial
management includes vigorous blood volume replacement and,
possibly, circumferential compression and mechanical tamponade
with some form of pelvic binder. External skeletal fixation may be
helpful if the fracture anatomy is appropriate, and an orthopedic
surgeon should be consulted early in the course of treatment. In
patients with arterial bleeding associated with pelvic injury, CT
scanning will reveal a blush of contrast. Pelvic angiography for
embolization should be considered in the hypotensive patient
because of an increased likelihood for arterial bleeding. Angiography
may be required in approximately 10% of patients with pelvic
fractures. Recently, angiography has become the treatment of choice
for control of bleeding from pelvic fractures and hematomas, even in
the unstable patient.

d. Fractures
Patients with fractures will likely have associated hemorrhage in the
surrounding injured tissue. Estimates of blood loss from various
fractures are: rib 125 mL, radius or ulna 250–500 mL, humerus
500–750 mL, tibia or fibula 500–1,000 mL, femur 1,000–2,000
mL, pelvis 1,000 mL to massive. Multi-injured patients can have
severe blood loss from their musculoskeletal injuries. This needs to
be recognized quickly and appropriate resuscitation initiated
promptly. In patients with long bone fractures, repeated physical
examination for soft-tissue swelling and development of compartment
syndrome is imperative in the management of these patients.

A pelvic binder may be a commercially available

device or a bedsheet wrapped tightly around the
pelvis. This maneuver should center the
compressive forces at the level of the greater
trochanters.
 e. External Hemorrhage
External hemorrhage can be very dramatic, as with a lacerated major
artery or vein where direct pressure will decrease blood loss. Other
cases, such as scalp lacerations, may go unrecognized as a possible
source of significant blood loss. Rapid application of direct pressure
(with or without hemostatic gauze), temporizing suture repair, or
application of a tourniquet to a bleeding extremity may be lifesaving.
If a commercially available tourniquet is not available, an alternative
method employs a blood pressure cuff inflated to a pressure higher
than the patient’s systolic blood pressure. Tourniquet use should be
followed by surgical consultation because the tourniquet places the
extremity at risk for ischemic injury. The time the tourniquet is
placed should be written on the tourniquet and communicated to the
receiving facility if the patient is transferred. In some situations,
including military conflict and intentional mass casualty events, the
early control of hemorrhage along with the liberal use of tourniquets
can be lifesaving and may take priority in the initial evaluation and
management.

8. Nonhemorrhagic Shock
The differential diagnosis of nonhemorrhagic shock in the trauma patient
includes obstructive shock (tension pneumothorax, cardiac tamponade),
cardiogenic shock (blunt cardiac injury), and distributive shock (neurogenic
shock with acute spinal cord injury). Head injury is a rare cause of
hypotension, but when it occurs, it is usually a preterminal event.

If tension pneumothorax is suspected in an

intubated patient, disconnect the patient from the
ventilator and vent the pleural space with a
finger thoracostomy or needle decompression
followed by a tube thoracostomy. Manually
ventilating the patient may reveal increased
resistance.
a. Tension Pneumothorax

Tension pneumothorax causes hemodynamic compromise and

pulmonary dysfunction because of acute compression of the lung
parenchyma and a shift of the mediastinum away from the
hemithorax with the increased pressure. Do not wait for a chest
radiograph to make this diagnosis. Breath sounds will be absent,
chest rise will be asynchronous, and patients may develop respiratory
distress, acute desaturation, bradycardia, and occasionally, distended
neck veins. Classic venous distension may be absent in the setting of
pneumothorax complicated by hypovolemia. All but gross changes in
breath sounds may be difficult to detect in the resuscitation room.
Tracheal shift is a late sign and may not be a presenting finding. In
adults, needle chest decompression in the midclavicular second
intercostal space or finger thoracostomy at the fifth intercostal space
anterior axillary line is performed; this is a lifesaving intervention that
is followed by placement of a chest tube.
b. Cardiac Tamponade

The classic signs of cardiac tamponade—hypotension, distant heart

sounds, jugular venous distension, and pulsus paradoxus—may be
obscured because of noise and hypovolemia (decreasing jugular
distension). Ultrasound (FAST) is a sensitive test for fluid in the
pericardial sac. A pericardial window should be performed for the
patient with refractory shock, persistent central venous hypertension,
and a high-risk penetrating wound (between the nipples, above the
costal margin, below the clavicles). When surgical expertise is not
available, a needle/catheter pericardiocentesis may be performed as
a temporizing measure. Occasionally, major blunt chest trauma
ruptures the cardiac surface. Most cases involve atrial tears and can
be repaired if diagnosed early.
c. Blunt Cardiac Injury
The diagnosis of blunt cardiac injury should be suspected in a patient
involved in a high-speed, frontal impact accident who has
unexplained hypotension or arrhythmia or, less commonly,
cardiogenic shock. Changes in the electrocardiograms (ECGs) are
usually nonspecific and can include premature ventricular
contractions, bundle branch block, atrial fibrillation, unexplained
sinus tachycardia, and ST-segment changes. If blunt cardiac injury is
a possibility, a screening ECG should be obtained in the emergency
department. If the patient has new abnormalities, the patient should
be admitted for continuous ECG monitoring. For patients with
preexisting abnormalities, comparisons with previous ECGs should be
made. Hemodynamically stable patients with no ECG abnormalities
and negative cardiac troponin need no further cardiac evaluation or
observation. Echocardiography is indicated in patients with
unexplained hypotension or arrhythmias to evaluate cardiac function
and structural heart injury. Treatment includes correction of acidosis,
hypoxia, and electrolyte abnormalities; judicious administration of
fluid; and pharmacologic treatment of life-threatening arrhythmias.

Inotropes may be indicated to support hemodynamic function. It is

important to ensure that refractory hypotension is not caused by
ongoing blood loss. Patients may present with acute myocardial
infarction secondary to cardiac injury, or an acute myocardial
infarction may have led to trauma (ie, fall, motor vehicle crash). At
times, these patients may need emergent cardiology consultation for
heart catheterization.

The right ventricle is most frequently involved in

blunt cardiac injury, and volume challenge is the
initial therapy for hypotension in the absence of
pulmonary edema.
 d. Neurogenic Shock
Neurogenic shock, a physiologic state of shock, occurs when a
cervical or high thoracic spinal cord injury (above T6 level) causes
sympathectomy. Loss of vasomotor tone causes vasodilation of
visceral and peripheral blood vessels. It is characterized by
hypotension, frequently associated with relative or absolute
bradycardia. Flaccid paralysis, loss of extremity reflexes, and
priapism may be some of the initial associated neurologic findings.
This is usually followed by spasticity. This spectrum of neurologic
findings comprises spinal shock. Treatment for hypotension includes
volume resuscitation and vasopressors (phenylephrine or
norepinephrine) if volume loading does not reverse the hypotension.
Atropine or dopamine may be considered in the presence of
bradycardia associated with hemodynamic instability.

B. Secondary Survey: Diagnosis and Treatment of Other Injuries

Most patients with acute injuries can be resuscitated to a hemodynamically
stable state. The primary survey should immediately identify acute life-
threatening injuries. The next goal is to complete a secondary assessment to
identify and treat other injuries. This assessment is crucial to allow proper
triage to the operating room, radiology suite, or ICU. Keep in mind that
should the patient’s condition change, return to the primary survey and repeat
the process.

1. History

Essential components of a patient’s history include details of the mechanism

of injury, previous medical illness, past surgical history (eg, inquiring about
surgical scars), current medications, allergies, and tetanus immunization.

2. Physical Examination
The patient should be examined from head to toe. The skull is carefully
inspected to identify occult injuries. Signs of basilar skull fracture include
hemotympanum, rhinorrhea, or otorrhea; Battle sign (ecchymosis of the skin
over the mastoid); and raccoon eyes. Facial bones, mandible, and neck are
palpated for tenderness and crepitus. The GCS score and limited neurologic
examination from the initial assessment are used to evaluate for head trauma
(Chapter 9). Extraocular eye movements are checked to exclude muscle or
nerve entrapment. The nares are inspected for blood and septal hematoma.
The neck is inspected for distended neck veins, the position of the trachea, or
subcutaneous emphysema. Neck pain or tenderness over the cervical spine
warrants additional radiographs (see later section), CT, or magnetic resonance
imaging. The chest is auscultated and palpated for tenderness and crepitus.
The patient is logrolled so that the thoracic and lumbar spine can be palpated
for tenderness and other injuries can be detected. In penetrating trauma,
exclude occult entrance or exit wounds in the axillary, cervical, or inguinal
regions. This may require a second full log roll to the opposite side or quarter
roll. The abdomen is likewise inspected, auscultated, and palpated. The
pelvic bones are assessed for stability with lateral compression, anterior-
posterior compression, and a gentle translational motion; lack of pain with
these motions in an awake patient without competing pain issues is usually
sufficient to rule out significant pelvic bone fractures. Repeated examinations
for pelvic stability should be avoided and may cause further injury. The
rectum is evaluated for tone and the presence or absence of blood and to
ensure that the prostate gland is not displaced or difficult to palpate. The
presence of perineal/scrotal hematoma and blood at the urethral meatus
implies potential urogenital injury, which is a risk for urinary catheter
insertion. The extremities are inspected, palpated, and evaluated for range of
motion and neurovascular integrity.

3. Laboratory Studies
Minimal testing includes complete blood count, electrolyte measurements,
blood glucose level, blood alcohol level, and toxicology screening. Viscoelastic
assays (TEG or ROTEM), if available, can better depict trauma-induced
coagulopathy and provide guidance of massive transfusion protocols. In any
patient with evidence of hypovolemia, blood-group typing, and a coagulation
profile should be performed. Arterial blood gas measurements should be
analyzed in selected patients to confirm adequate ventilation and perfusion
(presence of acidosis). An elevated serum amylase level may be an indicator
of pancreatic or bowel injury in the patient with blunt abdominal trauma,
although it tends to increase several hours after initial injury. Creatinine
phosphokinase should be checked and followed if rhabdomyolysis or
compartment syndrome is suspected. The hematocrit may not reflect the
patient’s acute volume status; ongoing resuscitation equilibration by
transcapillary fluid shifts can take hours to be reflected as a decrease in
hematocrit. In general, a fall of 3% in the hematocrit is equivalent to 1 unit of
blood loss. Serum lactate level measurements and follow-up to monitor
clearance can help management and prognosis.

Reevaluate laboratory results after initial

resuscitation. Absolute values may not be as
important as trends.

4. Radiologic Evaluation
a. General
In the evaluation of blunt multiple-system trauma, a supine chest
radiograph and supine view of the pelvis are generally obtained as
the primary survey is performed. This allows for interpretation of
completed radiographs as the secondary survey begins. Plain
radiographs of the pelvis are crucial for early identification of major
fractures and may allow for early placement of a pelvic binder to help
reduce ongoing blood loss

b. Head
CT scanning is essential for initial evaluation of a head-injured
patient or in any patient with a decreased or altered level of
consciousness. Special consideration should be given to patients
sustaining a blunt mechanism and are on anticoagulation and/or
antiplatelet medications, especially in the elderly population. Many
centers will also obtain a CT scan of the cervical spine when the head
scan is obtained.

c. Spine
The initial lateral C-spine radiograph has been largely abandoned for
the diagnosis of cervical spine injury. Given the common issues in
obtaining adequate cervical spine images, including inadequate
visualization of the spine between C7 and T1 and poor definition of
the occiput, most centers now obtain a CT evaluation of any areas
that cannot be clinically cleared or have concerning results on
physical examination. In the patient with increased risk of C-spine
injury, cervical immobilization is crucial until these studies are
reviewed and correlated with a reliable physical examination for
evidence of tenderness. However, patients should be removed from a
rigid spine board expeditiously because of the risk of skin pressure
injury with extended immobilization. Magnetic resonance imaging is
helpful for disc, spinal cord, and ligament injuries. If a C-spine
fracture is found, radiographic screening of the entire spine is
indicated because ~10% of these patients will have a second,
noncontiguous vertebral column fracture. CT scans of the chest and
abdomen often can be reformatted to provide information on spine
injury without the need for additional plain radiographs or additional
radiation exposure.
Neurologic examination alone does not exclude a C-spine injury. The
following considerations apply to patients at risk for C-spine injury:
Patients who are alert, awake, and have no changes in
neurologic status or neck pain may be considered to have a
stable C-spine and need no radiologic studies. Beware of
injuries that could distract the patient with C-spine injury.
Early CT scans may facilitate evaluation of the C-spine in any
head-injured or intubated patient. Adding CT evaluation of
the C-spine to the initial CT scan of the head is an appropriate
strategy after injury.
 The presence of paraplegia or quadriplegia is presumptive
evidence of spinal instability.
Patients with neurologic deficits potentially the result of a C-
spine injury require spine surgery consultation.
Exclusion of any bony injury does not eliminate the possibility
of ligamentous disruption. Magnetic resonance imaging can
facilitate clearance of ligamentous injury if the examination is
not reliable.

Persistent pneumothorax despite a functioning

chest tube or persistent air loss through the chest
tube system may indicate a tracheobronchial
injury.

d. Chest

Once the spine is cleared for fractures, an upright (or reverse

Trendelenburg) chest radiograph is indicated to better define or
identify pneumothorax, hemothorax, mediastinal widening or
irregularity (concern for aortic transection), or fractures, as well as to
confirm the position of various tubes. Chest radiographs are
inadequate to rule out aortic injury. When a significant lateral impact
or deceleration injury occurs, an aortic injury should be suspected in
a patient with a chest radiograph demonstrating a widened
mediastinum. CT angiography provides an excellent method to
screen for aortic injury and define other thoracic injuries. Its use has
largely replaced traditional angiography in the initial diagnosis of
thoracic aortic injuries.
e. Abdomen
 Plain abdominal radiographs in blunt trauma are not usually helpful.
In the hemodynamically stable patient, a CT scan of the abdomen
and pelvis and the FAST examination are the mainstays of abdominal
evaluation in a trauma patient. FAST can be followed up with a CT
scan of the abdomen if free peritoneal fluid is identified in the stable
patient. DPL may still be used in certain circumstances, but has
generally been replaced by CT imaging and the FAST examination.
A nasogastric tube serves to decompress the stomach and may
reduce the risk of pulmonary aspiration; however, it should be placed
orally in patients with midfacial fractures or possible basilar skull
fractures. Blood in the gastric aspirate may be the only sign of an
otherwise occult injury to the stomach or duodenum, and further
investigation may be indicated
f. Genitourinary Tract
Hematuria should be evaluated with a CT scan or other contrast
studies. It provides anatomic detail about abdominal and
retroperitoneal structures and any direct injury to the kidney(s). If
physical examination suggests that a urethral injury is present, a
urethrogram should be obtained before urinary catheterization. A
cystogram may be indicated if bladder injury is suspected.
Intravenous pyelograms are not overly valuable during the initial
assessment.

g. Skeletal Fractures
Films of the extremities (anterior posterior and lateral views) should
be obtained on the basis of physical examination or patient
complaint. Films should include the joint above and below the site of
fracture. Evaluation of the head and central injuries take precedence.
In stable patient with no signs of vascular compromise secondary to
their skeletal injuries deferring extremity radiographs is advisable to
avoid delay in proceeding to CT.

5. Other Issues
Systemic antibiotics should usually be withheld until a specific indication is
determined, but they are employed in three situations: (1) patients undergoing
intracranial pressure monitoring or chest tube placement frequently receive
gram-positive coverage when the device is inserted; (2) patients with
penetrating abdominal trauma may be given coverage for gram-negative
aerobic and anaerobic organisms for the first 24 hours after injury; and (3)
patients with low-grade open fractures are given gram-positive coverage for 24
hours while high-grade open fractures require broad-spectrum coverage for
48 hours as orthopedic evaluation is arranged.

Remember to consult specialty services early so

that they can offer input into treatment decisions.

Another important issue is the need for adequate tetanus prophylaxis in

patients with open wounds. The patient’s current vaccination status must be
verified and updated if needed. In those patients who have an unclear
immunization status or with especially contaminated tetanus-prone wounds,
the use of tetanus immune globulin should be considered (Table 12-3).

Table 12-3 Guide to Tetanus Prophylaxis in Routine Wound Managementa

Abbreviations: Tdap, tetanus toxoid, reduced diphtheria toxoid, acellular pertussis vaccine; Td, tetanus
toxoid and reduced diphtheria toxoid — for adult use (dose = 0.5 mL); TIG, tetanus immune globulin
— human (dose 250 IU).
aPatients who have completed a three-dose primary tetanus vaccination series and have received a
tetanus toxoid-containing vaccine <5 years before the injury do not require a tetanus toxoid-containing
vaccine for wound management.
bChildren <7 years – Tdap is recommended; if pertussis vaccine is contraindicated, Td is given.
Children 7-9 years or adults >65 years = Td is recommended. Children and adults 10-64 years =
Tdap is preferred to Td if the patient has never received Tdap and has no contraindication to pertussis
vaccine. For patients >7 years of age, if Tdap is not available or not indicated because of age, Td is
preferred to tetanus toxoid.
cSuch as (but not limited to) wounds contaminated with dirt, feces, soil, and saliva; puncture wounds;
avulsions; and wounds resulting from missiles, crushing burns, and frostbite.
dEquine tetanus antitoxin should be used when TIG is not available.
eIf only three doses of fluid toxoid have been received, a fourth dose = preferably an adsorbed toxoid
– should be given. Although licensed, fluid tetanus toxoid is rarely used.
fYes, if ≥ 10 years since the last tetanus toxoid-containing dose.
gYes, if ≥5 years since the last tetanus toxoid-containing dose; more frequent boosters are not needed
and can accentuate adverse effects.

Female patients of childbearing age should be questioned about the

possibility of pregnancy or be checked with a β-human chorionic
gonadotropin test before extensive radiographic evaluation is performed
unless significant hemodynamic instability is present. The priority with the
unstable pregnant patient always has to be maternal resuscitation and
stabilization. Any female in her second or third trimester should be positioned
with a wedge under her back to elevate the right side, avoiding compression
of the vena cava. This is done only after examination of the spine and pelvis
does not reveal any pain or tenderness, which may indicate a fracture.
Remember that the optimal care of the mother yields optimal care for the
fetus. Obstetrical consultation should be considered.
Case Follow-up: A 22-year-old woman presents to the emergency department
with a gunshot wound to the right thigh. She sustained a femoral shaft fracture
and superficial femoral artery laceration. She initially underwent external
fixation of the femur fracture and femoral artery reconstruction using
contralateral vein graft. Definitive fixation is performed with an intramedullary
nail.

C. Tertiary Survey: Ongoing Evaluation

 Case Study
An 18-year-old man is in the ICU after sustaining a gunshot wound to the left
chest traversing the diaphragm, left lobe of the liver, and spleen. In the
operating room he underwent a left diaphragmatic repair after confirmation of
no active bleeding coming from the thoracic cavity, left hepatic lobe repair,
and splenectomy. Urine output was initially adequate along with blood
pressure; however, it has been steadily decreasing along with increasing
bloody drainage from the nasogastric tube. A viscoelastic assay obtained prior
to the decline revealed no abnormalities.
– What is the possible cause of the bleeding?
– What should be the most appropriate first step in resuscitation?

Go back to the primary and secondary survey

when a patient has a negative change to provide
a framework to help organize the critical thinking
process.

After life- and limb-threatening injuries have been addressed and metabolic
derangements have been corrected, periodic systematic assessment is
performed to identify occult injuries not evident at presentation. In addition,
healthcare personnel must be prepared to return to the resuscitation phases
and/or when conditions change. In the immediate period of the patient’s
course, these changes must not be viewed as a failure or “something was
done wrong.” This type of thinking or judgment will invariably lead to delays
and potential adverse outcomes.
 The administration of atropine or dopamine, as
well as mydriatic agents, may dilate the pupils
and lead to a false diagnosis of a more severe
head injury.

1. Head Injury

Evaluation of the head-injured patient is an ongoing process requiring early

neurosurgical consultation. Serial assessment of the GCS scores, pupil size
and response, and the presence or absence of lateralizing neurologic signs is
crucial. Any changes in examination results are noted and acted on as they
are discovered. Typically any change in the neurologic examination for the
worse warrants a repeat head CT.
Serial CT scans of the head may offer clinically useful information, but the
key to patient management is detection of changes in the physical
examination. Repeat scheduled head CT is not uncommon for patients on
blood thinners, such as warfarin or direct-acting oral anticoagulants (DOACs).
Continued resuscitation is imperative to avoid secondary brain injury, which
typically occurs when a patient becomes hypoxic or hypotensive during acute
care. These secondary insults increase the likelihood of a poor outcome
(Chapter 9).

2. Pulmonary Injury
Trauma patients often have a full stomach at the time of injury and experience
aspiration. Aspiration of the acidic gastric contents may cause a chemical
pneumonitis initially and predispose patients to an infective pneumonia or
acute respiratory distress syndrome later. Antibiotics are not indicated in
initial management. Early antibiotics can also make the patient more
susceptible to resistant organisms. Bronchoscopy may be needed for removal
of large particulate matter.
Delayed onset of pneumothorax or hemothorax may follow chest trauma. In
addition, pulmonary contusions and resulting acute respiratory distress
syndrome may not become obvious until later (12 to 48 hours). Continued
assessment includes physical examination, oximetry and/or arterial blood gas
measurements, chest radiographs, and ventilatory mechanics.

3. Cardiac Injury
Continuous ECG monitoring and frequent measurements of blood pressure
are mandatory in the emergency department and ICU. Continuous arterial
blood pressure monitoring may be indicated (Chapter 7). Electrolyte
disturbances may lead to cardiac contractile dysfunction or arrhythmias in the
aggressively resuscitated trauma patient. Common electrolyte disturbances
include hyperchloremia, hypokalemia and hyperkalemia, hypomagnesemia,
and hypocalcemia.

4. Abdominal Injury
Substance abuse or neurologic injury may not allow for a reliable initial
abdominal examination. Perforation of a hollow viscus in blunt trauma is
sometimes difficult to diagnose. Free air under the diaphragm on an upright
chest radiograph, over the liver on a left lateral decubitus radiograph, or on
an abdominal CT necessitates the need for surgical exploration. CT scanning
also provides information about the retroperitoneum. In the head-injured
patient who is undergoing a head CT scan and has a nonsurgical neurologic
injury, abdominal scanning should be considered because physical
examination may be unreliable. However, caution must be used in the clinical
interpretation of CT imaging for a hollow viscus injury; a negative scan does
not absolutely rule out the possibility of an occult injury.

An underdiagnosed condition is abdominal compartment syndrome. This

condition occurs when intra-abdominal pressure increases because of
intraperitoneal or retroperitoneal hemorrhage, ascitic fluid accumulation,
edema secondary to massive fluid resuscitation, or intraoperative surgical
closure of the abdomen under tension. Increased intra-abdominal pressure
decreases cardiac output and compresses the vascular bed and kidneys. The
diaphragm is displaced upward by increased intra-abdominal pressure, which
results in decreased thoracic volume and compliance. Decreased volume
within the pleural cavity predisposes to atelectasis, and ventilated patients
with intra-abdominal hypertension require increased airway pressure to
deliver a fixed tidal volume. Vascular compression can decrease blood flow to
the liver and kidneys with resultant dysfunction. Finally, intra-abdominal
hypertension significantly increases intracranial pressure. Typically,
abdominal hypertension is manifested with decreased urine output, increasing
peak airway pressures, hypotension, and an expanding tense abdomen.

5. Musculoskeletal Injury

In compartment syndrome, urgent fasciotomy is

required with loss of pulse being a very late
finding.

The neurologic and vascular evaluation of the extremities is an ongoing

process. A swollen and tense extremity should be watched closely for the
development of a compartment syndrome, particularly in patients with
decreased responsiveness. In alert patients, serial physical examination is the
best monitoring method. Classic signs include pain, pallor, pulselessness,
paresthesia, and/or paralysis. The most helpful early signs are reports of pain
out of proportion to physical findings and severe pain on passive stretch of the
involved muscle groups. In the unconscious patient or when the examination
is unreliable, compartment pressure may be monitored using a needle with a
pressure transducer. Pressures > 30 mm Hg warrant consideration of
fasciotomy.
Musculoskeletal examination should be repeated, either as patients recover
from other injuries or as their mental status clears, to identify new pain or
tenderness. Plain radiographs should then be obtained to identify occult
fractures. Orthopedic injuries commonly identified in a delayed fashion
include fractures of the scapula, thoracic and lumbar spine, pelvis, ankle, and
wrist.
Crush syndrome should be considered when patients have been trapped,
injury to large muscle mass is involved, prolonged compression has occurred
with protracted immobilization, or vascular compromise is present (such as
tourniquet use or compartment syndrome). Crush syndrome develops when
damaged myocytes lyse, releasing myoglobin, potassium, phosphorus, and
calcium. Manifestations of this syndrome include cardiac dysrhythmias, renal
failure, metabolic acidosis, and hypovolemia. Preemptive hydration before
reperfusion of crushed muscle mass usually is accomplished before arrival at
the hospital. Revascularization of ischemic extremities, fasciotomy for
compartment syndrome, or release of tourniquets can mimic this situation.
Before reperfusion, normal saline should be administered (1- to 2-L bolus or
10–15 mL/kg/h). Careful monitoring for cardiac signs of hyperkalemia should
be instituted. After reperfusion, aggressive hydration to maintain urine output
above 3 to 4 mL/kg/h helps prevent heme pigment-associated renal injury.
Adjuvants, such as bicarbonate and mannitol, have been used.
The use of extremity tourniquets has become more frequent in the field. The
length of time the tourniquet was in place and whether it was effective should
be noted. Attention should be directed to the extremity(s) if effective
tourniquet time exceeded 90 to 120 minutes because of the increased risk for
complications such as compartment syndrome, rhabdomyolysis, reperfusion
injury, and nerve damage.

6. Other Considerations
Resuscitation is an ongoing process. Traditional end points, such as
normalization of blood pressure, heart rate, and urine output, may not always
reflect complete correction of the shock state. The attainment of normal vital
signs can occur even in the setting of tissue hypoperfusion, resulting in a
compensated state of shock. Lactate concentration and resolution of metabolic
acidosis may provide more definitive end points for adequacy of resuscitation.
Because the time to normalization of these parameters is predictive of
survival, additional resuscitation in the form of volume replacement, blood
product transfusion, or support with vasoactive agents may be indicated within
the first 24 hours following injury despite normal or near-normal vital signs.
Persistence of a metabolic acidosis or elevated lactate concentration may be
an early indicator of complications, including ongoing hemorrhage or
abdominal compartment syndrome.
Damage control surgery (abbreviated to control of bleeding and
decontamination of hollow organ ruptures with spillage) may be needed in the
first 24 to 48 hours, before definitive surgery is performed. Many trauma
patients benefit from delayed definitive surgery, particularly the repair of
fractures, during this period of ongoing stabilization. Decisions to proceed
with surgery should be made after appropriate consultation with the primary
surgical service, a critical care physician, and other consultants as indicated.

Some patients will benefit by undergoing

stabilizing procedures such as washout,
debridement, and placement of external fixation
for open fractures followed by delayed definitive
repair.

In the immediate resuscitation period, periodic reassessments are important.

Once a patient is stabilized, all intravenous access sites should be reassessed.
Because full sterile precautions to prevent line-related infections may not be
feasible during emergency vascular access, many lines will need to be
replaced. If central venous access is no longer indicated, it should be
discontinued.
Case Follow-up: An 18-year-old man is in the ICU after sustaining a gunshot
wound to the left chest traversing the diaphragm, left lobe of the liver, and
spleen. He underwent hemostatic resuscitation including packed red blood
cells, fresh frozen plasma, and platelet transfusions. Urine output improved as
did nasogastric drainage.
III. BURN INJURY: INITIAL EVALUATION AND
STABILIZATION

Case Study
A 56-year-old woman is brought to the emergency department after sustaining
injuries in a house fire with an explosion. The patient was found outside the
house, awake, alert, and reporting abdominal pain. On examination, she has
blistering of her cheeks, soot around her nares, and blistering over her
bilateral forearms and chest. You are asked to see the patient in the
emergency department to assist during her initial care.
– What are the initial evaluation priorities?
– What is the greatest risk to this patient?

A. General
Burn injuries represent a significant cause of morbidity and mortality. Near a
half million cases of burn injury occur each year with approximately 40,000
requiring hospitalization. Deaths from burn injury occur with greatest
frequency as a result of residential fires with smoke inhalation. Like other
forms of injury, burns tend to be frequent in the young and the elderly.
Scalds are the most common form of childhood injury, whereas electrical and
chemical injuries affect adults in the workplace. In 1975, mortality was
approximately 25% for severe burns; however, with improvements in burn
care, mortality is now around 4%. Factors that affect burn mortality include
size of cutaneous injury, patient age, and presence or absence of inhalation
injury. Burn injuries should not distract providers from seeking other potential
traumatic injuries. The initial evaluation and treatment of a serious burn
injury follows the same pathway as trauma, including the primary and
secondary surveys.
B. Airway/Breathing
The initial evaluation of the airway is directed, in part, by the history of the
injury. Patients who are at the greatest risk of smoke inhalation injury
typically have a history of being in a closed space with flame and smoke. With
increased exposure time, the likelihood of injury increases. Smoke inhalation
injury can be described by three mechanisms. These include particulate
injury, toxic byproducts of combustion injury, and direct thermal injury.
Particulates found in the soot and smoke of the fire are responsible for a
reactive airway injury that may result in bronchospasm. Toxic exposure may
have a direct cytotoxic effect on alveolar tissue or affect energy-generating
pathways, or bind hemoglobin and reduce the availability of oxygen for
intracellular use. Direct thermal injury can result in oral, nasal, and upper
respiratory injury with airway swelling.

At room air, the half-life of carbon monoxide in

association with hemoglobin is 3 to 4 hours;
breathing 100% oxygen, the half-life is only 30 to
90 minutes.

Inhalation injury, the leading cause of death in burns, is generally diagnosed

by a combination of clinical signs and symptoms confirmed by bronchoscopy.
Clinical findings include facial burns, parched oral mucosa, nasal singeing,
soot in the oral and nasal passages, and symptoms of reactive airway
exacerbation. Bronchoscopic findings include mucosal edema, ulceration,
sloughing, and mucus plugging. Chest radiographs are frequently normal at
admission, and hypoxemia often is not appreciated. Additional diagnostic
studies to consider are serial arterial blood gases, peak expiratory flow rates,
pulse oximetry, end-tidal CO2, serum lactate, and carboxyhemoglobin.

Three stages of inhalation injury have been identified:

 1. Acute hypoxia with asphyxia typically occurs at the scene of the
fire.
2. Upper airway and pulmonary edema may evolve during the first
hours to days after injury.
3. Infectious complications that stem from exposure to heat and
chemical irritants may appear later (eg, pneumonia).
Treatment of inhalation injury may include supplemental oxygenation and
bronchodilators. If exposure to carbon monoxide is suspected, 100% oxygen
should be provided. Early intubation is advocated, especially if the patient
will be transferred, because pulmonary and laryngeal injury may quickly
evolve even though the initial airway assessment is satisfactory.
Humidification of inhaled gases helps in secretion control and reduces
desiccation injury to the airway. In those patients with potential inhalation
injuries sustained in enclosed spaces, consideration should be given to the
potential for cyanide toxicity in which administration of methemoglobin
generators (eg, amyl nitrate, cyanocobalamin) is indicated.

C. Circulation
Patients with larger burns (> 20% total body surface area [TBSA]) may
develop burn shock. This is the result of a diffuse capillary leak syndrome
resulting from the release of cytokines, interleukins, and vasoactive amines
and causing third spacing of fluid. The combined loss of fluid from the
burned surface area and the interstitial edema may result in the loss of
circulating volume. Systemic hypotension may ensue. Resuscitation following
the American Burn Association recommendations (discussed later) should be
followed because it permits large volumes of fluid to be administered over an
extended period. Large-bore peripheral intravenous catheters should be
placed (through the burn, if necessary). The preferred resuscitation fluid is
lactated Ringer solution. Intravascular resuscitation should not be delayed or
withheld, especially in patients with inhalation injury, because this increases
resuscitation fluid requirements.
D. Assessment of Injury
The approach to the initial assessment is the same as in trauma. An initial
primary survey (ABCDE) is performed, followed by a head-to-toe
examination. All nonadherent clothing must be removed to determine burn
size, and the patient must be covered with blankets because heat is lost
quickly. Depending on the history, the patient may have other injuries and
should be assessed for trauma in accordance with the guidelines outlined.

1. Depth of Burns
There are classically three burn depths. However, some describe up to six
degrees of burn injury depending on the involvement of underlying
subcutaneous tissue, muscle, and bone. For this course we will use four burn
depths:
1. Superficial (first-degree): erythematous, painful
2. Partial thickness (second-degree)
a. Superficial: painful, pink, edematous, and blistered
b. Deep: red or mottled red and white, pinprick perceived as
pressure as opposed to pain, +/- blisters
3. Full thickness (third-degree): white, leathery, painless
4. Fourth-degree: all layers of skin, fat, muscle, and bone
Full-thickness injuries and deeper usually require surgical intervention.

2. Burn Area (Rule of Nines)

The rule of nines is commonly used to estimate the surface area that has been
burned (Figure 12-2). The head and upper extremities each represent 9% of
the TBSA. The anterior and posterior trunk and the lower extremities each
represent 18%, and the perineum represents 1% of the TBSA. In children,
the head is proportionally larger, leading to a relative decrease in the area of
other body segments. Alternatively, the patient’s palm, which equals roughly
1% of TBSA, may be used to estimate the size of a small or irregular burn.
An often-used tool to estimate the TBSA in children younger than 15 years is
the Lund-Browder Chart (Figure 12-3).

Figure 12-2. Rule of Nines

Most appropriate for adults and children over 15 years of age.

 Figure 12-3. Lund-Browder Chart

The Lund-Browder chart is the most accurate method for estimating burn extent and must
be used in the evaluation of pediatric patients under 15 years of age.

E. Resuscitation
Burn shock presents during the first 24 to 48 hours with profound
hypovolemia, which has both interstitial and intracellular components.
Increased capillary permeability is one of the key components of the burn
shock response. In small burns, maximal edema is seen 8 to 12 hours after
injury; larger burns at 12 to 24 hours. Plasma volume loss coincides with
edema formation and increased extracellular fluid. Edema is affected by fluid
administration during resuscitation. Fluid and electrolytes should be replaced
as dictated by organ perfusion indicators and electrolyte imbalance. Because
fluid and electrolyte losses in burns are primarily insensible, fluid lost cannot
be quantified adequately. Venous access should be obtained and a urinary
catheter placed. In the 2018 update to Advanced Burn Life Support, the
American Burn Association recommends fluids in patients older than 14
years of age initiated at 500 mL/h with rapid titration to weight-based fluid
infusion rates. For scald or flame burns, infants and young children weighing
less than or equal to 30 kg should receive 3 mL lactated Ringer per kg per
%TBSA and D5LR at maintenance rate. Children younger than 14 years of
age should receive 3 mL per kg per % TBSA; adult and older children should
receive 2 mL per kg per %TBSA. The rates are increased for electrical burns.
All patients with electrical burns should receive 4 mL lactated Ringer per kg
per %TBSA; however, infants and children should receive additional D5LR at
maintenance rate.

Although volume resuscitation formulas give a

good estimate of the initial volume requirements
for resuscitation in the critically burned patient,
the most important indicator of appropriate
resuscitation is adequate urine output.

Beginning at the low end may reduce edema and extra-vascular complications
such as abdominal compartment syndrome. The TBSA is calculated only for
second- or third-degree burns. Resuscitation is carried out with lactated
Ringer solution. Half of the crystalloid resuscitation should be administered in
the first 8 hours after time of injury, the remaining over the next 16 hours.
Confirming adequacy of resuscitation is more important than strict adherence
to formulas. Surrogate markers of adequate resuscitation include
normalization of blood pressure, heart rate, and urine output. Appropriate
urine output in adults is 0.5 to 1 mL/kg/h and in children > 30 kg up to age
17 is 0.5mL/kg/h and young children < 30 kg is 1mL/kg/h. An arterial
blood gas measurement to monitor the pH and base deficit and serum lactate
levels are also good markers of adequate resuscitation. Although appropriate
resuscitation is critical to maintain physiology, care must be taken to avoid
over-resuscitation because this can lead to significant increases in peripheral
edema, pulmonary edema, compartment syndromes, and result in increased
morbidity of the burn injury. Once target urine output is reached, a gradual
reduction of IV fluid administration is advised to prevent over-resuscitation.
F. Escharotomy
A circumferential burn to an extremity may develop significant edema that the
underlying tissue cannot accommodate because of the constrictive nature of
the burn wound. Impaired limb and tissue perfusion may ensue that can only
be managed by performing an escharotomy to the extremity and/or digits. In
larger burns of the abdomen and chest wall, a compartment syndrome may
develop whereby cardiovascular and respiratory compromise may mandate
torso escharotomies or abdominal decompression. Surgical consultation
should be sought immediately for any of these problems.

G. Carbon Monoxide Exposure

A fire in an enclosed space mandates consideration of carbon monoxide
poisoning in addition to the worry for inhalation injury. The typical oxygen
saturation monitor will not detect carbon monoxide and can give artificially
elevated oxygen saturation levels; therefore, if carbon monoxide poisoning is
suspected, an arterial blood gas with a carboxyhemoglobin level will clarify
the clinical picture. High-flow 100% oxygen will reduce the half-life of carbon
monoxide in the plasma and is the primary treatment. Early use of hyperbaric
oxygen for patients with high carboxyhemoglobin levels (> 25%) or evidence
of significant neurologic or cardiovascular toxicity has been recommended,
but data supporting this recommendation are limited.

H. Burn Wound
Local wound care begins with serial debridement of nonviable tissue and
blisters by appropriate surgical consultants. Little care, other than covering
with a dry clean dressing to prevent hypothermia, is required for the burn
wound before transfer to the burn center or surgical consultation. If gross
contamination is present, a gentle washing and coverage with clean linen may
be appropriate. If the patient cannot be transferred to a burn center within 24
hours, it may be necessary to cleanse the burns with a cleansing agent and
apply appropriate topical antibiotic ointment (ie, silver sulfadiazine or
bacitracin) and occlusive dressings to help prevent evaporative heat loss.
I. Other Considerations
Placement of a nasogastric tube and gastrointestinal stress ulcer prophylaxis
are indicated if the patient vomits, requires intubation, or has a burn > 20%
of TBSA. This may also prove beneficial to provide nutritional support for
large burns, given the high nutritional requirements. Intravenous opiates
should be given for pain. Rings and bracelets should be removed because
they may cause constriction early in resuscitation. Burns are tetanus-prone
injuries, and tetanus prophylaxis should be reviewed (Table 12-3).

J. Special Considerations
1. Chemical Burns

Hydrofluoric (HF) acid burns can be particularly

destructive, coagulating the skin on exposure as
a result of fluoride ions penetrating the skin
combining with cellular calcium and magnesium,
requiring urgent wound excision. HF acid is
commonly used in circuit boards, cleaning
solvents, and paint removers.

Chemical burns may be caused by acid (eg, cleaning products, industrial

applications), alkali (eg, hydrides of sodium, potassium, and sodas of
ammonia), or organic compounds (eg, petroleum products). Severity of injury
relates to the agent involved, its concentration, and the duration of contact.
Initial care requires removing the patient from the source of chemical injury
immediately. In general, removal of clothing is essential. Dry substances
should be brushed off and the area irrigated copiously with water. Do not use
neutralizing agents because they may increase the severity of burn.
Contact with petroleum products (such as spilled gasoline at the scene of a
motor vehicle crash) is associated with rapid skin penetration and late
multiple-organ failure. Again, rapid removal of the patient from the source
and vigorous irrigation of exposed surfaces are warranted. Advice regarding
chemical burns is available from regional burn centers.

2. Electrical Injury
Electrical injury is a syndrome with a variety of presentations. Exposure to an
electrical source of < 440 volts produces a low voltage injury similar to other
cutaneous burns. When exposure exceeds 1,000 volts, a greater potential for
deep as well as cutaneous injury exists.
Three types of skin injury can occur with electrocution:
1. Entrance and exit wounds, typically circumscribed, deep lesions,
occur at points of contact with the electrical source or ground
(usually hands and feet).
2. Cutaneous burns may be caused by arc injury from the primary
site to the patient, a flash injury, or an actual flame injury if
clothing catches fire.
3. Deep soft-tissue injuries involve muscle, nerve, or the vascular
bed as current passes through the tissue.
Beware of pneumothorax, airway compromise, cardiac arrest, and blunt
injury secondary to falls and violent muscle contraction. Muscle compartment
pressures may increase, necessitating fasciotomy, not just escharotomy. If
myoglobin is present in the urine or creatine kinase concentrations are
elevated, provide adequate intravascular fluid to increase the urine output to
3 to 4 mL/kg/h until resolution of the rhabdomyolysis. Patients may develop
ileus after electrocution. The ECG should be reviewed in electrical injury.

The initial priority in the management of electrocution is removal of necrotic

tissue and decompression of compromised deep tissue compartments,
particularly muscle. Resuscitation is begun at 4 mL/kg/% TBSA cutaneous
injury and titrated to maintain a urine output of 0.5 to 1 mL/kg/h unless
rhabdomyolysis is present and higher urine output is desirable. Aggressive
fluid resuscitation potentiates filtering of pigment and dilution of iron
(nephrotoxic). Alkalinization of the urine may be considered to decrease the
nephrotoxic potential despite lack of supportive evidence. If large areas of
soft-tissue injury are present, surgical consultation should be requested.
As with other burns, infection is the chief risk, but other potential problems
are myocardial and vascular injury, encephalopathy, cataracts, and bowel
perforation.
Lightning injury may be thought of as massive exposure to direct current.
Most injury is topical because exposure times are extremely brief. Mortality
rates associated with lightning relate to early cardiac and respiratory arrest.
Aggressive basic and advanced life support may be lifesaving for these
patients.

IV. REFERRAL AND TRANSFER CONSIDERATIONS

Early involvement of surgical expertise is important in the care of the injured
patient. A surgeon should be summoned as soon as it is known that a
seriously injured patient is arriving. Early neurosurgical consultation is
advised for patients with head injury.
General guidelines for field triage and interfacility transfer have used
physiologic, anatomic, and high-risk mechanistic criteria to suggest triggers for
triage and transfer. One may extrapolate that these parameters can be used to
initiate involvement of a trauma surgeon as well. The criteria for transfer of
patients to burn centers according to the American Burn Association:
Partial-thickness burns on greater than 10% TBSA
Burns involving the face, hands, feet, genitalia, perineum, and
major joints
Third-degree burns in any age group
Electrical burns, including lightning injury
Chemical burns
 Inhalation injury
Significant burns in patients at the extremes of age or with
significant comorbid disease
Patients with combined trauma and burn injury whose burn care
supersedes the trauma care*
Children at hospitals without qualified personnel or equipment to
care for pediatric burn patients
Burn injury in patients who will require special social, emotional,
or rehabilitative intervention
*Patients with severe trauma with burns should be addressed at the nearest trauma center prior to
consideration for transfer to burn center. For additional information on burn transfer criteria, see
https://ameriburn.org/public-resources/burn-centerreferral-criteria/. Some additional triggers are
suggested in Table 12-4.

If appropriate surgical services are unavailable, early transfer to the closest

trauma or burn center should be initiated. This should not be delayed for
additional radiologic studies if surgical resources are unavailable unless those
studies are requested by the accepting physician. The trauma center should
be contacted for advice and to discuss potential problems or concerns with
transport personnel.
Common pitfalls in the transfer of seriously ill patients include failure to
intubate before transfer, failure to recognize the need for transfer to a higher
level of care, and a general failure to stabilize the patient adequately before
transport. Unrecognized ongoing hemorrhage, delayed onset of tension
pneumothorax, and reversible/preventable causes of secondary brain injury
must be considered.
Case Follow-up: A 56-year-old woman is brought to the emergency
department after sustaining injuries in a house fire with an explosion. She was
intubated and placed on mechanical ventilation while her inhalation burns
improved. She sustained a pneumothorax that required tube thoracostomy
placement. The woman also underwent angioembolization of a splenic
laceration with active extravasation of intravenous contrast.
 Table 12-4 Indications for Field Triage and Interfacility Transfera

Adapted from Centers for Disease and Prevention. Guidelines for field triage of injured patients:
Recommendations of the National Expert Panel on Field Triage, 2011. MMWR Recomm Rep.
2012;61(1):1-21.
Key Points
Basic Trauma and Burn Support
The first goal in trauma management is to identify and treat
immediately life-threatening injuries by following the ABCDE
sequence of priorities.
After blunt trauma, airway control should proceed on the
assumption that an unstable cervical spine injury exists.
A diagnosis of tension pneumothorax should be based on clinical
criteria and not on a chest radiograph.
Hemorrhage is the most likely cause of shock after injury, and
initial empiric treatment consists of crystalloid infusion to normalize
blood pressure, reverse tachycardia, and maintain adequate organ
perfusion.
In general, blood should be added to resuscitation early if the
response is inadequate or if continued ongoing hemorrhage is
suspected. Uncrossmatched, type-specific blood can be
administered safely.
A secondary assessment includes a head-to-toe examination to
identify and treat potentially life-threatening injuries.
Computed tomographic scanning is essential for the initial
evaluation of head-injured patients with a depressed level of
consciousness.
Burn resuscitation is proportional to the area sustaining second-
and third-degree burns and is titrated to signs of perfusion.
Adequate urine output is one of the key indicators of adequate
resuscitation.
Closed-space smoke inhalation injury places the patient at high risk
for upper airway and inhalation injury that may not be obvious at
 the initial presentation.
Surgical expertise should be secured early and transfer considered
for those patients who require a higher level of care.
Transfer to a specialized care setting should not be delayed for
additional radiologic studies unless the accepting physician
requests the studies.

Suggested Readings
1. American Burn Association. Advanced Burn Life Support Course
Provider Manual. 2018 Update. Chicago, IL: American Burn
Association; 2018.
2. American College of Surgeons Committee on Trauma. Advanced
Trauma Life Support for Doctors (ATLS): Student Course
Manual. 10th ed. Chicago, IL: American College of Surgeons;
2018.
3. American College of Surgeons Committee on Trauma. Guidelines
for the operation of burn centers. In: Resources for Optimal
Care of the Injured Patient. Chicago, IL: American College of
Surgeons; 2014:100-104.
4. American College of Surgeons. Hartford Consensus Compendium.
Bulletin of the American College of Surgeons. 2015;100(1S):1-
88.
5. Bagley LJ. Imaging of spinal trauma. Radiol Clin North Am.
2006;44(1):1-12.
6. Brain Trauma Foundation. Management and prognosis of severe
traumatic brain injury. J Neurotrauma. 2007;24(Suppl 1):i-
S106.
 7. Chan O, Wilson A, Walsh M. Major trauma. BMJ.
2005;330(7500):1136-1138.
8. Cheatham ML, Malbrain ML, Kirkpatrick A, et al. Results from
the International Conference of Experts on Intra-abdominal
Hypertension and Abdominal Compartment Syndrome, II:
Recommendations. Intensive Care Med. 2007;33(6):951-962.
9. Elliott DC. An evaluation of the end points of resuscitation. J Am
Coll Surg. 1998;187(5):536-547.
10. Gunst M, Ghaemmaghami V, Gruszecki A, et al. Changing
epidemiology of trauma deaths leads to a bimodal distribution.
Proc (Bayl Univ Med Cent). 2010;23(4):349-354.
11. Gonzalez E, Moore EE, Moore HB. Management of Trauma-
Induced Coagulopathy with Thrombelastography. Crit Care Clin.
2017;33(1):119–134. doi:10.1016/j.ccc.2016.09.002
12. Herndon DN, ed. Total Burn Care. 3rd ed. Philadelphia, PA:
Saunders-Elsevier Inc; 2007.
13. Holcomb JB, Jenkins D, Rhee P, et al. Damage control
resuscitation: Directly addressing the early coagulopathy of
trauma. J Trauma. 2007;62(2):307-310.
14. Johnson JW, Gracias VH, Schwab CW, et al. Evolution in damage
control for exsanguinating penetrating abdominal injury. J
Trauma. 2001;51(2):261-271.
15. Latenser BA. Critical care of the burn patient: the first 48 hours.
Crit Care Med. 2009;37:2819-2826.
16. Mattox KL, Moore EE, Feliciano DV, eds. Trauma. 7th ed. New
York, NY: McGraw-Hill; 2012.
17. Morrison CA, Carrick MM, Norman MA, et al. Hypotensive
resuscitation strategy reduces transfusion requirements and severe
postoperative coagulopathy in trauma patients with hemorrhagic
 shock: Preliminary results of a randomized controlled trial. J
Trauma. 2011;70(3):652-663.
18. Pryor JP, Braslow B, Reilly PM, et al. The evolving role of
interventional radiology in trauma care. J Trauma.
2005;59(1):102-104.
19. Rhee P, Nunley MK, Demetriades D, et al. Tetanus and trauma:
A review and recommendations. J Trauma. 2005;58(5):1082-
1088.
20. Rossaint R, Bouillon B, Cerny V, et al. Management of bleeding
following major trauma: An updated European guideline. Crit
Care. 2010;14(2):R52.
21. Sarrafzadeh AS, Peltonen EE, Kaisers U, et al. Secondary insults
in severe head injury: Do multiply injured patients do worse? Crit
Care Med. 2001;29(6):1116-1123.
22. Sasser SM, Hunt RC, Faul M, et al; Centers for Disease Control
and Prevention. Guidelines for field triage of injured patients:
Recommendations of the National Expert Panel on Field Triage,
2011. MMWR Recomm Rep. 2012;61(1):1-21.
23. Society of Critical Care Medicine. Fundamental Disaster
Management. 3rd ed. Mount Prospect, IL: Society of Critical
Care Medicine; 2009.
24. Stengel D, Bauwens K, Sehouli J, et al. Emergency ultrasound-
based algorithms for diagnosing blunt abdominal trauma.
Cochrane Database of Syst Rev. 2005;(2):CD004446. doi:
10.1002/14651858.CD004446.pub2.

Suggested Websites
1. Society of Critical Care Medicine. www.sccm.org
2. American Burn Association. www.ameriburn.org
3. Burn Surgery. www.burnsurgery.org.
4. Brain Trauma Foundation. www.braintrauma.org
5. American Association for the Surgery of Trauma. www.aast.org
6. Eastern Association for the Surgery of Trauma. www.east.org
7. World Society of the Abdominal Compartment Syndrome.
www.wsacs.org
8. American College of Surgeons. www.facs.org/quality-
programs/trauma/atls
 Chapter 13
ABDOMINAL SURGICAL
EMERGENCIES: PART 1

Objectives
Recognize the various patient presentations of abdominal emergencies
and determine whether surgical consultation is necessary.
Identify the signs and symptoms of toxic megacolon and discuss the
importance of a multidisciplinary approach to toxic megacolon including
early consultation of surgical and other specialty services.
Compare and contrast etiologies and differing management approaches
for small bowel obstructions (SBO).
Define primary, secondary, and tertiary peritonitis.
Recognize symptoms and grades of acute cholecystitis and discuss
clinical guidelines to select appropriate treatment.
Explain the etiology, presentation, diagnosis, and management of
esophageal perforation.

I. INTRODUCTION
This chapter will review the pathophysiology and management of five common
abdominal surgical emergencies which include toxic megacolon, small bowel
obstruction, peritonitis, biliary emergencies, and esophageal perforation.
II. TOXIC MEGACOLON

Case Study
A 69-year-old man with a medical history including atrial fibrillation and
congestive heart failure was involved in a motorcycle crash and sustained an
open left femur fracture. He underwent open reduction and internal fixation
(ORIF) of his femur fracture 3 days ago and received cephalosporin and
gentamicin preoperatively. This morning his WBC is 17,000/mm3, his
abdomen is tender without peritonitis, and he had multiple loose bowel
movements overnight.
– Which differential diagnoses need to be considered?
– Which diagnostic tests could provide helpful information?
– Which findings are important in deciding on medical versus surgical
management?

A. Background and Pathophysiology

Toxic megacolon (TM) describes severe total or segmental colonic distension
associated with systemic toxicity and signs of sepsis. An increasing incidence
and severity of Clostridioides difficile infection in hospitals in the United States
has contributed to a rise in the incidence of TM, which was classically
associated with inflammatory bowel disease (IBD). Less common causes of TM
include colitides due to other infections including Salmonella, Campylobacter,
enterohemorrhagic Escherichia coli (E. coli), and cytomegalovirus (CMV),
ischemia, or mechanical obstruction from volvulus or cancer.

A basic understanding of large bowel anatomy is helpful when interpreting

imaging studies. The colon can be divided into the cecum; ascending,
transverse, descending, and sigmoid colon; and rectum. The cecum has the
largest diameter at baseline and is therefore particularly at risk for distension,
ischemia, and perforation. Cecal diameter of more than 10 cm is concerning for
the development of ischemia and perforation, and one of the indications to
consider for surgical intervention or at least immediate decompression. The
transverse colon has the smallest diameter at baseline, and dilation beyond 6
cm is considered “megacolon.” Duration, etiology of colonic dilation, and
clinical examination are more important than absolute diameter with regard to
prognosis and need for interventions.

From inside to outside, the colonic wall consists of mucosa, submucosa,

muscularis, and serosa. Many processes eventually resulting in TM start in the
mucosal layer and therefore patients may not have abdominal pain until further
advancement of this process (Figure 13-1). Similarly, a severely diseased colon
can appear “normal” on the outside during surgical inspection and might result
in false reassurance that the colon is not the etiology of clinical deterioration.

Figure 13-1. Severe Pancolonic Distension

Image courtesy of S. Leichtle, MD, FACS

In TM from inflammatory, infectious, or ischemic etiology, an initially mucosal

abnormality becomes a transmural process which ultimately leads to full-
thickness pathology, peritonitis, and possible perforation. Colonic distension
associated with these processes, or due to mechanical distal obstruction, causes
stretching of the colonic wall, excessive tension, and local ischemia which
progresses to transmural necrosis and perforation.

B. Clinical Presentation and Laboratory Findings

Severe lactic acidosis should raise concern for the

presence of ischemic or necrotic bowel, which is a
surgical emergency.

Acute illness and systemic toxicity are part of the definition of TM and patients
will have leukocytosis (or worse, leukopenia), tachycardia, and likely
hypotension. Other inflammatory markers, such as lactate levels and C-reactive
protein (CRP), are elevated. Severe lactic acidosis should raise concern for the
presence of ischemic or necrotic bowel, which is a surgical emergency. In
addition, patients may present with bloody diarrhea, but the absence of loose
bowel movements should not lead the clinician to abandon a possible diagnosis
of TM because ileus and obstipation are also a possible presentation.
Examination of the patient’s abdomen often demonstrates distension and
tenderness, although true peritonitis is often absent unless perforation has
occurred. Patients who are immunosuppressed either due to underlying
comorbidities or due to their acute critical illness may have less obvious
symptoms or laboratory abnormalities.

As demonstrated in the description of the patient at the beginning of the

chapter, patient presentation and underlying etiology may vary substantially.
TM due to Clostridioides difficle (C. difficle) infection usually follows
worsening diarrhea in the setting of current or recent antibiotic use. Those
patients with IBD often have a history of several days to a few weeks of
worsening symptoms such as bloody diarrhea and malaise leading up to the
acute presentation. Fulminant colitis marked by numerous, bloody bowel
movements can also be the initial presentation of patients with newly diagnosed
IBD. In patients with TM due to CMV, a diagnosis of immunosuppression due
to human immunodeficiency virus (HIV) or transplant is usually present, and in
cases of TM due to other bacterial infections, a history of recent exposure to
risk factors may be elicited.

Acute mechanical obstruction from cancer or volvulus as a cause of TM always

needs to be ruled out. Obtaining a history of risk factors or associated
symptoms is important. However, TM also needs to be considered in the
intubated, critically ill patient for whom only a limited history and examination
are available.

C. Diagnosis
If circumstances, history, and/or physical examination raise concern for TM, the
actual diagnosis is often confirmed on imaging studies. A supine abdominal
radiograph will demonstrate a severely distended colon (Figure 13-1) or signs
of mechanical obstruction such as the classic “coffee-bean” sign of sigmoid
volvulus or apple core lesion of colorectal cancer. An upright chest radiograph
or lateral decubitus abdominal radiograph will demonstrate free air in the
setting of perforation, which would indicate a very severe presentation or late
diagnosis of TM. In patients in whom the diagnosis is in question, a computed
tomography (CT) scan of the abdomen and pelvis should be performed. A CT
scan allows for more accurate determination of colon diameter (Figure 13-2),
visualization of signs of bowel ischemia (pneumatosis or wall thickening), and
can rule out the presence of distal obstruction. To achieve these goals, the CT
scan should be performed with IV contrast and careful (risk of perforation)
administration of rectal contrast.
In patients who cannot undergo CT imaging or in whom the diagnosis still is
unclear, further clarification can be done with bedside sigmoidoscopy. This
bedside procedure can be performed in the intensive care unit in patients who
are too unstable to travel to the CT scanner. Sigmoidoscopy can demonstrate
signs of C. difficile infection (pseudomembranes), mucosal necrosis (ischemic
colitis), or ulcerations (IBD). Bedside sigmoidoscopy needs to be performed
with extreme care with little to no insufflation to decrease the risk of iatrogenic
perforation, which nevertheless exists. Full colonoscopy should not be
performed due to the excessive risk of perforation.

Figure 13-2. Distention of Transverse Colon

Image courtesy of S. Leichtle, MD, FACS

D. General Management
When the initial workup raises concern for colonic distension and megacolon,
the following steps should rapidly be instituted (not all might be applicable to an
individual patient).

Strict nil per os (NPO) and decompression with a nasogastric tube.

The latter does not decompress the colon, but it is helpful if ileus is
present because this is common in critical illness.
Surgical consultation to assess for surgical intervention and help with
interventions such as decompression via rectal tube or bedside
procedures such as sigmoidoscopy.
 Any electrolyte abnormalities (common are abnormal potassium,
magnesium, and phosphorus levels) need to be aggressively treated.
A rectal examination needs to be performed carefully to rule out
distal obstruction and assess for melena. A rectal tube (a soft catheter
such as a large indwelling catheter) can be inserted, which may help
with decompression.
Attention should be paid to the fluid status of the patient and
appropriate resuscitation should be ensured.

Unless the patient has indications to immediately undergo surgical intervention

(see the following), the next steps include:
Serial abdominal examinations and abdominal radiographs with a
focus on worsening pain, development of peritonitis, enlarging
diameter of the colon, or presence of free air.
Serial complete blood count (CBC) and lactate measurements, with
particular attention to worsening leukocytosis, worsening anemia, and
increasing lactic acidosis.
Further workup to confirm the diagnosis (if not yet established), such
as testing for Clostridioides difficile (C. difficile) and presence of
CMV.
If C. difficile infection is confirmed or suspected, empiric treatment
for C. difficile should be initiated (see next section). For other
etiologies, broad antibiotic coverage against gram-negative and
anaerobic bacteria (eg, piperacillin/tazobactam) and/or specific
treatment (ie, ganciclovir for CMV colitis) should be initiated.
Mechanical obstruction as a cause of TM requires surgical or
procedural intervention (see next section).

Laxatives and motility agents are absolutely

contraindicated because they might precipitate
colonic perforation, and opioid pain medication
 should be avoided or limited because it further
diminishes intestinal motility.

E. Specific Management for Important Causes of Toxic Megacolon

1. Clostridioides difficile Infection

Medical management of severe Clostridioides difficile (C. difficile) infection

with or without TM includes stopping causative antibiotics (if possible) and
initiating specific antibiotic therapy against C. difficile. A 10-day course of
either oral vancomycin or fidaxomicin is recommended for an initial infection.
In fulminant, or severely ill and/or complicated infection, oral vancomycin is
preferred. If patients have ileus and are unable to tolerate oral vancomycin, it
can be administered rectally every 6 hours as a retention enema. While no
longer recommended in mild C. difficile infection, IV metronidazole should be
administered along with the oral or rectal vancomycin in patients with fulminant
C. difficile infection. Patients who experience a recurrence of C. difficile
infection should be managed with either a tapered and pulsed vancomycin
regimen or 10 days of fidaxomicin (if not used for the initial episode). There is
no evidence that longer courses of vancomycin or fidaxomicin are helpful, even
in those with fulminant disease. For patients with multiple recurrences of C.
difficile infection despite appropriate antibiotic treatment, fecal microbiota
transplantation should be considered.

The mortality of advanced C. difficile infection with TM is excessive and there

should be a low threshold for considering surgical intervention, despite the
morbidity of a major operation. Patients with peritonitis or perforation have a
clear indication for emergent operation, but those with severe leukocytosis
(WBC more than 20,000/mm3), worsening lactic acidosis, or septic shock
without another obvious source, may also benefit from early surgical
intervention. Among the risk factors for death were age 70 years or older,
severe leukocytosis (35,000/mm3) or leukopenia, and a need for vasopressors
or mechanical ventilation. In the operating room, a subtotal colectomy (ie,
leaving a short rectal stump behind) with end ileostomy is the current standard
treatment. Due to the high morbidity and mortality of a subtotal colectomy,
particularly in elderly and/or critically ill patients, other surgical strategies are
being studied and used. The most promising of these consists of colonic lavage
via loop ileostomy which allows for colonic preservation. There is, however, a
risk of residual or recurrent C. difficile infection, and this novel approach
should only be considered in experienced hands. In elderly, multi-morbid
patients, a frank family discussion about expected outcomes and goals of care
as well as involvement of the palliative care service, if available, are important.

2. Inflammatory Bowel Disease

The indications for emergent surgical intervention are similar as for other
causes of TM and include impending perforation, peritonitis, worsening clinical
examination and/or laboratory studies, or lack of improvement with optimal
medical treatment within 48 to 96 hours. Colectomy should also be considered
for persistent, intractable symptoms of IBD. Immunosuppressive medications
can be part of the medical regimen of patients with IBD and obscure their
presentation by preventing the development of severe leukocytosis or clear signs
of peritonitis.

For medical management, consultation of the specialty service for IBD (often
gastroenterology or colorectal surgery) should be initiated early to optimize
medical management. Initial treatment includes IV steroids such as
hydrocortisone or methylprednisolone, while medications for maintenance
therapy, such as sulfasalazine and 5-ASA compounds, are not used in TM.
Immunomodulators may be used if conventional medical therapy fails.

3. Mechanical Obstruction
TM as a result of mechanical obstruction suggests a late presentation. Rectal
examination or, more frequently, imaging such as abdominal radiograph or CT
scan will suggest an obstructing mass (eg, due to cancer or a benign stricture)
or volvulus. Whereas a sigmoid volvulus can be decompressed colonoscopically
followed by non-emergent surgical colectomy, any volvulus causing TM, or any
complete colonic obstruction due to a mass is a surgical emergency. In select
cases of obstructing masses, colonoscopic stenting can be an option, while
surgical therapy consists of partial or total colectomy. In frail patients who are
considered to be poor candidates for colectomy, decompressive loop colostomy
is an option to provide temporary decompression.

III. SMALL BOWEL OBSTRUCTION

Case Study
A 75-year-old woman with a history of hypertension and type 2 diabetes
mellitus arrives to the emergency department reporting abdominal pain for the
past 3 days associated with nausea and vomiting. Her last bowel movement was
4 days ago. Her vital signs reveal a blood pressure of 90/68 mm Hg, heart rate
of 110 beats/min, respiratory rate of 24 breaths/min, and temperature of 38° C
(100.4° F). Her oxygen saturation on room air is 90%, but she reports dyspnea
only with exertion. Her oxygen saturation increased to 96% on 2 liters of
oxygen. You are called to evaluate her.
– Based on patient clinical findings, what are the potential differential
diagnoses?
– What tests are indicated immediately?

A. Introduction
Small bowel obstruction (SBO) is a common reason for consultation in the
emergency department and inpatient setting. The presentations range from mild
abdominal distension and nausea to peritonitis and critical illness. Morbidity
and mortality rates rise dramatically in the setting of bowel ischemia, requiring
immediate recognition and treatment. Prompt and detailed clinical history, early
recognition, and intervention are keys to minimizing morbidity and mortality.
Clinical presentation and radiographic findings both need to be considered
when making management decisions because they do not necessarily correlate.

B. Etiology
There are three main causes of SBO. In Western countries the most common
cause is adhesive disease, accounting for 65% to 75% of cases. While there are
a very small number of patients who can have adhesions in the absence of prior
abdominal surgeries, in general, the diagnosis of adhesive SBO should not be
made in the absence of an abdominal surgical history. The second most
important cause of SBO is hernias (often ventral and inguinal, but also including
internal hernias without obvious findings on examination). In developing
countries, hernias are the leading cause of SBOs with the third important cause
being malignancy. Other less common causes of SBO include inflammatory
bowel disease, intussusception, volvulus, gallstones, trauma, foreign bodies, and
bezoars.

C. Types
SBO can be categorized as partial, high-grade, complete, or closed-loop. The
risk of bowel compromise and need for surgical management increase with
worsening degree of obstruction (a true closed-loop obstruction requires
immediate surgical attention), but general clinical presentation is more
important than radiographically determined degree of obstruction. More
recently, there have been attempts to develop a systematic approach to
categorize the clinical findings, severity, and outcomes.

Complete bowel obstruction is a complete occlusion of the lumen without

allowing a path for gas or abdominal fluid content to pass at the obstruction site.

Partial bowel obstruction is the narrowing at the site of the obstruction of the
lumen; gas and abdominal fluid content are still able to pass at some level.

Closed-loop bowel obstruction is a segment of bowel that is obstructed at two

points preventing prograde and retrograde decompression. This leads to a rapid
increase in intraluminal pressure, distension, ischemia, and perforation if not
addressed urgently.

D. Initial Assessment
 Hemodynamic instability, organ failure, severe
leukocytosis, and lactic acidosis are concerns for
bowel ischemia and a surgical consult should be
obtained immediately.

Initial assessment of an SBO needs to focus on ruling out intestinal strangulation

or presence of irreversible bowel ischemia, both of which require emergent
surgical exploration. The physical examination includes determining the degree
of abdominal distension, pain, or presence of peritonitis. Hemodynamic
instability, organ failure, severe leukocytosis, and lactic acidosis are concerns
for bowel ischemia and a surgical consult should be obtained immediately.
Patients also need to undergo a thorough examination from “head-to-toe” to
detect ventral, flank, inguinal, or femoral hernias. Initial assessment and
evaluation of a patient’s fluid status is essential in SBO because most patients
are severely dehydrated with concomitant acute kidney injury.

E. Diagnosis
1. Radiographic Examinations

Radiographic examinations are critical to the diagnosis and severity of SBO.

Initial imaging studies include supine or upright abdominal radiographs. Lateral
decubitus radiographs or an upright chest radiograph can rule out the presence
of free air (ie, perforation). Small bowel dilation (Figure 13-3A and 13-3B),
multiple air-fluid levels in the small bowel, or a “string of beads” sign suggest
the diagnosis of SBO.
 Figure 13-3A and 13-3B. Small Bowel Dilatation

A CT scan of the abdomen and pelvis with IV contrast is the best imaging
modality to assess a patient with suspected SBO with high sensitivity and
specificity. The classic CT appearance of an SBO includes a lead point with
small bowel dilatation proximally and decompression distally (Figure 13-4).
 Figure 13-4. Small Bowel Obstruction with Transition Point (arrow)

Image courtesy of S. Leichtle, MD, FACS

However, often a clear transition point cannot be visualized on imaging. CT

imaging can also demonstrate mesenteric swirling or a C-shaped segment of
small bowel concerning for closed-loop obstruction. An abdomen/pelvis CT can
also detect hernias as a cause of the SBO that might have been missed on
physical examination (ie, a femoral hernia or internal hernia). CT with IV
contrast should be given whenever possible because it allows for the detection
of ischemic bowel, characterized by increased bowel wall thickness or
pneumatosis.

Other radiographic examinations may include fluoroscopic small bowel follow

through (SBFT) or abdominal radiograph with water-soluble oral contrast.
These should only be performed in clinically stable patients in whom
perforation has been ruled out. These examinations provide further evaluation
of the degree of the bowel obstruction and there may be therapeutic benefit, the
latter remains controversial.

2. Laboratory Examinations
Routine laboratory assessment should include a CBC, basic metabolic panel,
and lactate level. Coagulation panel and type and screen should be added if
surgical intervention is likely. Severe, persistent, or worsening leukocytosis
and/or lactic acidosis in the presence of a SBO are concerning for ischemic
bowel and should prompt surgical consultation. Most patients with SBO have
electrolyte abnormalities and are dehydrated due to nausea, emesis, and
inadequate oral intake. They often present with acute kidney injury and may
have hyperkalemia. A basic metabolic panel in addition to calcium, magnesium,
and phosphorus levels is important to obtain to address these abnormalities. An
infrequent cause of SBO is “gallstone ileus,” in which imaging and an abnormal
hepatic panel are helpful in this case.

F. Management
1. Nonsurgical Management

Patients with SBO and little improvement after

48–72 hours of nonsurgical management or
worsening clinical examination and/or laboratory
studies should strongly be considered for surgical
consultation.

Nonsurgical patients with SBO should have strict NPO status and placement of a
nasogastric tube to decompress the gastrointestinal (GI) tract, resuscitation with
balanced crystalloid solutions such as lactated ringer solution, and correction of
electrolyte imbalances. Acute kidney injury due to dehydration is often present
and patients are at risk for electrolyte abnormalities and fluid overload. Patients
with SBO and little improvement after 48–72 hours of nonsurgical management
or worsening clinical examination and/or laboratory studies should strongly be
considered for surgical consultation. Nontoxic patients with adhesive obstruction
etiology who do not improve early in their course may be candidates for enteral
hypertonic water-soluble contrast challenge which can be therapeutic by
decreasing bowel wall edema and stimulating bowel peristalsis.
2. Surgical Management

Most patients requiring surgical management of their SBO are comprised of

those who either failed to respond to nonsurgical management or had findings
concerning for bowel ischemia on initial presentation. Either exploratory
laparotomy or diagnostic laparoscopy is the surgical intervention. The latter is
absolutely contraindicated in patients with hemodynamic instability. Relative
contraindications to laparoscopic (ie, minimally invasive) exploration are severe
bowel distension, multiple prior abdominal surgeries, and lack of experience
with advanced laparoscopy. Preoperatively, patients (or their families) need to
be informed that extensive bowel resection, stoma creation, and further
reoperations might be necessary. Patients with extensive bowel necrosis might
be dependent on total parenteral nutrition postoperatively, and some patients
might have surgical findings not compatible with curative treatment.
Fortunately, in many patients, lysis of adhesions or sometimes transection of a
single adhesive band can resolve their SBO and postoperative recovery can be
fast. Patients with SBO due to hernias require reduction of their hernia,
possible bowel resection, and hernia repair, depending on the type of hernia
and intraoperative findings (Figure 13-5).

Figure 13-5. Summary and Algorithm for Management of Small

Bowel Obstruction
Postoperatively, patients need to be monitored closely. Even after successful
lysis of adhesions or reduction of a hernia, they are at risk for postoperative
ileus, delayed development of missed ischemic bowel, and abdominal
compartment syndrome. The latter is of particular concern in patients who
underwent aggressive fluid resuscitation.

IV. PERITONITIS

Case Study
A 58-year-old man with a history of diverticulosis presents with diffuse
abdominal pain, nausea, vomiting, and fever. He reports a preceding 5-day
history of worsening nausea, abdominal discomfort predominantly in the left
lower abdomen, and malaise. On examination, he has a diffusely tender
abdomen with guarding.
– What is the patient’s likely diagnosis based on his clinical findings?
– What diagnostic studies are indicated?

A. Definition
Peritonitis is defined as inflammation of the peritoneum. It can be classified into
primary, secondary, and tertiary peritonitis.

Primary Peritonitis – often referred to as spontaneous bacterial peritonitis

(SBP). It can occur from spontaneous bacterial invasion of the peritoneal cavity
and usually occurs in the immunocompromised individual such as a patient with
cirrhosis.

Secondary Peritonitis – peritoneal infections secondary to an intra-abdominal

source such as hollow viscus perforation, necrotic bowel, nonbacterial
peritonitis, or penetrating infectious process. This is the most common form of
peritonitis.

Tertiary Peritonitis – characterized by persistent or recurrent infections after

adequate initial therapy. It usually follows after surgical attempts to treat
secondary peritonitis and can be seen in the immunocompromised patient.

B. Etiology and Pathogenesis

1. Primary peritonitis – diffuse bacterial infection without the loss of the GI
tract integrity. The highest risk is among patients with decompensated liver
cirrhosis. Approximately 10–30% of patients with cirrhosis and ascites
develop SBP. In most cases, SBP is due to a single organism. The presence
of multiple organisms should raise concern for the presence of secondary
rather than primary peritonitis. The most common gram-negative bacteria
include E. coli (40%), followed by Klebsiella pneumonia, Pseudomonas
aeruginosa, Proteus species, and other gram-negative bacteria. Frequent
gram-positive organisms include Streptococcus pneumoniae and other
 Streptococcus species (30%), as well as Staphylococcus species. Less than
5% of SBP are due to anaerobic organisms.
2. Secondary peritonitis – acute peritoneal infection due to loss of GI tract
integrity or from an inflamed or infected abdominal organ. This can be the
result of hollow viscus perforation, such as perforated sigmoid diverticulitis,
an anastomotic leak in the postoperative setting, or due to severe
inflammation of an abdominal organ such as gangrenous cholecystitis.
Secondary peritonitis can be localized, ie, the “classic” right lower quadrant
pain in acute appendicitis, or diffuse. The latter indicates spread of the
infection throughout the abdominal cavity and urgent need for source control.

Most common gram-negative organisms to cause secondary peritonitis include

E. coli (60%), followed by Enterobactor/Klebsiella species, Proteus species,
and Pseudomonas aeruginosa. Gram-positive organisms include Streptococci
species (28%), followed by Enterococci species, and Staphylococci species.
The most common anaerobic organisms to cause secondary peritonitis are
anaerobes which include Bacteroides (72%), Clostridioides,
Peptostreptococcus, and Peptococcus. Candida species accounts for 2% of
cases. In secondary peritonitis, multiple organisms are usually found in the
peritoneal fluid (Table 13-1).

The vast majority of primary peritonitis is due to a

single organism.

3. Tertiary peritonitis – more commonly occurs in patients who are

immunocompromised and those with significant preexisting comorbidities. It
usually follows an attempt to surgically treat secondary peritonitis and is
almost exclusively associated with a systemic inflammatory response.
4. Chemical peritonitis – Sterile peritonitis caused by irritants such as bile,
blood, barium, or other substances or by transmural inflammation of visceral
organs such as in Crohn’s disease without introduction of bacteria into the
peritoneal cavity.
C. Diagnosis
The diagnosis of peritonitis is primarily clinical. Patients can have focal,
localized peritonitis with voluntary guarding on palpation, or diffuse abdominal
pain with rebound tenderness and abdominal rigidity. Associated symptoms are
often anorexia, nausea, vomiting, diarrhea, fever, tachycardia, and tachypnea.
The latter symptoms can indicate the presence of septic shock, particularly in
the setting of concomitant metabolic acidosis, hypotension, and other organ
system failure.

A high gradient serum ascites albumin gradient

(SAAG >1.1 g/dL) indicates portal hypertension
and suggests a nonperitoneal cause of ascites.

Radiologic tests to affirm the diagnosis of secondary peritonitis can include

plain abdominal radiographs (assessment for free air), ultrasound
(demonstrating an inflamed abdominal organ such as appendix), and CT scan of
abdomen and pelvis. Laboratory tests include complete blood count (CBC),
comprehensive metabolic panel, lactate, and blood cultures.

Table 13-1 Common Causes of Secondary Peritonitis by Regions of the Body

*Iatrogenic trauma can result from endoscopic procedures.

If there is concern for primary peritonitis (SBP) and imaging workup is not
suggestive of secondary peritonitis, paracentesis should be performed prior to
administering antibiotics. The ascitic fluid should be tested for the following:

Aerobic and anaerobic culture (use blood culture bottles)

Cell count and differential
Gram stain
Albumin
Protein
Glucose
Lactate dehydrogenase (LDH)
Amylase
Bilirubin (if fluid is dark orange or brown)

An elevated ascitic fluid absolute polymorphonuclear cell neutrophil (PMN)

count ≥250 cells/mm3, a positive bacterial culture, and absence of secondary
causes of peritonitis, such as bowel perforation, suggest SBP.

D. Management
Source control is the single most important step in the treatment of peritonitis.
In addition, patients need to undergo prompt antibiotic administration and
appropriate fluid resuscitation.
1. Fluid resuscitation – Fluid resuscitation with crystalloids,
supplemented by vasoactive medications, and following current sepsis
treatment guidelines should be initiated promptly. The treatment
strategy should be tailored to the individual patient and adjusted based
on patient response.
2. Source Control – Elimination of the source of infection is the single
most important step in the treatment of peritonitis. Depending on the
etiology, this may include surgical intervention, placement of
percutaneous drains, or administration of broad antibiotic coverage.
Managing source control early is important in preventing severe
adverse consequences. Determining whether the intra-abdominal
infection is uncomplicated (limited to a single organ) or complicated
(spread to involve the entire abdominal cavity) can be helpful when
deciding on how aggressive treatment needs to be, but most
importantly requires individual patient assessment and early surgical
consultation.
3. Antimicrobial Therapy – The choice of antibiotics should be based
on the patient’s clinical condition, risk for multidrug-resistant bacteria,
and the local resistant epidemiology. In critically ill patients, antibiotic
coverage should be broad initially, and then tailored to specific micro-
organisms once this information becomes available. First choice in
patients, even critically ill but somewhat stable, is either cefotaxime or
ceftriaxone. Beta-lactam/beta-lactamase inhibitor combinations and
carbapenems are effective against gram-positive, gram-negative, and
anaerobe organisms. For severe infections, piperacillin/tazobactam,
meropenem, or the combination of a third- or fourth-generation
cephalosporin or ertapenem with metronidazole are common empiric
regimens. Ceftazidime and cefoperazone are third-generation
cephalosporins with antipseudomonal coverage. Eravacycline is a
viable option for complicated infections where P. aeruginosa is not a
concern, particularly in patients with beta-lactam allergies or in those
with extended spectrum betalactamase (ESBL) infections. It has a wide
spectrum of activity including many ESBL and carbapenemase-
producing organisms, anaerobes, Acinetobacter baumannii,
methicillin-resistant Staphylococcus aureus (MRSA), and vancomycin-
resistant Enterococcus (VRE). Ciprofloxacin and levofloxacin are no
longer first-line treatment in many geographic regions due to a
prevalence of fluoroquinolone resistance. However, fluoroquinolones
can be used for patients with an allergy to beta-lactams but only in
combination with metronidazole. Eravacycline is a viable treatment for
complicated infections due to its favorable activity against anaerobic
 organisms, enterococci species, several extended-spectrum beta-
lactamase (ESBL) and carbapenemase-producing Enterobacteriaceae,
and Acinetobacter species.

The single most important step in the treatment of

peritonitis is source control.

In patients who underwent source control of uncomplicated intra-abdominal

infections such as non-perforated appendicitis or cholecystitis, postoperative
antibiotic coverage is not recommended. In patients with complicated intra-
abdominal infection who have undergone source control via surgical
interventions, a 3- to 5-day course of antibiotics postoperatively is
recommended. Patients with ongoing sepsis or peritonitis beyond 5 to 7 days of
antibiotic treatment should warrant a diagnostic investigation. Single or multiple
antibiotic regimens may be used.

V. BILIARY EMERGENCIES
A. Introduction
Diseases of the gallbladder and biliary system are among the most commonly
encountered urgent and emergent surgical problem. Presentations range from
infectious or inflammatory problems, such as gallstones, pancreatitis, or
cholangitis, to the result of external or iatrogenic trauma. Patients’ acuity can
range from minor abdominal discomfort to life-threatening critical illness, ie, in
cases of severe pancreatitis with a mortality of 15% to 20%. These patients are
commonly managed in an ICU setting.

B. Initial Assessment
Patients presenting with the severe forms of gallbladder and pancreas-related
disease such as cholangitis or necrotizing pancreatitis are at risk for distributive
and/or hypovolemic shock, septic, and sometimes hemorrhagic shock. In
addition, patient condition is often worsened as a result of dehydration from
vomiting and poor oral intake. Rapid assessment and source control are
essential. The preferred resuscitation solution for septic and/or hypovolemic
shock is balanced crystalloids. Concomitantly with resuscitation, patients must
undergo investigation to determine the etiology of the biliary disease.
Laboratory tests, diagnostic imaging, and a patient’s history and events leading
up to presentation (duration of pain) should be used to quickly determine the
etiology and guide further treatment. Depending on the level of instability,
diagnostic imaging will range from abdominal ultrasound (Figure 13-6), which
can be easily performed at the bedside in the ICU, to CT and hepatobiliary
scintigraphy (HIDA), or magnetic resonance imaging (MRI). The latter can only
be performed safely in hemodynamically stable patients. Invasive procedures,
such as endoscopic retrograde cholangiography (ERCP), cholangiography,
and/or endoscopic ultrasound (EUS), may be beneficial. Determination
regarding the patient’s tolerance for these procedures must be made before
they are performed.
 Figure 13-6. Ultrasound Diagnosis of Cholecystitis: Presence of
Gallstones, GB Wall Thickening, and Pericholecystic Fluid

Abnormal gallbladder ultrasound consistent with acute calculous cholecystitis. Image

courtesy of Mary Jane Reed, MD

1. Cholecystitis and Cholangitis

Acute calculous cholecystitis typically presents with right upper quadrant pain.
Diagnostic workup reveals systemic signs of inflammation such as fever or
elevated WBC and imaging characteristics of cholecystitis. According to the
Tokyo Guidelines 2018, patients with grade I (mild) or grade II (moderate)
acute cholecystitis should undergo early laparoscopic cholecystectomy, and
barring unforeseen complications, these patients are unlikely to be ICU
patients. Patients who have cholecystitis that goes unrecognized may develop
grade III cholecystitis. These patients should wait to undergo cholecystectomy
until they have been resuscitated and organ dysfunction is reversed. In the face
of prohibitive surgical risk, including persistent organ failure, cholecystectomy
should be deferred in favor of treatment with antibiotics and percutaneous
cholecystostomy. Patients with grade III acute cholecystitis are patients with
cholecystitis and concomitant organ dysfunction (Table 13-2). Patients with
untreated cholecystitis may also develop: 1) gallbladder empyema, where the
distended gallbladder is filled with pus, 2) emphysematous cholecystitis, gas in
the wall of the gallbladder, 3) perforation, or 4) gallbladder torsion. Any of
these can result in severe sepsis and carry much higher mortality. Early surgical
consultation to determine the best course of management in a collaborative
fashion is highly recommended and the Tokyo Guidelines may not be
appropriate for every patient.

In patients with cholecystitis or cholangitis, early

surgical consultation is highly recommended.

Table 13-2 Severity Grading for Acute Cholecystitis

From N Engl J Med., Strasberg SM, Acute Calculous Cholecystitis, 358, 2804-2811. Copyright © 2008
Massachusetts Medical Society. Reprinted with permission from Massachusetts Medical Society.

2. Acalculous Cholecystitis

Acalculous cholecystitis is serious and an

uncommon complication seen in septic,
immunocompromised, or otherwise critically ill
patients.

Acalculous cholecystitis (ACC) is an uncommon and serious complication seen

in septic, immunosuppressed, or otherwise critically ill patients. Risk factors are
male sex, diabetes mellitus, vascular disease, and injury due to external trauma
or systemic stressors such as burns or the major surgical interventions. The
pathogenesis is a combination of bile stasis related to the NPO state combined
with hypoperfusion. The hypoperfusion may be related to intravascular
depletion or related to vasoactive medications. It may also be related to intra-
abdominal hypertension or gallbladder distension causing local ischemia.
Diagnosis can be difficult. Patients may or may not be able to report pain
depending on level of consciousness and sedation. Physical examination may be
unreliable for the same reason. Fevers and WBC and liver function tests (LFTs)
elevations may be attributed to other causes as well. The primary imaging test
of choice is ultrasound, which can be performed at the bedside of a critically ill
patient and will demonstrate signs of acute cholecystitis without the presence of
gallstones. Ultrasound in this setting has good sensitivity and excellent
specificity. A HIDA scan not only has a high false-negative rate in ACC, but
also requires a significant period out of the ICU, so this modality should be
used with caution. CT scans are an alternative to ultrasound and may be helpful
to rule out other causes of acute illness. Because ACC is most often found in
critically ill patients, organ dysfunction is typically present, and therefore
patients are not candidates for laparoscopic cholecystectomy. Percutaneous
cholecystostomy tube placement and antibiotics are the treatment of choice, but
open cholecystectomy might be required in patients with gangrenous or necrotic
gallbladder to achieve source control.

3. Acute Cholangitis

Acute cholangitis is defined as acute inflammation and infection of the biliary

tree. This is most commonly a consequence of bile duct obstruction and
subsequent bacterial proliferation in the bile. As with all infections, avoiding
systemic progression is the key to improving survival. Charcot’s triad (fever,
jaundice, and right upper quadrant pain) has long been considered the
hallmark of cholangitis. The Tokyo Guidelines for diagnosis require systemic
inflammation and either cholestasis or specific findings on imaging for a
suspected diagnosis, and all three for a definitive diagnosis. Using these criteria
in the appropriate clinical situations resulted in 91.8% sensitivity and 77.7%
specificity for cholangitis. Management includes resuscitation, hemodynamic
monitoring, NPO, and antibiotics. Diagnostic imaging is used to identify the
etiology and location of the obstruction. Maneuvers should be undertaken to
address the obstruction as soon as the patient can tolerate an intervention. This
is usually endoscopic retrograde cholangiopancreatography (ERCP)
decompression or percutaneous transhepatic cholangiography and drainage.

4. Biliary Injury

Hemobilia is gastrointestinal hemorrhage emanating from a lesion or injury in

the biliary tree. In most studies, trauma, including blunt and penetrating,
iatrogenic, and accidental, is the most common etiology of bleeding. Other
causes include inflammation, tumors, and vascular conditions. Patients may
possibly present with Quincke’s triad which includes abdominal pain,
gastrointestinal bleeding, and jaundice.

The diagnosis of hemobilia can be difficult because bleeding is often

intermittent. Patients with gastrointestinal hemorrhage often undergo upper
endoscopy which can reveal the diagnosis if blood is seen coming from the
ampulla of Vater. Other imaging, such as ultrasound and CT, may reveal
layering and filling defects in the gallbladder and bile ducts due to blood and
clots. The patient may require active resuscitation from shock. The key to
successful management of hemobilia is recognition and prompt
angioembolization by interventional radiology.
5. Bile Duct Injury

Postoperative bile duct injury is a serious complication of upper abdominal

operations and can occur even in “routine” laparoscopic cholecystectomies.
Injury is often not immediately recognized and delayed presentations may be
severe with bile leak, cholangitis, and severe sepsis. After appropriate
resuscitation, the next step involves early surgical consultation to establish a
surgical plan. This will include draining abdominal fluid collections and major
hepatobiliary reconstruction to restore the flow of bile.

VI. ESOPHAGEAL PERFORATION

A. Introduction
Esophageal perforation can rapidly progress to life-threatening sepsis and
death. Rapid stabilization and early intervention to establish source control are
essential. Individual or institutional inexperience with this condition may result
in a delay in diagnosis, dramatically increasing rates of morbidity and mortality.
Early recognition is facilitated by a high index of suspicion based on patient
history and prompt recognition of signs and symptoms on examination and
imaging.

B. Etiology of Esophageal Perforation

1. Spontaneous
Spontaneous esophageal perforation is generally due to sudden high
intraluminal pressure. The classic example is Boerhaave syndrome, where
prolonged or forceful retching causes a transmural rupture, usually in the distal
esophagus just proximal to the gastroesophageal junction. Sepsis is due to
contamination of the mediastinum, left pleural space, or drainage into the
peritoneum. Other mechanisms of esophageal perforation include weakened
tissue due to erosion of ulcers, infection, immunodeficiency, or chemoradiation.

2. Foreign Body
While foreign body ingestion is relatively common, it results in perforation in
only about 1–2% of cases. Foreign body perforations are more likely in the
cervical esophagus, one of the areas of physiologic narrowing of the esophagus.
As a result, cervical esophageal perforations are typically less morbid because
there is more access for drainage and the spread of infection can be limited.

3. Iatrogenic
Due to the increase in endoscopic procedures, iatrogenic perforation is an
important etiology of esophageal perforation. Unrecognized intra-operative
laceration of the esophagus is rare, but procedures associated with this type of
esophageal perforation include:
Operations at the hiatus such as fundoplication, vagotomy, and hiatal
hernia repair
Operations in the mediastinum including lung transplantation,
pneumonectomy, and thoracic aortic aneurysm repair
Cervical operations such as thyroidectomy, tracheostomy,
mediastinoscopy, and cervical spine surgery

The key to optimal outcome is immediate recognition of the injury because any
delay in treatment, particularly beyond 24 hours, dramatically increases
morbidity and mortality rates.

4. Trauma

Most esophageal injuries are penetrating injuries. The incidence of blunt

esophageal injuries is very low. The most common penetrating etiology is
gunshot wound (75%) in the United States, followed by stab wounds, and other
mechanisms. Suspicion should always be high for esophageal or
hypopharyngeal injury in any penetrating wound to the lower head or neck,
particularly zones I and II of the neck.

C. Presentation
Esophageal perforation often presents with nonspecific symptoms such as chest
pain, dysphagia, dyspnea, subcutaneous emphysema, epigastric pain, fever,
tachycardia, and tachypnea. The two pathognomonic signs of esophageal
perforation are Hamman’s sign and Mackler’s triad. Hamman’s sign is a
rasping or crunching heard on auscultation over the precordium caused by the
heartbeat against air-filled tissue. Mackler’s triad is chest pain, vomiting, and
subcutaneous emphysema. These “classic presentations” are rare.
Subcutaneous emphysema, while a highly suspicious finding, is detectable by
physical examination in only 30% of patients after thoracic perforation and
60% of patients after cervical perforation.

Patients with cervical perforations can present with neck pain, dysphonia,
hoarseness, and cervical dysphagia. Acute chest pain, back pain, or pain that
radiates to the back is more likely a mid-esophageal injury and peritoneal signs
correspond to intraperitoneal injuries. Signs of an inflammatory response sepsis,
such as tachycardia, tachypnea, elevated white blood cell count, and fever, can
develop in any esophageal injury and represent the development of sepsis. This
is an ominous development. A CT scan of the neck and chest demonstrating a
large amount of subcutaneous air in the setting of penetrating trauma is highly
suspicious of esophageal trauma.

D. Diagnosis
Prompt diagnosis of esophageal perforation can be difficult due to its
nonspecific symptoms. The median time to diagnosis of esophageal perforation
can be up to 12 hours (range 1–120 hours), with a high index of suspicion and
attention to detail being important for a successful diagnosis. In a recent review,
odynophagia and dysphagia were the most common presenting symptoms.
Particular attention should be paid to patients with risk factors for perforation
such as trauma, instrumentation, or foreign body ingestion. These patients need
further evaluation.

Prompt diagnosis of esophageal perforation can

be difficult due to nonspecific symptoms. A high
index of suspicion and attention to detail are
important.
Evaluation begins with plain chest radiographs in which signs of esophageal
injury may include pleural effusion (mostly on the left), pneumomediastinum,
subcutaneous emphysema, or pneumothorax. A swallow study with water-
soluble contrast medium (if the patient can swallow) is the next step and will
reveal a contrast leak in most cases of esophageal perforation (Figure 13-7).
Water-soluble contrast should be used instead of barium contrast to prevent
barium-related inflammation of the mediastinum if there is perforation. If the
water-soluble contrast study is negative for an obvious leak, it can be followed
by a swallow study with diluted barium for optimal sensitivity. CT is frequently
used in patients who cannot undergo esophagography (Figure 13-8). Patients
who are unable to swallow or who are critically ill may proceed directly to CT.
Patients who have other injuries and who may need CT for other reasons may
forgo esophagography in favor of CT. This may be beneficial in preoperative
planning, and findings in esophageal perforation are similar to plain film
findings and include pleural effusion, pneumomediastinum, subcutaneous
emphysema, and pneumothorax.
There is significant controversy regarding the use of endoscopy to identify
perforation. In evaluating penetrating esophageal injury, endoscopy has been
shown to have a sensitivity of 100% and specificity of 83%. In foreign body
perforation, laryngoscopy and flexible endoscopy had long been considered the
standard for diagnosis, but recently have been shown to miss a number of
foreign bodies, particularly fish bones, which were identified by CT. Flexible
esophagoscopy is generally avoided when other forms of injury are suspected
due to the potential risk to convert a small or partial tear into a larger
laceration.

Figure 13-7 and 13-8. Esophageal Perforation

(Figure 13-7) Extraluminal contrast on esophagography. Used with
permission. Courtesy of Matthew A. Facktor, MD
 (Figure 13-8) Contrast extravasation into mediastinum consistent
with esophageal perforation.
Used with permission. Courtesy of Matthew A. Facktor, MD

E. Management
The management in esophageal perforation begins with resuscitation and the
principles of critical care. There is the potential for airway compromise due to
an expanding hematoma or abscess. The airway should be evaluated and
secured prior to any other intervention. There may be an empyema, pleural
effusion, or pneumothorax interfering with respiration. Adequate gas exchange
must also be ensured. The patient may already show signs of sepsis with
circulatory compromise. Hemodynamic monitoring should be initiated. Lactate
levels should be monitored. It is likely that fluid resuscitation will be required to
restore circulating blood volume.
Identifying and controlling the source of ongoing contamination is the next step.
It is critical to avoid further spillage and to try to remove any spillage from the
perforation that has already occurred. If chest radiographs reveal pleural
effusions or pneumothorax, it is likely that tube thoracostomy will be required.
This may be accomplished in the emergency department or ICU, or in a
procedures or operating area depending on the facility and the next steps.
Aside from tube thoracostomy, all other interventions to control mediastinal,
pleural, cervical, or peritoneal contamination would likely require a surgical
intervention. While primary surgical repair seems desirable, it is extremely
morbid. Minimally invasive therapies, such as stenting and drainage
procedures, have come into greater favor as a result. Any intervention should
include establishing enteral access for long-term nutrition.

After initial resuscitation, it is critical to avoid

further spillage and to try to remove any spillage
from the perforation that has already occurred.

Once the stabilization and source control are established, transfer to a tertiary
care facility should be considered. The patients often need to undergo multiple
procedures during the initial hospitalization. They will require long-term follow-
up with repeat procedures; thus, they are best served in a facility that offers
those resources.

F. Conclusion
Esophageal perforation is deadly if it is not quickly recognized and treated. A
high index of suspicion based on a patient’s history or trauma mechanism is
key, and clinicians need to be aware of the nonspecific and sometimes subtle
signs of esophageal injury. Once the diagnosis is established, immediate
administration of broad antibiotic coverage followed by surgical consult and
subsequent control of the perforation are critical. Definitive repair or
stabilization can be accomplished either through an open surgical approach or a
minimally invasive approach depending on each individual patient’s situation.
Key Points
Abdominal Surgical Emergencies: Part 1
TM should be considered in critically ill patients with classic risk
factors such as IBD and C. difficile infection, but also in those with
multi-system organ failure of unclear etiology.
Early diagnosis and aggressive treatment are essential. Plain
abdominal radiographs should be the first imaging modality and may
demonstrate an excessively dilated (frequently right side) colon.
Distal obstruction as etiology of colonic dilation needs to be ruled out
via contrast enema, abdomen and pelvis CT scan with rectal contrast,
or bedside sigmoidoscopy.
Medical treatment needs to be started immediately for all cases of
TM and consists of specific antimicrobial therapy or steroids and
immunomodulators for infectious or inflammatory colitides,
respectively. However, early surgical consultation and a low
threshold for surgical intervention are essential.
First-line surgical treatment of TM consists of colectomy with end
ileostomy, although for select cases of C. difficile infection other
surgical treatment, such as lavage through a loop ileostomy, are novel
strategies.
Patients with SBO are a heterogenous group and appropriate
management ranges from serial examinations and fluid resuscitation
to immediate surgical intervention. SBO due to adhesions often
responds to nonsurgical management, while patients with hernias
most often require surgical management, and those with obstruction
due to cancer or volvulus always do.
In a patient with SBO, regardless of etiology, peritonitis, severe
leukocytosis, or lactic acidosis, or imaging findings of pneumatosis
and bowel wall thickening are concerning for bowel ischemia or
 necrosis and require surgical consultation and most likely
intervention.
Patients with SBO who do not respond to nonsurgical management
after 48–72 hours should be considered for surgical intervention.
Peritonitis is defined as inflammation of the peritoneum and can be
classified as primary, secondary, and tertiary.
Secondary peritonitis is the most common type of peritonitis.
Treatment for peritonitis includes prompt administration of
crystalloids, source control, and antimicrobial therapy.
Patients presenting with the severe forms of gallbladder and
pancreas-related disease such as cholangitis or necrotizing
pancreatitis, respectively, are at risk for distributive and/or
hypovolemic shock, septic, and sometimes hemorrhagic shock.
Esophageal perforation often presents with nonspecific symptoms
such as chest pain, dysphagia, dyspnea, subcutaneous emphysema,
epigastric pain, fever, tachycardia, and tachypnea.

Suggested Readings
1. Aquina CT, Becerra AZ, Probst CP, et al. Patients With Adhesive
Small Bowel Obstruction Should Be Primarily Managed by a
Surgical Team. Ann Surg. 2016;264(3):437-447.
2. Asensio JA, Chahwan S, Forno W, et al. Penetrating esophageal
injuries: multicenter study of the American Association for the
Surgery of Trauma. J Trauma. 2001;50(2):289.
3. Barie PS, Eachempati SR. Acute acalculous cholecystitis. Gastro
Clinics N Am. 2010;39(2):343-357.
4. Biffl WL, Moore EE, Feliciano DV, et al. Western Trauma
Association Critical Decisions in Trauma: Diagnosis and
 management of esophageal injuries. J Trauma Acute Care Surg.
2015;79(6):1089-1095.
5. Cherry-Bukowiec JR, Miller BS, Doherty GM, et al. Nontrauma
emergency surgery: optimal case mix for general surgery and acute
care surgery training. J Trauma. 2011;71(5):1422-1426.
6. Davis CA, Landercasper J, Gundersen LH, et al. Effective Use of
Percutaneous Cholecystostomy in High-Risk Surgical Patients
Techniques, Tube Management, and Results. Arch Surg.
1999;134(7):727-732.
7. Ferrada P, Patel MB, Poylin V, et al. Surgery or stenting for colonic
obstruction: a practice management guideline from the Eastern
Association for the Surgery of Trauma. J Trauma Acute Care Surg.
2016;80(4):659-664.
8. Ferrada P, Velopulos CG, Sultan S, et al. Timing and type of
surgical treatment of Clostridium difficile-associated disease: a
practice management guideline from the Eastern Association for the
Surgery of Trauma. J Trauma Acute Care Surg. 2014;76(6):1484-
1493.
9. Hawser SP, Bouchillon SK, Hoban DJ, Badal RE: In vitro
susceptibilities of aerobic and facultative anaerobic Gram-negative
bacilli from patients with intra-abdominal infections worldwide from
2005-2007: Results from the SMART study. Int J Antimicrob
Agents. 2009;34(6):585-588. 10.1016/j.ijantimicag.2009.07.013.
10. Horwitz B, Krevsky B, Buckman RF Jr, et al. Endoscopic
evaluation of penetrating esophageal injuries. Am J Gastroenterol.
1993;88:1249-1253.
11. Huffman JL, Schwenker S. Acute acalculous cholecystitis: a review.
Clin Gastroenterol Hepatol. 2010;8:15-22.
12. Kimura Y, Tadaka T, Strasburg SM, et al. TG13 current
terminology, etiology, and epidemiology of acute cholangitis and
cholecystitis. J Hepatobiliary Pancreat Sci. 2013;20(1):8-23.
13. Kiriyams S, Takada T, Strasberg SM, et al. New diagnostic criteria
and severity assessment of acute cholangitis in revised Tokyo
Guidelines. J Hepatobiliary Pancreat Sci. 2012;19(5):548-556.
14. Ross H, Steele SR, Varma M, et al. Practice parameters for the
surgical treatment of ulcerative colitis. Dis Colon Rectum.
2014;57(1):5-22.
15. Sailhamer EA, Carson K, Chang Y, et al. Fulminant Clostridium
difficile colitis: patterns of care and predictors of mortality. Arch
Surg. 2009;144(5):433-439; discussion 9-40.
16. Sartelli M, Malangoni MA, Abu-Zidan FM, et al. WSES guidelines
for management of Clostridium difficile infection in surgical
patients. World J Emerg Surg. 2015;10:38.
17. Sartelli M, Viale P, Catena F, et al. 2013 WSES guidelines for
management of intraabdominal infections. World J Emerg Surg.
2013;8(1):3. doi:10.1186/1749-7922-8-3.
18. Scotte M, Mauvais F, Bubenheim M, et al. Use of water-soluble
contrast medium (gastrografin) does not decrease the need for
operative intervention nor the duration of hospital stay in
uncomplicated acute adhesive small bowel obstruction? A
multicenter, randomized, clinical trial (Adhesive Small Bowel
Obstruction Study) and systematic review. Surgery.
2017;161(5):1315-1325.
19. Søreide JA, Viste A. Esophageal perforation: diagnostic work-up
and clinical decision-making in the first 24 hours. Scand J Trauma
Resusc Emerg Med. 2011;19:66. doi:10.1186/1757-7241-19-66.
20. Strong S, Steele SR, Boutrous M, et al. Clinical Practice Guideline
for the Surgical Management of Crohn’s Disease. Dis Colon
Rectum. 2015;58(11):1021-1036.
21. Vial CM, Whyte RI. Boerhaave’s syndrome: diagnosis and
treatment. Surg Clin North Am. 2005;85:515-524. doi:
10.1016/j.suc.2005.01.010. ix.
Suggested Websites
1. http://www.aasld.org/practiceguidelines/Documents/ascitesupdate20
13.pdf
2. C-diff - https://www.east.org/education/practice-management-
guidelines/clostridium-difficile-associated-disease---timing-and-
type-of-surgical-treatment
3. SBO - https://www.east.org/education/practice-management-
guidelines/smallbowelobstruction-evaluation-and-management-of
4. Cholecystitis https://www.east.org/education/publications/landmark-
papers-in-trauma-and-acute-care-surgery/emergency-general-
surgery/cholecystitis
 Chapter 14
ABDOMINAL SURGICAL
EMERGENCIES: PART 2

Objectives
Classify and predict severity of acute pancreatitis.
Recognize complications associated with acute pancreatitis.
Outline appropriate management of acute pancreatitis.
Outline the diagnostic methods for determining location and type of
severe gastrointestinal hemorrhage.
Review the general management principles of severe upper and lower
gastrointestinal hemorrhage.
Identify the diagnosis and management of intra-abdominal
hypertension and abdominal compartment syndrome.

Case Study
A 58-year-old man with cirrhosis secondary to chronic alcohol abuse arrives
in the emergency department reporting upper abdominal pain and
generalized weakness for the past 2 days. He is currently intoxicated and is
unable to provide a detailed history. His vital signs reveal a temperature of
37.5°C (99.5°F), respiratory rate of 28 breaths/min, blood pressure of
92/70 mm Hg, and a heart rate of 115 beats/min. On physical examination,
his abdomen is rotund and tender to palpation in the mid-epigastrium. As an
intravenous crystalloid fluid infusion is started, the patient becomes more
lethargic.
– What is the differential diagnosis based on the patient’s risk factors and
clinical findings?
– What diagnostic studies would be indicated?
– What would your initial management consist of?

I. INTRODUCTION
The conditions covered in this chapter highlight the need for closely
coordinated, multidisciplinary and multi specialty care of the seriously ill.
Severe pancreatitis, gastrointestinal (GI) hemorrhage, and abdominal
compartment syndrome require initial and continuing communication among
the primary provider team and various consultants. Expedient discussion,
planning and implementation of resuscitation and interventions often requires
a lead service to strategize the patient’s care and organize alternative
treatment if initial therapy failed.

II. PANCREATITIS
A. Diagnosis and Classification
Pancreatitis is the most common GI condition requiring hospitalization in the
United States and United Kingdom. A worldwide increase in the incidence of
pancreatitis is most likely associated with the concurrent increase in obesity
and gallstones. Pancreatitis is defined by having two of the three following
criteria:
1. Symptoms consistent with pancreatitis (eg, epigastric pain)
2. Serum amylase and/or lipase greater than three times the upper limit
of normal
 3. Cross-sectional imaging or transabdominal ultrasonography revealing
pancreatitis
The two most frequent causes of acute pancreatitis include gallstones and
alcohol. Other causes are:

Hypertriglyceridemia
Hypercalcemia
Endoscopic retrograde cholangiopancreatography
Trauma
Associated conditions (diabetes mellitus, obesity, smoking)
Genetic causes
Autoimmune disorders
Medications(furosemide, steroids)
Infection (mumps)
Post-cardiopulmonary bypass
Obstruction of pancreatic duct
Idiopathic

There are two types of acute pancreatitis: interstitial edematous pancreatitis

and necrotizing pancreatitis. Although most patients admitted with pancreatitis
will have the interstitial edematous type characterized with a mild disease
course and a mortality rate around 2%, about 20% of patients will develop
necrotizing pancreatitis associated with local and systemic complications and a
mortality rate that exceeds 30% in the most severe bouts.

Twenty percent of patients with pancreatitis will

develop necrotizing pancreatitis that can have a
mortality rate upwards of 30%.
Methods to classify the severity of acute pancreatitis include the Revised
Atlanta Classification (RAC) and the Determinant-Based Classification (DBC)
as shown below.

Severity of pancreatitis is based on an associated

level of organ dysfunction or failure.

The RAC sought to clarify terminology used in the original Atlanta

Classification to differentiate the two types of acute pancreatitis, interstitial
edematous pancreatitis and necrotizing pancreatitis, and describe fluid
collections which are viewed as local complications of acute pancreatitis.
These fluid collections are defined as acute peripancreatic fluid collection
(APFC), acute necrotic collection (ANC) (sterile or infected), pancreatic
pseudocyst (PP), and walled-off necrosis (WON) (sterile or infected) (Table
14-1).

Revised Atlanta Classification (RAC) (2012)

Mild acute pancreatitis

No organ failure
No local or systemic complications

Moderately severe acute pancreatitis

Transient (< 48 hours) organ failure and/or
Local or systemic complications without persistent organ failure
Severe acute pancreatitis
 Persistent organ failure (> 48 hours), single or multiorgan

Data from Banks PA, et al. Gut. 2013;62:102-111.

Determinant-Based Classification (DBC)

Mild acute pancreatitis

No organ failure
No (peri)pancreatic necrosis

Moderate acute pancreatitis

Sterile (peri)pancreatic necrosis and/or transient organ failure

Severe acute pancreatitis

Infected (peri)pancreatic necrosis or persistent organ failure

Critical acute pancreatitis

Infected (peri)pancreatic necrosis and persistent organ failure

Data from Talukdar R and Vege R. Acute pancreatitis. Curr Opin

Gastroenterol. 2015;31:376.

Table 14-1 Definition of Pancreatic and Peripancreatic Collections

Reproduced from Gut. Banks PA, et al. 62, 102-111, 2013, with permission from BMJ Publishing
Group Ltd.

The morphologic characteristics of acute pancreatitis are best seen on

contrast-enhanced computed tomography (CECT). The fluid collections that
may result from interstitial edematous pancreatitis (Figure 14-1) are APFC
and PP; ANC and WON develop from necrotizing pancreatitis. On CECT, the
pancreas in interstitial edematous pancreatitis is enlarged secondary to
edema, has relatively homogenous enhancement, and the peripancreatic fat
shows inflammatory changes. There may be the development of an APFC
which occurs during the first 4 weeks after the onset of interstitial edematous
pancreatitis. An APFC appears on CECT as a homogenous collection with
fluid density confined by the fascial planes surrounding the pancreas. After at
least 4 weeks, this collection of fluid may develop a mature, well-
circumscribed inflammatory wall at which time it is referred to as a PP
(Figure 14-2).
Figure 14-1. Interstitial Edema Pancreatitis

Image courtesy of Daniel Wu, DO.

 Figure 14-2. Pancreatic Pseudocyst (starred area)

Image courtesy of Daniel Wu, DO.

Necrotizing pancreatitis is defined as necrosis of the pancreatic parenchyma,

the peripancreatic tissue, or both. Necrosis is evident on CECT as poorly
enhanced pancreatic parenchyma and surrounding tissue. This impairment of
perfusion evolves over several days which explains why an early CECT may
underestimate the eventual amount of pancreatic and peripancreatic necrosis.
An ANC occurs only in the setting of necrotizing pancreatitis and is
characterized as a heterogenous collection of solid and liquid densities without
a definable wall. After 4 weeks, encapsulation of the necrotic tissue may form
and is termed WON. Both ANC and WON may be sterile or infected (Figures
14-3 and 14-4).
Figure 14-3. Pancreatic Necrosis without Fluid Collections (circled
area necrosis-no contrast)

Image courtesy of Daniel Wu, DO.

 Figure 14-4. Pancreatic Necrosis with Peripancreatic Fluid
Collections (starred areas)

Image courtesy of Mary Jane Reed, MD.

Suspicion for the presence of local complications, which include gastric outlet
obstruction, splenic and portal vein thrombosis, and colonic necrosis, is
heightened because of persistent or recurrent abdominal pain, worsened
organ function, and clinical signs of sepsis including fever and leukocytosis.
These local complications can be confirmed on CECT. Systemic complications
confer greater severity of illness in acute pancreatitis. According to the RAC,
the organ systems that should be assessed for organ failure are respiratory,
cardiovascular, and renal. Persistent organ failure (> 48 hours) is the
defining feature of severe acute pancreatitis. Exacerbation of comorbid
illnesses such as coronary artery disease, chronic obstructive pulmonary
disease, or diabetes mellitus is also considered a systemic complication.

The ability to predict which patients will develop severe acute pancreatitis is
useful in that this allows appropriate triage to the proper level of monitoring
(intermediate or intensive care unit [ICU]) and early initiation of appropriate
therapy. Multiple scoring systems, combining clinical and laboratory
parameters, are available to predict the severity of acute pancreatitis. These
include Ranson score, Acute Physiology and Chronic Health Evaluation II
(APACHE II), Bedside Index for Severity in Acute Pancreatitis, Glasgow
Imrie, and Systemic Inflammatory Response Syndrome (SIRS) criteria.
Unfortunately, most of these scoring systems have a low-positive predictive
value and, therefore, no consistently reliable system for severity prediction
exists. However, signs of persistent SIRS (> 48 hours) increase the risk of
organ failure associated with acute pancreatitis and portend a poor prognosis.
Other predictors of severity in acute pancreatitis include elevated C-reactive
protein level and indicators of intravascular depletion as a result of third-
space fluid losses such as hemoconcentration and azotemia.

B. Management

Tailor fluid therapy based on intravascular

depletion and risk of cardiopulmonary overload.

Management consists of optimal fluid resuscitation with the goal to provide

enough intravascular volume to maintain pancreatic perfusion. Fluid therapy
needs to be tailored to the degree of intravascular volume depletion and the
cardiopulmonary reserve that is available to handle the fluid because volume
overload is a major risk of fluid resuscitation. Maintaining hemodynamic
stability and targeting a urine output of at least 0.5 mL/kg/h aids in
preventing acute kidney injury. Lactated Ringer solution is preferred by some
clinicians over normal saline in reducing inflammatory markers although
further studies need to be done.

The enteral route for provision of nutrition is preferred in patients with acute
pancreatitis. Early enteral nutrition helps to maintain gut mucosal barrier
integrity, decreases pathogenic intestinal flora, and reduces infection and
mortality compared with parenteral nutrition. No evidence exists to suggest
the superiority of elemental or semi-elemental formulas compared with
polymeric formulas. Post-pyloric feeding has not been shown to be superior to
gastric enteral feeding in acute pancreatitis. Delay in gastric emptying, reflux,
gastric feeding intolerance, and increased risk of aspiration would be
indications to pursue the post-pyloric route.

Total parenteral nutrition (TPN) is more expensive and is associated with

increased infectious complications, organ failure, and mortality than enteral
nutrition in patients with severe acute pancreatitis. TPN should be used in
those situations when enteral feeding is not tolerated or does not provide
adequate nutrition to meet caloric needs.

Most APFCs remain sterile, typically resolve spontaneously, and therefore do

not need treatment. A PP may require therapy if patients experience
symptoms such as abdominal pain, early satiety, fever, chills, or jaundice.
Endoscopic and occasionally percutaneous catheter drainage approaches have
supplanted surgical techniques for management.

ANCs and WON are composed of necrotic pancreatic parenchyma and/or

peripancreatic tissue. These collections may be sterile or become infected.
There is no benefit of providing prophylactic antibiotics in an attempt to
prevent secondary infection. In addition, surgical debridement of sterile
necrosis has not been proven to be helpful in the absence of obstructive
symptoms or failure to thrive.

The distinction between sterile and infected necrosis is imperative because

infected pancreatic and peripancreatic necrosis is associated with increased
morbidity and mortality. Once infection is confirmed, antibiotics with high
inhibitory concentrations within pancreatic tissue (eg, carbapenems,
fluoroquinolones, metronidazole) are administered which have been shown to
successfully treat infected necrosis in stable patients, obviating the need for
other intervention. For patients who fail to improve or show signs of
deterioration, a step-up approach with a delay in definitive treatment is
standard practice. This step-up approach consists of, in addition to antibiotic
administration, percutaneous drainage as needed, and after a delay of several
weeks, minimally invasive debridement (eg, percutaneous, endoscopic,
laparoscopic, and retroperitoneal approaches), if necessary. This approach is
superior to open necrosectomy with respect to the risk of major complications
or death. Approximately one-third of patients will not require debridement.
Open surgery should be reserved for when less invasive techniques fail.

The step-up approach to pancreatic and

peripancreatic necrosis includes antibiotics,
percutaneous drainage, then invasive
debridement, if necessary.

Patients diagnosed with acute pancreatitis should have an evaluation for

gallstones with abdominal ultrasonography. In those patients determined to
have mild gallstone pancreatitis, cholecystectomy performed during the initial
hospital admission prevents recurrent disease. Cholecystectomy may need to
be deferred in cases of necrotizing pancreatitis to allow for resolution of the
acute inflammatory changes, thereby improving surgical exposure of the
gallbladder.

Inflammation as a result of pancreatitis can lead to both thrombotic and

hemorrhagic complications. These vascular complications occur in 1–23% of
patients with pancreatitis and are associated with considerable morbidity and
mortality. Although rarely developing with mild acute pancreatitis, the
pancreatic and peripancreatic fluid collections, necrosis, and infection that
define more severe bouts of acute pancreatitis contribute to the development
of vascular complications.
Venous injuries occur more frequently than arterial injuries. Portal and
splenic vein thrombosis happen in 23% and 22% of cases of pancreatitis,
respectively. Because splanchnic thrombosis may spontaneously resolve with
appropriate management of pancreatitis, treatment with anticoagulation
should be instituted when clot burden results in hepatic decompensation or
compromise of bowel perfusion.

Pseudoaneurysms are the predominant cause of arterial hemorrhage

associated with pancreatitis. Direct trauma to adjacent vessels from
radiologically placed drains may also lead to arterial hemorrhage. Because
arterial complications are associated with 34–52% mortality, early recognition
and treatment are warranted. Symptomatic pseudoaneurysms lead to
abdominal pain because of retroperitoneal bleeding. The most common site
for pseudoaneurysms is the splenic artery (35–50%), followed by
gastroduodenal and pancreaticoduodenal arteries and, less commonly,
mesenteric, colic, and hepatic vessels. Identification of a pseudoaneurysm on
CECT can be managed with angiographic embolization. The need for surgical
management, especially with active hemorrhage and unsuccessful
interventional radiology attempts at hemorrhage cessation, remains a viable
option.

Pancreatitis recurs in nearly half of occurrences

when patient risk factors are not recognized and
addressed.

Determining the etiology of and providing appropriate management for acute

pancreatitis offers an effective strategy to prevent recurrence of the disease.
The recurrence rate of acute pancreatitis, which can be as high as 25%,
approaches 50% in patients whose risk factors have not been recognized or
addressed. After acute pancreatitis, pancreatic exocrine and endocrine
insufficiency develop in 20–30% of patients and chronic pancreatitis arises in
one-third to one-half of those patients. Risk factors for the transition to
recurrent attacks and chronic pancreatitis include the severity of the initial
attack, the extent of pancreatic necrosis, and the cause of acute pancreatitis.
Long duration heavy alcohol use as the cause and smoking as a cofactor
significantly increase the risk of progression to chronic pancreatitis.

III. GASTROINTESTINAL HEMORRHAGE

Mortality from a GI bleed could be high, especially if associated with other
risk factors. The most important first step is to obtain hemodynamic stability.
Adequate IV access is crucial, whether it be large-bore peripheral or central
access, and consider an arterial line for hemodynamic monitoring. Initially,
resuscitation will begin with intravenous fluids and may transition to the
administration of blood products if the hemodynamic status of the patient
does not improve. The goal of massive blood resuscitation (>10 units of
packed red blood cells within 24 hours) should be to provide products in the
1:1:1 method (packed cells: plasma: platelets) unless whole blood is available.
Vasopressor agents should be used as an adjunct to appropriate volume
resuscitation. The American College of Gastroenterology (ACG) recommends
maintaining a hemoglobin level of 7 g/dL in patients with massive bleeding, 9
g/dL in those with comorbid illness, especially cardiac ischemia, or a
predicted delay to intervention. This low threshold reduced the amount of
blood product transfused and incidence of rebleeding while improving
survival.

Once intravenous resuscitation has begun, blood tests should be drawn and
are recommended to be drawn serially. Hemoglobin and hematocrit,
coagulation studies (including prothrombin time [PT], partial thromboplastin
time [PTT], international normalized ratio [INR], and fibrinogen), a basic
metabolic panel, and type and crossmatch should be obtained.
Thromboelastography, which is a method to test for the efficiency of blood
coagulation, is being used more frequently in ICUs and is used to guide
resuscitation.

A complete history should be obtained from the patient or a spokesperson for

the patient. Special note should be taken to inquire about events leading up to
the hospitalization as well as any known history of liver disease, previous GI
bleeds, surgeries, or other GI disorders. Use of nonsteroidal anti-
inflammatory agents, antiplatelet agents, or anticoagulants should also be
discussed.
Reversal of anticoagulants is imperative in the actively bleeding patient. The
process by which to achieve this is becoming increasingly difficult with the
ever-expanding types of anticoagulants available. For patients receiving
coumadin therapy, the INR should be reversed to 1.5 or less. This has
proven to decrease the risk of rebleeding. Any INR > 1.5 is an independent
predictor of mortality.

Standard laboratory testing is not accurate for

direct-acting oral anticoagulants. Reversal
agents are more readily available.

Many new anticoagulants have been introduced and will likely continue to be
developed. These agents have brought about new considerations in GI
hemorrhage. Standard laboratory testing performed to evaluate coagulation is
not accurate for these medications. INR, activated partial thromboplastin time
(aPTT), and PT may variably be elevated but the level of elevation does not
correspond to the level of active medication in the bloodstream.
Thromboelastography is helpful in evaluating the degree of medication effect.
Reversal of these direct-acting oral anticoagulants (DOACs) was not initially
available when these products were approved for use. Reversal agents have
been developed and are becoming more readily available. For the type of
anticoagulant and its reversal refer to Table 14-2.

Table 14-2 Anticoagulants and Their Properties

Abbreviations: FFP, fresh frozen plasma; MOA, mechanism of action; 4F-PCC, 4-Factor prothrombin
complex concentrate; u/kg, units per kilogram; * suggest Pharmacy consultation

The first key in diagnosis of GI hemorrhage is differentiation of upper GI

hemorrhage from lower. The ACG divides GI bleeding into three distinct
categories:
1. Upper GI bleeding originating proximal to the ligament of Treitz
2. Middle GI bleeding from the small intestine
3. Lower GI bleeding from the colon or rectum
For the purposes of this chapter, the traditional definition utilizing the
ligament of Treitz as the division between the upper and lower GI tract will be
used as reference. We will be discussing upper GI bleeding and lower GI
bleeding separately.

A. Upper Gastrointestinal Bleeding (UGIB)

The traditional division between upper

gastrointestinal bleeding and lower is the
ligament of Treitz.
Upper GI bleeding can be mild to immediately life-threatening. Blood loss
originates proximal to the ligament of Treitz and can involve the esophagus,
stomach, and/or the duodenum. Treatment of Helicobacter pylori infection
and the use of acid-suppressive therapy for peptic ulcer disease (PUD) has led
to a decline in the incidence of UGIB to 100 cases per 100,000 population
per year. Despite improved management, morbidity and mortality from GI
bleeding have remained relatively stable at 6% to 10%. The aging population
presenting with an increasing number of comorbidities and the use of newer
anticoagulant medications are at increased risk of bleeding. Approximately
80% of mortality in patients with GI bleeding is attributed to the exacerbation
of other illnesses. Patients with GI bleed require close monitoring and
management in an ICU.

1. Diagnosis and Presentation

A team approach that involves an intensivist, gastroenterologist, radiologist,

and surgeon are needed to most effectively treat the patient with rapid
assessment, diagnosis, and intervention. A careful history and physical
examination should provide information to identify the cause and source of
the bleeding and discover any complicating conditions or medications.
Questioning should reveal timing, duration, volume, and severity of bleeding.
UGIB can have findings of coffee ground emesis, hematemesis, melena, or
even hematochezia if bleeding is rapid. A medical history of previous UGIB,
abdominal pain, change in bowel habits, the presence of PUD, alcohol
consumption, vomiting or retching, stigmata of cirrhosis, hepatitis, liver
disease, coagulation disorders, inflammatory bowel disease, weight loss,
anorexia, or malignancy should be obtained. Inquiry about surgical history,
including gastrectomy and abdominal aortic aneurysm repair, is also
important. Medications should be reviewed for the use of nonsteroidal anti-
inflammatory drugs (NSAIDs), aspirin, anticoagulants, and antiplatelet agents.
A family history of coagulation disorders or a history of recurrent bleeding
should be discussed.
Assessment of vital signs may indicate hypovolemia, including tachycardia
and orthostatic hypotension. Abdominal and rectal examination with guaiac
testing should be performed. Laboratory tests should include a complete
blood count, coagulation studies, type and cross match, creatinine level,
blood urea nitrogen level, and liver enzymes.

The placement of a nasogastric tube in patients presenting with GI bleeding is

a common practice that remains controversial. The benefits of nasogastric
lavage include confirmation of an upper GI source of bleeding, better
visualization during endoscopy, and prediction of high-risk lesions based on
the severity of the bleeding. The return of bilious material without any blood
makes a distal source more likely.
Non-variceal upper GI bleeding (NVUGIB) must be differentiated from
variceal upper GI bleeding (VUGIB). The differential diagnosis diverges
based on the type of bleeding.
Diagnostic tools for the evaluation of UGIB include endoscopy and
angiography. These tests are aimed at detecting the location, source, and
activity of bleeding. Other tests may be necessary in specific clinical
situations, such as computed tomography (CT) scanning when abdominal pain
is a prominent symptom to rule out ischemia, infarction, and perforation.
Endoscopy and to some extent angiography have the advantage of allowing
both diagnosis and therapy.

NVUGIB
Causes of NVUGIB include peptic ulcer disease (duodenal and gastric ulcers),
Mallory-Weiss tear, stress gastritis, Dieulafoy lesion, angiodysplasia, benign or
malignant neoplasms, hemobilia, and aortoduodenal fistula. These sources
account for 80–90% of upper GI bleeding.

a. Peptic Ulcer Disease

Peptic ulcer disease (PUD) is the most common cause of NVUGIB,

approximately 40% of all cases. NSAID use and Helicobacter pylori
infection are the common causes of PUD. Bleeding develops as a
consequence of peptic acid erosion of the mucosal surface.
Significant bleeding results when there is involvement of an artery of
the submucosa or with penetration of the ulcer into an even larger
vessel (gastroduodenal artery, pancreaticoduodenal artery, or left
gastric artery).

Peptic ulcer disease is the most common

source of non-variceal upper
gastrointestinal bleeding. This can
commonly be caused by NSAID use or H.
pylori infection.

b. Mallory-Weiss Tears
Mallory-Weiss tears are mucosal and submucosal tears that occur
near the gastroesophageal junction from sudden increases in pressure
within the cardia and lower esophagus. They develop after a period
of intense retching and vomiting commonly following binge drinking
in alcoholic patients but can occur in any patient who has a history of
repeated emesis. They account for 5% to 15% of cases of upper GI
bleeding. Ninety percent of bleeding episodes are self-limited and the
mucosa often heals within 72 hours.

c. Stress-Related Gastritis
Stress-related gastritis is characterized by the appearance of multiple
superficial erosions of the entire stomach, most commonly in the
body. The entity is thought to result from the combination of acid and
pepsin injury in the context of ischemia from hypoperfusion states.
Ventilator dependence for longer than 48 hours and coagulopathy
are risk factors for increased bleeding from stress gastritis. Two
patient populations in which this can be seen are patients with
increased intracranial pressure (Cushing ulcer) and major burns
(Curling ulcer).

d. Dieulafoy Lesions
Dieulafoy lesions are vascular malformations found primarily along
the lesser curve of the stomach within 6 cm of the gastroesophageal
junction. They are the result of the rupture of unusually large visible
vessels (1 to 3 mm) found in the gastric submucosa. Erosion of the
gastric mucosa overlying these vessels leads to bleeding. The mucosal
defect is usually small (2 to 5 mm) and may be difficult to identify
because of normal surrounding mucosa. They account for less than
5% of cases of upper GI bleeding.

e. Angiodysplasia

Angiodysplasia (arteriovenous malformation or vascular ectasia) is

another source of upper GI bleeding and accounts for approximately
5% to 10% of cases.

f. Neoplasms

Benign or malignant neoplasms are usually associated with chronic

anemia or hemoccultpositive stool. They can also present as
ulcerative lesions seen with gastrointestinal stromal tumor, lipomas,
leiomyomas, and lymphomas. They account for less than 5% of cases
of upper GI bleeding.

g. Hemobilia
Hemobilia is associated with trauma, liver biopsy, recent
instrumentation of the biliary tree (endoscopic retrograde
cholangiopancreatography [ERCP]), and biliary or hepatic
neoplasms. Suspect the diagnosis in patients who present with
bleeding, right upper quadrant pain, and jaundice.

h. Aortoenteric Fistula
Aortoenteric fistula typically develops in a patient with previous
repair of an abdominal aortic aneurysm but could occur with an
inflammatory or infectious aortitis, and it may develop in up to 1% of
aortic graft cases. It can also occur days to years after surgery, with 3
years being the median interval. Fistulas are located in the third
 portion of the duodenum. Patients will usually have a small bleed
(herald bleed) that occurs before the major bleeding that is often
massive and fatal unless immediate intervention is undertaken.

VUGIB

Have a high index of suspicion for hemobilia in

patients who present with bleeding, right upper
quadrant pain, and jaundice.

VUGIB is a serious complication of portal hypertension, most often in the

setting of cirrhosis. In patients with cirrhosis, 25% to 50% of patients have
varices. One-third of patients with varices will develop a variceal bleed. The
dilated submucosal veins develop in response to the portal hypertension,
providing a collateral pathway for decompression of the portal system into the
systemic venous circulation. Varices are most common in the distal esophagus
and can reach sizes of 1 to 2 cm. As they enlarge, the overlying mucosa
becomes increasingly tenuous, excoriating with minimal trauma. Varices are
most commonly seen in the esophagus but may also develop in the stomach
and hemorrhoidal plexus of the rectum. The likelihood of developing a bleed
increases with the size of the varices and worsening portal hypertension.
Bleeding is frequently massive, accompanied by hematemesis and
hemodynamic instability. Mortality secondary to variceal hemorrhage is
approximately 20–30%.

2. Treatment

Therapeutic options range from pharmacologic, endoscopic, angiographic, to

surgical. They are often complementary and require a multidisciplinary team
approach.

a. Proton Pump Inhibitors

The introduction of proton pump inhibitors (PPIs) and the progress
made in endoscopic technology have revolutionized the management
of GI bleeding. Acid suppression has been shown to play a role in the
inactivation of pepsin, optimization of platelet function, and inhibition
of fibrinolysis. Subsequently, clot stabilization and ulcer healing may
be more effective and rapid within a less acidic environment.
Infusions of PPIs are used when NVUGIB is suspected. Effective
acid suppression reduces the rate of bleeding recurrence, use of
surgery, and mortality. An intravenous bolus followed by a twice-
daily PPI is recommended prior to endoscopy and has been shown to
reduce the need for therapeutic endoscopic interventions. If high-risk
stigmata are seen during endoscopic therapy, a continuous infusion
of a PPI is recommended for 24–72 hours.

b. Vasoconstrictors

Prophylactic use of second- or third

generation cephalosporins should be
considered in patients with variceal
hemorrhage because of the risk of
spontaneous bacterial peritonitis.

The goal of pharmacologic therapy in VUGIB is to reduce portal

venous blood flow and thus pressure. Useful medications include
vasopressin, terlipressin, octreotide, and somatostatin. These agents
are successful in controlling variceal hemorrhage in up to 80% of
cases. Vasopressin promotes splanchnic arteriolar constriction,
leading to decreased portal venous pressure along with systemic
vasoconstriction. Vasopressin may cause coronary artery vasospasm,
angina, or hypertension. Administration of nitroglycerin along with
vasopressin may prevent the deleterious effects on the coronary
circulation. Somatostatin and its longer acting analog, octreotide,
inhibit the release of vasodilator hormones and indirectly cause
splanchnic vasoconstriction without affecting the systemic circulation
and thus results in a decrease in portal pressure. They are the agents
of choice because of their adverse effect profile. Somatostatin is
administered as a 250-µg IV bolus followed by an infusion of 250
µg/h for up to 5 days to prevent rebleeding. Octreotide has a longer
half-life than somatostatin and is administered as a 25- to 100-µg IV
bolus followed by infusion at 25–100 µg/h. Continuous IV infusion
of these agents results in temporary control of bleeding and allows
time for resuscitation and appropriate diagnostic and therapeutic
interventions. Vasoactive medications have been shown to decrease
mortality, decrease hospital stay, improve hemostasis, and decrease
blood transfusion requirements.

c. Antibiotics

Prophylactic antibiotics should be started early in patients with

variceal hemorrhage because they have a risk of developing
spontaneous bacterial peritonitis. Second-or third-generation
cephalosporins have been used with good success. The use of
prophylactic antibiotics in patients with variceal bleeding has been
shown to decrease their mortality rate.

d. Endoscopy

Endoscopy has become the preferred

diagnostic and therapeutic modality for
upper gastrointestinal bleeding with
diagnosis achieved in 95% of patients.

Endoscopy has become the preferred diagnostic and therapeutic

modality for upper GI bleeding because of its accuracy and low
complication rate. Specific diagnosis can be achieved in 95% of
patients. The optimal timing of endoscopy remains a balance between
clinical need and resources. Endoscopy should ideally be performed
when the patient is clinically stabilized and able to tolerate the
procedure. It is recommended that upper endoscopy be performed
within 24 hours in patients with suspected NVUGIB. If endoscopy is
not quickly available, consider transfer to a facility with endoscopic
capabilities.
Endoscopy can identify stigmata of a recent bleed known to correlate
well with an increased risk for rebleeding and thus a need for
endoscopic therapy. In patients undergoing upper GI endoscopy,
20% to 35% will require a therapeutic endoscopic intervention.
Different forms of endoscopic therapy include injection technique,
thermal technique, and mechanical technique. In many cases, a
combination of these modalities is used to treat a single bleeding
lesion or one at high risk of bleeding. Endoscopy is successful at
stopping acute bleeding in 90% of cases. Rebleeding occurs in about
20% of patients and increases the risk of mortality. With rebleeding,
repeated endoscopy is typically justified.
In patients with VUGIB, endoscopic sclerotherapy and endoscopic
band ligation are the mainstays of therapy. These procedures are
successful in achieving hemostasis in 80% to 90% of patients.
Despite its high effectiveness in controlling bleeding, the complication
rate with sclerotherapy can be as high as 40%. Band ligation has a
lower rate of complications, but it can be difficult to perform during
acute bleeding. Even when bleeding is short lived, endoscopy should
be pursued because the rate of significant rebleeding is high.

e. Angiography with Embolization

When endoscopy fails to control bleeding, angiography with
embolization is now considered the second-line treatment before
proceeding with surgical intervention in the 5–10% of patients who
are unresponsive to pharmacologic or endoscopic treatment.
Embolization has a 90% success rate and is less invasive than
surgical intervention. Prior endoscopic tattooing can facilitate the
procedure. Super-selective embolization is preferred because it
carries a lower complication rate than embolization of larger vessels.

f. Balloon Tamponade

In patients for whom pharmacologic or endoscopic therapy fails to

control variceal hemorrhage, balloon tamponade can be used to
temporize the bleeding for 24 hours. A high risk of rebleeding exists
after deflation of the balloon, in addition to the risk of esophageal
rupture; therefore, a more definitive therapy should be undertaken
(Figure 14-5).
Figure 14-5. Diagram of Variceal Balloon Tamponade Device

g. Surgery
Surgical intervention is usually reserved for cases in which endoscopy
and angiography with embolization have failed to control the bleeding
due to PUD. Patients requiring surgery are typically critically ill and
have higher rates of mortality. Indications for surgery were
traditionally based on the blood transfusion requirements. Although
not absolute, many surgical consultants consider an ongoing blood
transfusion requirement in excess of 6 U is an indication for surgical
consultation and possible intervention in older patients, and 8 to10 U
for younger patients. Hemodynamic instability despite significant
resuscitation (> 6 U transfusion), recurrent hemorrhage after initial
stabilization (with up to two attempts at obtaining endoscopic
hemostasis), continued slow bleeding with a transfusion requirement
greater than 3 U/day may all prompt evaluation and consideration for
surgery. If surgery is required, the procedure of choice depends on
the underlying pathophysiology.

h. Transjugular Intrahepatic Portosystemic Shunt (TIPS)

Emergent portal decompression with a TIPS should be considered in
patients with refractory variceal bleeding despite medical
management. The TIPS procedure involves the creation of a
nonselective, low-resistance shunt between the portal vein and the
hepatic vein through which blood is shunted from the portal to the
systemic circulation. The procedure is performed by angiographic
technique. TIPSs are required in approximately 10% of patients with
variceal bleeding. The TIPS procedure can be lifesaving with 90% to
100% of patients achieving hemostasis. A major complication
associated with this procedure is the development of hepatic
encephalopathy in 10% to 20% of patients as a result of shunting of
the blood from the portal to the systemic circulation. Rebleeding
occurs in up to 20% of patients within the first month, usually related
to occlusion. TIPSs are associated with significantly less morbidity
and mortality than surgical decompression. Surgery is considered
only when medical and endoscopic therapy fails to control bleeding
and a TIPS is not available.

A major complication of a transjugular

intrahepatic portosystemic shunt is acute
encephalopathy in 10% to 20% of patients.
B. Lower Gastrointestinal Bleeding
Lower GI hemorrhage can present in a myriad of ways and be self-limiting or
life-threatening. In this section, we will focus on the evaluation, diagnosis, and
management of clinically significant bleeding.
Lower GI bleeding comprises approximately 20% of all GI bleeds. Five
percent to 10% of all GI bleeds are isolated to the small bowel. Common
causes of lower GI bleeding include diverticular hemorrhage, angioectasia,
post-polypectomy bleeding, ischemia, polyps, neoplasia, inflammatory bowel
disease, Meckel’s diverticulum, rectal ulcers, or radiation proctitis.

1. Diagnosis

Diagnosis of a GI bleed can be diagnosed with fecal occult blood testing or

observation of blood expelled from the rectum. The color of the output may
range from bright red to maroon or black. Hematochezia commonly emanates
from a lower GI source, but can result from a brisk upper GI bleed. Black
stool is also likely from an upper GI source but can result from the small
bowel or right colon as well.

The source of blood expelled from the rectum

may be from an upper gastrointestinal location
regardless of color of output.

a. Laboratory Values

Laboratory values may be altered in the patient with GI bleeding.

Hemoglobin and hematocrit (H&H) will likely demonstrate anemia.
Early in the course of the bleeding, the H&H may remain normal.
Blood urea nitrogen (BUN) can be elevated in the absence of acute
renal disease. An elevated BUN to creatinine ratio of greater than
30:1 could be indicative of an upper GI source.

b. Radionuclide Scans
Multiple radiologic modalities are available for diagnosis and/or
localization of the source of the GI hemorrhage. Radionuclide scans
have a high sensitivity and detect bleeding at 0.05 to 0.1 mL/min.
This study is not specific because localization is not as precise as with
other modalities. The most common radionuclide study is the
technetium-99m (Tc-99m) red blood cell scan. Angiography should
be performed immediately after a positive result to maximize the
odds of a positive angiography. If the study is negative, repeat
imaging can be performed without repeat Tc-99m dosing should the
patient again demonstrate signs of hemorrhage.
An uncommon source of lower GI hemorrhage is a Meckel’s
diverticulum. This can be diagnosed with a Meckel’s scan, a
radionuclide scan using technetium-99m pertechnetate, which
illustrates the gastric mucosa found in the diverticulum.

c. Computed Tomography Scan

A contrast-enhanced computed tomography (CTA) scan can detect
bleeding at a rate as low as 0.3 mL/min. Sensitivity is improving with
continued development in technology. CTA is often more timely and
specific than a Tc-99m study but does require administration of
contrast, potentially increasing the prevalence of contrast-induced
nephropathy. This should be taken into account if consideration is
being made for transcatheter angiography for treatment because
further contrast will need to be administered.
Computed tomographic enterography (CTE) can be used to diagnose
small bowel bleeding after a negative capsule endoscopy or in those
patients in which capsule endoscopy is contraindicated (inflammatory
bowel disease, history of radiation, small bowel surgery, or stenosis
of the small bowel). There is an increase in the localization of masses
in the small bowel compared with video capsule endoscopy. (See
discussion on capsule endoscopy.)

d. Angiography
Transcatheter arteriography (TCA) can detect bleeding at a rate of
0.5 to 1.0 mL/min, a higher rate than a Tc-99m study or CTA.
Therefore, negative angiography is common after a positive initial
study. Source identification is obtained in 25% to 70% of cases.
Provocative angiography can be performed. This involves the infusion
of anticoagulants, vasodilators, or thrombolytics to increase the
likelihood of bleeding. Identification occurs in 31% to 89% of cases
of provocative angiography. Angiography can be more beneficial in
the patient with the massive GI bleed because diagnosis and
intervention can be performed via catheter-directed therapy. It is the
preferred initial test if the patient is hemodynamically unstable or has
received a transfusion of greater than 5 units of packed red blood
cells.

e. Endoscopy
Endoscopic evaluation of the small bowel and colon can be
performed as standalone studies or in conjunction with radiographic
modalities. Per the ACG, a colonoscopy should be performed as the
initial diagnostic procedure for nearly all patients presenting with
acute lower GI bleeding. Colonoscopy can be a diagnostic and also
therapeutic modality. In lower GI bleeds, 48% to 90% can be
localized with colonoscopy. It is imperative to intubate the ileocecal
valve and examine the terminal ileum during the procedure to rule
out a more proximal source of bleeding. Bowel preparation should be
performed when able because this can improve localization and
decreases the rate of colon perforation. A nasogastric tube may be
placed to aid in administration of the solution. Large-volume tap
water enemas may also be given to allow better visualization.
 More than half of lower gastrointestinal bleeds
can be localized using colonoscopy. Bowel
preparation improves visualization.

Push enteroscopy is usually performed with a pediatric colonoscope and can

reach up to 150 cm from the ligament of Treitz. This can diagnose up to 70%
of lesions which are usually vascular in nature. This is considered a second-
look endoscopy and the majority of identified lesions are in a location that are
visualized on standard upper endoscopy.
Video capsule endoscopy (VCE) has emerged as the diagnostic test of choice
for small bowel bleeding. The source of bleeding is identified in 38% to 83%
of patients with high positive and negative predictive values, 94% to 97% and
83% to 100%, respectively. Performing the examination within 2 weeks of
the bleeding episode increases localization from 34% to 91%, with the
greatest yield within the first 72 hours. VCE should be performed if other
imaging modalities have been used without achieving localization of the
bleeding source.

2. Treatment
Therapeutic modalities for lower GI bleed include interventions in the
radiology suite, GI lab, and operating room. Medical management of lower GI
bleeding can include the use of somatostatin analogs, which can lead to a
decreased need for blood transfusion in refractory bleeding (Figure 14-6).
Transcatheter angiography can be immediately followed by intervention
during the same procedure. Super-selective embolization (SSE) succeeds in
obstructing the bleeding source in 73% to 100% of cases. Clinical success
(defined as cessation of bleeding without early rebleeding) is achieved in 63%
to 96% of cases. Secondary clinical success rate (after a second
angioembolization) is 79%. Transcatheter angiographic intervention (TAI)
provides definitive treatment in 81% to 86% of patients. Rebleeding is more
common in small bowel sources as a result of the large amount of collateral
vessels present. Embolization does frequently result in minor ischemic injury
to the bowel, but major events occur in 4% of the cases.

Figure 14-6. Algorithm for the Management of Lower

Gastrointestinal Bleeding

Interventions in the endoscopy suite can be performed at the time of the

diagnostic evaluation via colonoscopy or push enteroscopy. Application of
clips, argon plasma coagulation, electrocoagulation, banding, and injection of
epinephrine are all employed to obtain hemostasis. These modalities are more
effective in the large bowel than the small bowel. Up to 46% of patients
experienced rebleeding within 36 months in small bowel lesions treated
endoscopically.

In extreme cases, emergent subtotal colectomy

can be performed once an upper gastrointestinal
source has been ruled out. Persistent hemorrhage
after this suggests a small bowel source.

Surgical intervention is usually reserved for cases in which the location of

bleeding has definitively been located. In extreme cases, emergent subtotal
colectomy can be performed once an upper GI source has been ruled out. If
an emergent subtotal colectomy is performed and continued hemorrhage is
encountered, the small bowel is the most likely source of bleeding. Surgical
resection is the treatment of choice for the bleeding Meckel’s diverticulum.

IV. INTRA-ABDOMINAL HYPERTENSION AND

ABDOMINAL COMPARTMENT SYNDROME
Intra-abdominal pressure (IAP) is a steady-state pressure contained within the
abdominal cavity. Normal IAP ranges from 5–7 mm Hg. However, patients
with morbid obesity and individuals that are pregnant may have higher
baseline IAPs. Short periods of increased IAP occur during sneezing,
coughing, Valsalva maneuvers, defecation, and weight lifting.
IAP can also vary with spontaneous respirations. In addition, positive
inspiratory-expiratory pressures during mechanical ventilation can indirectly
increase IAP. Increases in the volume of intra-abdominal contents can also
increase IAP. Although it does not increase IAP directly, compliance of the
abdominal wall (ie, burns, edema, and prone positioning) may also affect the
pressures contained within.
 In clinical practice, intraabdominal pressure is
almost always measured indirectly via bladder
pressures.

Pressures in the abdomen increase with intra-abdominal volume increases or

decreased compliance. Massive intravenous fluid resuscitation with capillary
leak, positive fluid balance, and rapid increase in visceral edema are directly
associated with the development of increased intra-abdominal volumes, thus
increasing IAP. No matter what the cause, elevated IAP threatens perfusion
and viability of the organs of the intra-abdominal compartment. The terms
intra-abdominal hypertension (IAH) and abdominal compartment syndrome
(ACS) represent stages along the spectrum of IAP that affects intra-abdominal
tissue viability and organ dysfunction.

1. Diagnosis
IAH is defined by a sustained or repeated pathologic elevation in IAP greater
than or equal to 12 mm Hg. In clinical practice, IAP is almost always
measured indirectly by way of bladder pressures transduced through an
indwelling catheter. This measured pressure correlates well with directly
measured IAP. Intermittent bladder pressure measurement equipment is
readily available in most ICUs. Grades of IAH are noted in Table 14-3.
Abdominal compartment syndrome is not graded; it is solely present or
absent.

Table 14-3 Grading of Intra-abdominal Hypertension

 Sustained intra-abdominal pressures greater than
10 mm Hg in the pediatric population constitutes
intra-abdominal hypertension.

Abdominal compartment syndrome is defined as a sustained IAP greater than

20 mm Hg that is associated with new organ dysfunction or failure. In the
pediatric population, IAH is defined as sustained or repeated pathologic
elevation of IAP greater than 10 mm Hg and ACS defined as IAH with new
or worsening organ dysfunction attributable to elevated IAP. IAH and ACS
can be further classified as primary, secondary, or recurrent. Primary is when
the condition is associated with injury or disease in the abdominal pelvic
region that frequently requires surgical or interventional radiologic
intervention. Secondary refers to conditions that do not originate from the
abdominal pelvic region. Recurrent refers to IAH or ACS that redevelops
following previous surgical or medical treatment of the primary or secondary
IAH. Many different conditions can lead to IAH and ACS. Risk factors for
IAH are listed in Table 14-4.

2. Clinical Presentation
Early detection and recognition of IAH is paramount so that it can be treated
before progressing to ACS. The presentation of acute IAH is varied, but
progressive oliguria and increased ventilatory requirements are common.
Other findings include hypotension, tachycardia, elevated jugular venous
pressure, jugular venous distension, peripheral edema, abdominal tenderness,
or acute pulmonary decompensation. There may be evidence of
hypoperfusion, including cool skin, obtundation, restlessness, or lactic
acidosis. Physical examination has a low sensitivity of around 40–60%, but
nearly all patients have a tensely distended abdomen.

Table 14-4 Risk Factors

Abbreviations: APACHE II, Acute Physiology and Chronic Health Evaluation II, BMI, body mass
index, PEEP, positive end-expiratory pressure, SOFA, Sequential Organ Failure Assessment
Reproduced with permission Kirkpatrick AW, Roberts DJ, De Waele J, et al. Intraabdominal
hypertension and the abdominal compartment syndrome: updated consensus definitions and clinical
practice guidelines from the World Society of the Abdominal Compartment Syndrome. Intensive Care
Med. 2013;39(7):1190-206. Used under a CC BY4.0 license.

IAH and ACS can have effects both intra-abdominally and extra-abdominally.
Some of these effects are directly associated with the pressure causing
impaired perfusion of the abdominal organs, while other effects are the result
of the change in thoraco-abdominal compliance.
Gastrointestinal tract: Increased vascular resistance of the
splanchnic vessels leads to hypoperfusion and visceral ischemia,
potentially leading to bacterial translocation and lactic acid
production.
Renal: Direct compression of the renal parenchyma and
compression of renal vessels resulting in increased venous
congestion and decreased arterial perfusion that can activate the
renin-angiotensin system leading to oliguria and acute kidney
injury.
Cardiovascular: Inferior vena cava compression which can decrease
the preload; decreased arterial outflow to the lower extremities;
increase in right ventricular afterload; decreased cardiac output.
Respiratory: Decreased functional residual capacity; increased
ventilation/perfusion mismatch; increased intrathoracic pressures
during mechanical ventilation.
Central nervous system: Impaired venous return from the brain as
a result of increased jugular venous pressures which may result in
increased intracranial pressure.
 Abdominal compartment syndrome can affect
both intra-abdominal and extra-abdominal organ
systems.

3. Management
Early detection of IAH and ACS remains the mainstay of optimal
management. The use of serial monitoring is recommended in any patient at
risk. Supportive care should consist of maintaining adequate perfusion with
prompt intervention with medical therapies designed to decrease rising intra
abdominal pressure. These therapies include the following examples.
Improving abdominal wall compliance: optimize sedation and
analgesia; avoid elevation of head of bed greater than 30 degrees;
remove constrictive dressings; escharotomies; and use of
neuromuscular blockers.
Evacuation of intra-luminal contents: nasogastric decompression;
prokinetic agents; rectal decompression; decrease or discontinue
enteral nutrition; enemas; and colonoscopic decompression.
Evacuation of abdominal fluid collections: paracentesis;
percutaneous drainage of fluid collections/abscesses; and surgical
evacuation.
Correct fluid balance: avoid excessive fluid; aim for zero to
negative balance; diuresis; and renal replacement therapy.
Optimize systemic and regional perfusion: use of goal directed
therapies; and hemodynamic monitoring devices to guide
resuscitation.

Decompressive laparotomy remains the standard

and most definitive treatment for abdominal
 compartment syndrome.

Surgical treatment, the decompressive laparotomy, remains the gold standard

and most definitive treatment for ACS. However, even after a decompressive
laparotomy is performed, the procedure does not prevent recurrent intra-
abdominal hypertension. The temporary abdominal closure device used to
protect the viscera can result in a constrictive bandage that decreases
abdominal wall compliance and can allow for increased IAP.

Key Points
Abdominal Surgical Emergencies: Part 2
Although no current scoring system exists to accurately predict
patients at risk for severe acute pancreatitis, stratification of
severity remains important.
Antibiotic prophylaxis is not recommended to prevent infected
pancreatic necrosis.
Oral feeding is feasible and recommended if the patient can
tolerate; otherwise, enteral tube feedings should be instituted.
Upper gastrointestinal bleeding originates proximal to the ligament
of Treitz, and lower gastrointestinal bleeding originates distal to the
ligament of Treitz.
Medical treatment has greatly decreased the incidence of upper
gastrointestinal bleeding with endoscopy being the mainstay of
treatment refractory to medical treatment.
Localization of the site of the lower gastrointestinal bleeding will
help determine the management pathway.
 Intra-abdominal pressures should be measured via bladder
pressures early in patients at risk for intra-abdominal hypertension
and abdominal compartment syndrome.
Treatment to maintain abdominal organs perfusion and methods to
mediate and prevent increasing intra-abdominal pressure should be
instituted early in patients with intra-abdominal hypertension.
Decompressive laparotomy remains the most definitive treatment
for abdominal compartment syndrome but does not obviate the risk
of recurrent abdominal compartment syndrome.

Suggested Readings
1. Banks PA, Bollen TL, Dervenis C, et al. Classification of acute
pancreatitis—2012: revision of the Atlanta classification and
definitions by international consensus. Gut. 2013;62(1):102-111.
2. Chaptiti L, Peikin S. Gastrointestinal Bleeding. In Parrilo JE,
Dellinger RP, eds. Critical Care Medicine. 4th ed. Philadelphia,
PA: Saunders Elsevier; 2014; Chapter 76.
3. Coccolini F, Montori G, Ceresoli M, et al. The role of open
abdomen in non-trauma patient: WSES Consensus Paper. World
J Emerg Surg. 2017;12:39.
4. Darcy MD, Cash BD, Feig BW, et al. Appropriateness Criteria-
Radiologic Management of Lower GI Tract Bleeding. American
College of Radiology.
https://acsearch.acr.org/docs/69457/Narrative/
5. Evans RPT, Mourad MM, Pall G, et al. Pancreatitis: Preventing
catastrophic haemorrhagic. World J Gastroenterol.
2017;23(30):5460-5468.
6. Forsmark CE, Vege SS, Wilcox CM. Acute pancreatitis. N Engl J
Med. 2016;375(20):1972-1981.
 7. Feinman M, Haut ER. Upper gastrointestinal bleeding. Surg Clin
North Am. 2014:94(1):43-53.
8. Gerson LB, Fidler JL, Cave DR, Leighton JA. ACG Clinical
Guideline: Diagnosis and Management of Small Bowel Bleeding.
Am J Gastroenterol. 2015;110(9):1265-1287.
9. Kirkpatrick AW, Roberts DJ, De Waele J, et al. Intra-abdominal
hypertension and the abdominal compartment syndrome: updated
consensus definitions and clinical practice guidelines from the
World Society of the Abdominal Compartment Syndrome.
Intensive Care Med. 2013;39(7):1190-206.
10. Maheshwari R, Subramanian RM. Severe acute pancreatitis and
necrotizing pancreatitis. Crit Care Clin. 2016;32(2):279-290.
11. Rahman SI, Saeian K. Nonvariceal upper gastrointestinal
bleeding. Crit Care Clin. 2016:32(2):223-239.
12. Rogers WK, Garcia L. Intraabdominal Hypertension, Abdominal
Compartment Syndrome, and the Open Abdomen. Chest.
2018;153(1):238-250.
13. Strate LL, Gralnek IM. ACG Clinical Guideline: Management of
Patients with Acute Lower Gastrointestinal Bleeding. Am J
Gastroenterol. 2016:111(4):459-474.
14. Tavakkolizadeh A, Ashley S, Acute Gastrointestinal Hemorrhage.
In: Townsend CM, Beauchamp RD, Evers BM, Mattox KL, eds.
Sabiston Textbook of Surgery. 9th ed. Philadelphia, PA:
Saunders Elsevier; 2012; Chapter 48.
15. van Brunschot S, van Grinsven J, van Santvoort HC, et al.
Endoscopic or surgical step-up approach for infected necrotising
pancreatitis: a multicentre randomised trial. Lancet.
2018;391(10115):51-58.
16. Wybourn C, Campbell A. Gastrointestinal Bleeding. In: Vincent
JL, Abrahm E, Moore FA, Kochanek PM, Fink MP, eds.
 Textbook of Critical Care. 7th ed. Philadelphia, PA: Elsevier;
2017: Chapter 24.

Suggested Websites
1. American Pancreatic Association. https://www.american-
pancreatic-association.org
2. American College of Gastroenterology. http://www.gi.org
3. WSACS - the Abdominal Compartment Society.
http://www.wsacs.org
4. EMCrit Blog – Emergency Department Critical Care &
Resuscitation. https://emcrit.org/emcrit/blakemore-tube-
placement/
 Chapter 15
ACUTE CORONARY SYNDROMES

Objectives
Identify patients who have acute coronary syndromes with various
electrocardiographic and clinical presentations.
Outline diagnostic procedures and the acute management of non–ST-
elevation acute coronary syndrome (NSTE-ACS) and ST-elevation
myocardial infarction (STEMI).
Identify appropriate reperfusion interventions for patients with STEMI and
high-risk patients with NSTE-ACS.
Recognize the complications of myocardial infarction and outline the
appropriate management.

Case Study
A 58-year-old man with a long-standing history of type 2 diabetes mellitus and
hyperlipidemia develops sudden-onset severe chest pain while mowing grass. It was
associated with dyspnea, nausea, and diaphoresis. His vital signs on arrival in the
emergency department are as follows: blood pressure of 148/84 mm Hg, heart rate
of 94 beats/min, respiratory rate of 26 breaths/min, and oxygen saturation
measured by pulse oximetry of 97% on room air. His physical examination is
remarkable only for dyspnea and mild diaphoresis.
– What features make acute coronary syndrome more likely to have occurred?
– What information is needed to determine whether this patient has an acute
coronary syndrome?
 – What are the recommended immediate management/interventions?

I. INTRODUCTION
Acute coronary syndrome (ACS) refers to a group of conditions characterized by
acute myocardial ischemia resulting from reduction in myocardial blood flow. An
important distinction is made clinically on the basis of an electrocardiogram (ECG)
between patients with ACS who have ST-elevation myocardial infarction (STEMI),
who should be considered for immediate revascularization, and those who do not
(non–ST-elevation acute coronary syndrome [NSTE-ACS]). ACSs account for nearly
2 million hospitalizations annually in the United States, and, if patients who die
before reaching the hospital are included, mortality may be as high as 25%.

ACSs share similar pathogenic mechanisms and represent different points along a
common continuum. ACSs are usually precipitated by rupture of an atherosclerotic
plaque, leading to a complex process of inflammation, platelet activation and
aggregation, thrombus formation, and microembolization to the distal vasculature
that results in decreased myocardial oxygen supply. Plaque erosion may play a role
in some patients with NSTE-ACS. Possible sequelae of plaque rupture include
thrombus formation with total occlusion, with ST-elevation myocardial infarction;
dissolution of thrombus and healing of the fissure, with clinical stabilization; and
subtotal occlusion, which can lead to either NSTE-ACS or unstable angina.

The distinction between NSTE-ACS and unstable angina is made on the basis of
biochemical evidence of myocardial injury manifested as elevation of cardiac
troponin. Such injury confers a higher risk and is usually an indication for coronary
revascularization. Patients without elevated troponins are said to have unstable
angina. The spectrum of ACS is shown in Figure 15-1.

Be aware of changes in the management of ACS as

new evidence becomes available.

It is important to recognize that other conditions can increase cardiac troponin. The
Universal Definition of Myocardial Infarction makes a distinction between troponin
elevation consequent to plaque rupture or erosion (Type 1 MI) and troponin
elevation that is the result of an imbalance between myocardial demand and supply
(Type 2 MI), which is treated differently, usually by addressing the underlying
hemodynamic precipitant. Inflammatory, infectious, renal failure, and other
conditions can lead to elevated troponin levels not related to myocardial ischemia.

A multidisciplinary team approach is important in the

recognition and management of patients with ACS.

Patients presenting with chest discomfort should be evaluated expeditiously for life-
threatening conditions, including not only ACS but also other conditions such as
pulmonary embolism and aortic dissection; those conditions should be treated
promptly when diagnosed. An ECG should be obtained and interpreted within 10
minutes of presentation. Results are best when an organized approach to triage and
diagnosis of suspected ACS is employed. Hospitals should establish
multidisciplinary teams (including primary care physicians, emergency medicine
physicians, cardiologists, nurses, and others) to develop evidence-based protocols
for triaging and managing patients with symptoms suggestive of ACS. These
protocols must be updated periodically based on the best current evidence.
 Figure 15-1. Overlapping Spectrum of Acute Coronary Syndromes

Abbreviations: ECG, electrocardiogram; MI, myocardial infarction; NSTE-ACS, non–ST-elevation

acute coronary syndrome
Acute coronary syndromes are distinguished by initial ECG findings and cardiac markers. The
term NSTE-ACS is preferred to non-ST elevation MI because the latter does not distinguish
between Type 1 and Type 2 myocardial infarction (see text).

The consequences of ACS are often so severe that

therapy is indicated even when the diagnosis is
presumptive.

Patients with other critical illness or injury have an increased risk for ACS and
frequently have atypical presentations. Definitive diagnosis of ACS may not be
possible on initial evaluation and requires continuous observation, ECG monitoring,
and/or laboratory evaluations. The initial physical examination should include vital
signs and general observation, assessment of jugular venous distension, auscultation
of the lungs and heart, evaluation of the peripheral pulses, detection of neurologic
deficits, and assessment for evidence of systemic hypoperfusion.
II. NON—ST-ELEVATION ACUTE CORONARY SYNDROME
If ST elevation is not present on the presenting ECG, the likelihood that symptoms
represent ACS can be evaluated based on an assessment of risk factors for coronary
artery disease (Table 15-1), the history and presenting symptoms, physical
examination, the ECG, and biochemical markers. Accelerated diagnostic pathways
using validated risk scores can augment the accuracy of clinical judgment and can
be beneficial to assess prognosis.

Table 15-1 Risk Factors for Coronary Artery Disease

At presentation, patients with ischemic-type chest pain and an ECG with no ST-
segment elevation are presumed to have NSTE-ACS. Other causes of prolonged
chest pain (Table 15-2) should also be considered. Myocardial damage is assessed
using biochemical markers of cardiac injury.

Table 15-2 Differential Diagnosis of Prolonged Chest Pain

Data taken from the Agency for Healthcare Research and Quality. Braunwald E, Mark DB, Jones RH, et al.
Unstable angina: diagnosis and management. AHCPR Publication 94-0602. Rockville, MD: Agency for Health
Care Policy and Research and National Heart, Lung, and Blood Institute; 1994.

A. Diagnosis
The most important factors that suggest the likelihood of myocardial ischemia are
the character of the pain, prior history of coronary artery disease, age, and number
of risk factors. Results of the physical examination may be normal, although a
fourth heart sound (S4) may be heard during episodes of pain. A 12-lead ECG is
most helpful if it shows ST-segment depression (Figure 15-2) during anginal
episodes, especially if those changes are dynamic and relieved by nitrates, but the
ECG may be normal or may reveal nondiagnostic T-wave inversions or peaked T
waves.

Some patients may not have classic features of ACS. Patients with diabetes mellitus
may not feel chest discomfort but rather present with dyspnea or other atypical
symptoms. Elderly patients with ACS may present only with lethargy, irritability, or
altered mental status.
 Figure 15-2. Electrocardiogram of a Patient With NSTE-ACS

The ST-segment depression is characteristic of non–ST-elevation acute coronary syndrome.

Courtesy of Kehllee Popovich, ACPN, MSN

Some women may not present with typical left-sided pressure or squeezing-type
chest pain but may have nonspecific symptoms often described more as discomfort
rather than pain. Women also have a greater prevalence of other features such as
nausea, shortness of breath, palpitations, jaw and neck pain, as well as back pain.
Nonetheless, chest pain remains the predominant symptom reported in those
ultimately diagnosed with ACS, with the frequency in women equal to men.
If equipment and expertise are available, the use of transthoracic echocardiography
allows bedside assessment of wall motion abnormalities as a marker for current or
past ischemia and the detection and follow-up of new abnormalities. It also provides
an estimate of left ventricular (LV) function and identification of valvular
dysfunction and/or pericardial fluid.

New-onset shortness of breath and/or new left bundle

branch block should be considered possible evidence
of ACS, particularly in women and patients with
 diabetes mellitus, who may have atypical
presentations.

The differential diagnosis of chest pain is broad and includes aortic dissection or
aneurysm, myocarditis, pericarditis, aortic stenosis, pulmonary embolism,
pneumothorax, esophageal and gastrointestinal disorders, pneumonia, pleuritic
pain, musculoskeletal or chest wall diseases, hyperventilation, and other causes.
Additional tests, such as hemoglobin/hematocrit, electrolytes, thyroid function, and
arterial oxygen saturation, may be helpful in identifying precipitating factors for
demand ischemia or ACS, or may identify alternate diagnoses. Other imaging tests
may be indicated as warranted by the clinical presentation.
Several risk-stratification scores have been developed and validated to assist in
predicting the risk of death and ischemic events in NSTE-ACS. The GRACE 2.0
(Global Registry for Acute Cardiac Events) score (https://www.outcomes-
umassmed.org/risk_models_grace_orig.aspx) requires an app or a web-based
calculator, whereas the TIMI (Thrombolysis in Myocardial Infarction) risk score can
be easily determined at the bedside (Table 15-3). High-risk patients are considered
to have a greater than 6% risk of dying within 6 months, and intermediate-risk
patients have a 6-month mortality rate of 3% to 6%. Risk assessment has
implications for the location of care, selection of medical therapy, and use of
reperfusion interventions.

Table 15-3 TIMI Risk Score for Adverse Cardiac Events

Abbreviation: TIMI, thrombolysis in myocardial infarction

B. Management
Reversing myocardial ischemia and confirming the diagnosis of NSTE-ACS are the
initial priorities. Patients with NSTE-ACS should be admitted to a unit with cardiac
monitoring and placed on bed or chair rest (Figure 15-3). Emerging data suggest
that routine use of supplemental oxygen in cardiac patients with normal oxygenation
may have untoward effects, but patients with hypoxemia (oxygen saturation
measured by pulse oximetry < 90% on room air), respiratory distress, heart
failure, or shock should receive oxygen by nasal cannula. If precipitating, reversible
causes, such as fever, anemia, hypoxemia, infection, hypertension, anxiety,
hyperthyroidism, arrhythmias, or sympathomimetic drug ingestion (eg, cocaine,
amphetamines) can be identified, they should be treated aggressively. Further
management includes anti-ischemic therapy, therapy for platelet
aggregation/thrombosis, ongoing risk stratification, and consideration of invasive
reperfusion procedures.
 Figure 15-3. Evaluation and Treatment of Acute Coronary Syndromes

*Intervention by emergency medical services or in the emergency department

1sildanefil, vardenafil, tadalafil
Abbreviations: ABCs, airway, breathing, circulation; ACE, angiotensin converting enzyme
inhibitor; ARB, angiotensin receptor blocker; ECG, electrocardiogram; LBBB, left bundle branch
block; LMWH, low-molecular-weight heparin; NSTE-ACS, non–ST-elevation acute coronary
syndrome; STEMI, ST-elevation myocardial infarction; UFH, unfractionated heparin

1. Anti-ischemic Therapy

Immediate control of ischemic pain is typically accomplished with a combination of

nitrates, β-blockers, and opiates. Antianginal medications that are effective in
stabilizing patients with unstable angina are listed in Table 15-4. The goal is to
reduce ischemia without causing hypotension or reflex tachycardia. Patients with
ongoing ischemic discomfort should receive up to three doses of sublingual or spray
nitroglycerin. Nitrates should not be administered if the systolic blood pressure
measures < 90 mm Hg or ≥ 30 mm Hg below the patient’s baseline blood
pressure. Additional contraindications to nitrate administration are a heart rate of
< 50 beats/min, tachycardia > 100 beats/min in the absence of heart failure
symptoms, and in suspected right ventricular infarction or severe aortic stenosis.
Nitrates are also contraindicated in patients who have received a phosphodiesterase
inhibitor for erectile dysfunction in the previous 24 hours (48 hours for tadalafil).

Table 15-4 Anti-ischemic Therapy

Prominent hypotension with administration of

nitroglycerin should raise the suspicion of right
ventricular infarction.

If sublingual or spray nitroglycerin does not relieve pain, an assessment should be

made about the need for IV nitroglycerin for persistent ischemia. Decreases in
blood pressure with nitroglycerin are predominantly the result of increased venous
capacitance and can often be treated with careful IV crystalloid infusion, but if the
systolic pressure falls below 110 mm Hg in normotensive patients, the nitroglycerin
dose should not be increased. Tolerance to the hemodynamic effects of
nitroglycerin becomes important after 24 hours of continuous infusion, and efforts
should be made to switch to other dosing regimens. The dose of IV nitrates should
be tapered and discontinued when ischemic manifestations have resolved for 12 to
24 hours.

Morphine sulfate is a reasonable analgesic for management of pain refractory to

initial antianginal therapy. Nonsteroidal anti-inflammatory drugs other than aspirin
should be discontinued during hospitalization.

Aspirin improves survival and reduces the incidence

of MI.

Routine use of IV β-blockers in the initial management of patients with suspected

NSTE-ACS is not supported by current evidence, but may be considered in patients
with ongoing chest pain, especially with concomitant hypertension or tachycardia;
IV dosing should be followed by oral administration. IV β-blockers are
contraindicated in patients with shock, heart rate < 50 beats/min, decompensated
heart failure, advanced heart block (type II second-degree or third-degree),
hypotension, or active bronchospastic disease. Caution is advised with the use of β-
blockers in patients with risk factors for shock (age > 70 years, heart rate > 110
beats/min, systolic blood pressure < 120 mm Hg, or late presentation).
Oral β-blockers should be initiated within the first 24 hours in patients when
possible; an attempt should be made to start even in patients with initial
contraindications to their use.

Avoid use of diltiazem in cases of reduced left

ventricular function.

Non-dihydropyridine calcium channel blockers (eg, diltiazem, verapamil) do not

reduce mortality risk in myocardial infarction (MI). In the absence of
contraindications (such as significant LV dysfunction), they may be considered only
if patients cannot tolerate a β-blocker or symptoms are not controlled with
nitroglycerin and β-blockers together.

2. Antiplatelet Therapy

The use of antiplatelet and anticoagulant agents (Table 15-5) is important in

patients with NSTE-ACS because of the contributions of platelet
activation/aggregation and the coagulation system to platelet-rich thrombus
formation. Dual antiplatelet therapy is indicated in patients undergoing
revascularization with percutaneous coronary intervention (PCI). The intensity of
therapy with these agents is often tailored to the patient’s risk assessment and to
plans for early invasive procedures. Non−enteric-coated aspirin at a dose of 162 to
325 mg should be administered (and chewed) as soon as possible to all patients
with NSTE-ACS (including those in the prehospital setting) if no aspirin allergy is
suspected. Aspirin should be administered indefinitely. Clopidogrel or ticagrelor
should be considered as an alternative antiplatelet agent if aspirin is
contraindicated.

Table 15-5 Antiplatelet Drugs Used in Acute Coronary Syndromes

Abbreviations: P2Y12, The P2Y12 receptor is the predominant receptor involved in the ADP-stimulated
platelet activation; PCI, percutaneous coronary intervention; STEMI, ST-elevation myocardial infarction; NSTE-
ACS, non–ST-elevation acute coronary syndrome
*Individuals >75 years of age, and those receiving fibrinolysis, should receive a loading dose of 75 mg
because of increased bleeding risk

If an early invasive strategy (angiography within 24–48 hours with revascularization

if appropriate) or noninterventional conservative approach is planned, clopidogrel or
ticagrelor should be added to aspirin to decrease the risk of cardiovascular death,
MI, and stroke. Clopidogrel, prasugrel, or ticagrelor should be administered in
patients undergoing PCI, but prasugrel is contraindicated in those with a history of
stroke or transient ischemic attack and is associated with an increased risk of
bleeding. The choice of a specific adenosine diphosphate inhibitor should be
discussed with the cardiologist when possible.

3. Anticoagulant Therapy

The combination of aspirin and an anticoagulant agent is more beneficial than

aspirin alone in NSTE-ACS. The selection of a specific agent should take into
account the risks of ischemia and bleeding complications, as well as the presence of
renal dysfunction. In patients with ACS treated with a conservative ischemia-guided
approach, low-molecular-weight heparin, unfractionated heparin, bivalirudin, or
fondaparinux should administered as soon as possible unless there are significant
contraindications. Patients managed with fondaparinux require an additional
anticoagulant to prevent catheter thrombosis if a PCI is subsequently performed.
Unfractionated heparin is continued for at least 48 hours, and enoxaparin or
fondaparinux for the duration of the hospital stay (up to 8 days) in patients managed
with medical therapy or until PCI is performed. If an early invasive strategy is
planned, unfractionated heparin, enoxaparin, or bivalirudin should be initiated as
soon as possible. Serial platelet counts are required to monitor for heparin-induced
thrombocytopenia (HIT). Argatroban is an alternative anticoagulant in patients with
known HIT. Patients who are adequately anticoagulated with warfarin still require
antiplatelet therapy, but anticoagulation with heparin or alternative agents is
generally not needed unless the international normalized ratio is less than 2.0.

4. Reperfusion Interventions

Fibrinolytic agents have no proven efficacy in NSTE-ACS. Patients with NSTE-ACS

and shock benefit from early reperfusion with PCI or coronary artery bypass graft
and should be triaged to the catheterization laboratory as soon as possible. An early
invasive approach is clearly indicated in patients who have hemodynamic or electric
instability, or refractory angina, and who lack serious comorbidities such as
bleeding, advanced liver or renal failure, or end-stage disease such that the risk of
PCI outweighs the benefit.
In other patients with NSTE-ACS, risk stratification is the key to the decision about
an invasive strategy; cardiology consultation is usually warranted to help with the
decision. An initial strategy of medical management with attempts at stabilization is
warranted in patients with lower risk, but patients at higher risk should be
considered for cardiac catheterization. Calculation of a GRACE risk score can be
helpful with respect to timing; patients with a score > 140 benefited from early
revascularization (< 24 hours) in the Timing of Intervention in Acute Coronary
Syndromes (TIMACS) trial.

5. Other Interventions

An echocardiogram should be part of the workup in

ACS.

High-dose statins are indicated for all patients with ACS. Echocardiography should
be performed to evaluate LV performance because an angiotensin-converting
enzyme (ACE) inhibitor or angiotensin receptor blocker should be administered to
patients with NSTE-ACS and evidence of pulmonary congestion or LV ejection
fraction < 40% unless contraindications are present. Aldosterone antagonist is an
option in patients receiving an ACE inhibitor and β-blocker who have an ejection
fraction < 40%, diabetes mellitus or heart failure, and no contraindications. Risk
factor modification, including exercise, weight reduction, and smoking cessation, is
recommended for all patients with ACS. Patients should be evaluated for diabetes
mellitus even if not previously diagnosed.

III. ST-ELEVATION MYOCARDIAL INFARCTION

Patients with STEMI usually have plaque rupture with an occlusive coronary
thrombus, resulting in a wave front of myocardial necrosis that begins at the
endocardial surface within 15 minutes. The infarction progresses outward to the
epicardium over approximately 6 hours unless collateral flow, spontaneous
reperfusion, or reperfusion via an intervention is established. This progression may
be modulated by the extent of collateral flow and determinants of myocardial
oxygen consumption, which affords an opportunity for myocardial salvage. As with
the patient with NSTE-ACS, prompt diagnosis and early treatment of the patient
with STEMI is vital to optimize outcomes.

A. Diagnosis
Patients with STEMI typically present with prolonged chest pain and associated
symptoms, but some patients have MIs that are painless (silent infarction/ischemia)
or have other related symptoms, such as dyspnea and fatigue. In the critically ill
patient population, STEMIs may not be associated with classic symptoms and are
often suspected when complications occur, new arrhythmias develop, or ECG
changes are noted. The physical examination findings are nonspecific.

The most common finding in patients with normal sinus rhythm is the S4 heart
sound, indicating decreased left ventricular compliance at the end of ventricular
filling. Bibasilar crackles as a result of pulmonary edema may be present and are
helpful in assessing hemodynamic status. A brief focused physical examination aids
in the diagnosis and assessment of possible complications of STEMI. A limited
neurologic examination for evidence of prior stroke or cognitive deficits also should
be conducted.

When possible, a prehospital 12-lead ECG should be obtained and interpreted to

facilitate diagnosis, triage, and treatment on arrival at the medical facility.
Otherwise, a patient with chest discomfort or symptoms suggestive of ACS should
have this ECG performed and read within 10 minutes of arrival or detection of
symptoms. The ECG is diagnostic of STEMI in the absence of QRS confounders (ie,
bundle branch block, pacing, LV hypertrophy, Wolff-Parkinson-White syndrome) if
it shows ≥ 2 mm of ST-segment elevation in two or more contiguous leads in men
or ≥ 1.5 mm of ST-segment elevation in women in leads V2-V3 and/or ≥ 1 mm
in other contiguous leads (Figure 15-4).
Patients with ECG findings of new or undiagnosed left bundle branch block and
chest pain compatible with myocardial ischemia are treated similarly to those
patients with ST-segment elevation. If the initial ECG is not diagnostic but the
patient remains symptomatic with a high clinical suspicion for ischemia, serial ECGs
at 5- to 10-minute intervals may be performed to detect the development of ST-
segment elevation. A right-sided ECG showing ST elevation in right-sided V leads
may suggest right ventricular infarction is present.

Cardiac catheterization in STEMI should not be

delayed waiting for troponin results.
If the diagnosis is in doubt, echocardiography may add helpful information by
showing focal wall motion abnormalities. The diagnosis is confirmed by elevated
serum levels of cardiac-specific troponin, but reperfusion should not be delayed or
deferred pending troponin levels.

Figure 15-4. ECG Indicating an Inferolateral STEMI

This electrocardiogram (ECG) shows classic findings of ST elevation in the inferior (II, III, and
aVF) and lateral (V4, V5, V6) leads, indicating an inferolateral ST-elevation myocardial infarction
(STEMI).

B. General Management
Once STEMI is suspected or diagnosed, the immediate concerns are to ensure
hemodynamic stability and to limit infarct size by restoring blood flow to the
affected artery as soon as possible (Figure 15-5). Cardiology expertise should be
sought promptly. Treatment of STEMI in the patient with other critical illness
requires careful individualization. Absolute and relative contraindications to
therapies must be considered and relative risk assessed. Choices may be limited by
significant comorbidities, bleeding risk, the availability of specialized procedures,
and the underlying prognosis.

1. Early Therapy
Immediate 12-lead ECG, cardiac-specific troponin measurement, and related
laboratory tests should be completed. Aspirin should be administered immediately,
and supplemental oxygen should be given in the presence of dyspnea, hypoxemia,
heart failure, or shock.
Early restoration of flow in the infarct-related coronary artery is associated with
improved survival in patients with STEMI; therefore, some type of reperfusion
should be chosen as soon as possible. Primary PCI with stent placement is the
preferred method if it can be performed quickly by experienced personnel; patients
should be transferred directly to the catheterization laboratory in preference to
other intensive care units when this is feasible. The door-to-balloon time goal is 90
minutes, but 60 minutes is preferable. Recent studies suggest that first medical
contact to balloon time is a more relevant measure, with a goal set at 90 minutes.
Activating the catheterization laboratory by obtaining and transmitting a prehospital
ECG and taking appropriate patients directly to PCI-capable centers are strategies
that can reduce time to revascularization.

The addition of a loading dose and subsequent maintenance doses of clopidogrel or

ticagrelor as part of dual antiplatelet therapy may improve outcomes prior to PCI for
STEMI, but consultation with the cardiology team is advisable because other
options, such as short-acting intravenous platelet inhibition, may be advisable in
some situations, especially if surgical intervention may be needed. An anticoagulant
agent, unfractionated heparin or bivalirudin, should also be administered to patients
undergoing PCI. Intravenous nitroglycerin may be useful in patients with STEMI
and ongoing chest pain, hypertension, or heart failure, unless the systolic blood
pressure is below 90 mm Hg. Intravenous β-blockers are not routinely administered
but may be considered at presentation if hypertension or ongoing ischemia is
present and there are no contraindications.

2. Acute Reperfusion Therapy

A plan for early reperfusion in patients with STEMI should be developed based on
the resources available in the facility and community.

a. Percutaneous Coronary Intervention (PCI)

PCI involves deployment of an intracoronary drug-eluting stent, along with

pharmacologic measures to prevent thrombosis. Primary PCI results in
higher patency rates of the infarct-related coronary artery and lower rates
of recurrent ischemia, reinfarction, and death. Primary PCI is the preferred
reperfusion technique if the procedure can be performed by experienced
personnel within 90 minutes of hospital presentation being preferred with
clinical or electrocardiographic evidence of ongoing ischemia, even if more
than 12 hours have elapsed since symptom onset.

If primary PCI is not available, and transfer to a facility with invasive

reperfusion capability can be accomplished within 30 minutes, for a door-
to-balloon time of less than 120 minutes, then this is the preferable option.
If this is not an option because of logistic or other challenges, then
fibrinolytic therapy is recommended, and this should be initiated within 30
minutes of hospital presentation.
Potential complications of an invasive strategy for treating STEMI include
problems with the arterial access site, dye allergy, contrast nephropathy,
complications of antithrombotic medications, technical complications, and
reperfusion events.

Recent data indicate that a radial artery approach for primary PCI reduces
major bleeding and access site complications and is associated with
improved outcomes. This may shift the risk-benefit calculation in some
patients prone to bleeding complications.
b. Fibrinolysis

If PCI is not available or cannot be performed within 120 minutes of

arrival, fibrinolytic therapy should be considered. Limitation of infarct size
is optimized when fibrinolytics are administered within 6 hours of symptom
onset. The physician must weigh the potential risks against the benefits of
fibrinolysis for each patient. If the decision to proceed is made and no
absolute contraindications exist (Table 15-6), fibrinolytic therapy should be
administered expeditiously. Several agents are available, including
alteplase, reteplase, and tenectaplase, and all are effective. Doses are listed
in Table 15-7. Findings that suggest reperfusion include relief of
symptoms, maintenance or restoration of hemodynamic and/or electrical
stability, and reduction of at least 50% of the initial ST-segment elevation
injury pattern on a follow-up ECG performed 60 to 90 minutes after the
initiation of therapy.

After fibrinolysis with a plasminogen activator, heparin should be used to

maintain vessel patency for at least 48 hours. Aspirin should be continued.
 Routine use of PCI in the first 2 to 3 hours after fibrinolytic therapy
(“facilitated angioplasty”) is not recommended.

Table 15-6 Contraindications for Fibrinolytic Therapy

Table 15-7 Fibrinolytic Agents Used in ST-Elevation Myocardial Infarction

 Time to open the infarct-related coronary artery is
the most important determining factor when choosing
options for reperfusion.

STEMI patients who develop cardiogenic shock or severe heart failure, or

who have evidence of reperfusion failure or re-occlusion after fibrinolytic
therapy, should be transferred to PCI-capable facilities as soon as possible.
Patients with STEMI who are hemodynamically stable and achieve
successful reperfusion also should be considered for transfer to a PCI-
capable facility. Antiplatelet and anticoagulant therapy is continued after
fibrinolysis and before transfer. The algorithm for triage and transfer of
patients for reperfusion therapy in STEMI is found in Figure 15-5. For
specific American Heart Association guidelines, see
https://professional.heart.org/en/guidelines-and-statements.
Figure 15-5. Reperfusion Therapy for Patients with STEMI

c. Coronary Artery Bypass Graft (CABG) Surgery in Patients with STEMI

Subsets of patients who present with STEMI may be better served with
CABG. Patients with failed PCI or whose coronary anatomy is not
amenable to PCI but who have ongoing symptoms of ischemia, cardiogenic
shock, severe heart failure, or other high-risk features should be
considered for CABG. CABG is also recommended in patients who require
not only revascularization but also repair of a mechanical defect such as
ventricular septal defect, free wall rupture, or papillary muscle rupture.
The previously reported increased mortality in CABG patients who recently
had a STEMI, and the increased bleeding in patients given recent dual
antiplatelet therapy needs to be balanced against the need for
revascularization.
 PCI is not contraindicated by the presence of coma
or a need for targeted temperature management after
cardiac arrest.

3. Adjunctive Therapy

a. Antiplatelet Therapy

Dual antiplatelet therapy with aspirin and P2Y12 inhibition is given to all
patients undergoing PCI, as described previously. However, data suggest
that even patients not undergoing PCI benefit from the addition of
clopidogrel or ticagrelor to aspirin.

Ideally, thrombolytic therapy should be

initiated within 30 minutes of the patient’s
arrival to the hospital.

Glycoprotein IIb/IIIa receptor antagonists inhibit the final common pathway

of platelet aggregation, blocking crosslinking of activated platelets, but in
the era of dual antiplatelet therapy, the role of addition of a glycoprotein
IIb/IIIa inhibitor in primary angioplasty for STEMI is uncertain.
“Upstream” (prior to PCI) use of GP IIb/IIIa receptor antagonists has failed
to show benefit and is no longer recommended. They may be considered
on an individual patient basis, if a patient has a large thrombus burden at
PCI or if there was insufficient loading with a P2Y12 receptor antagonist.

b. Anticoagulant Therapy
 If PCI is not possible within 120 minutes, then
fibrinolysis should be considered.

After fibrinolysis with a plasminogen activator, heparin should be used to

maintain vessel patency for 48 hours, adjusted to keep the partial
thromboplastin time at 1.5 to 2 times the control value. Heparin
anticoagulation after use of streptokinase is not necessary. Patients who
have intramural thrombus detected or suspected on echocardiography
should receive heparin, and heparin should be considered in patients with
large anterior infarctions who do not receive PCI or fibrinolysis.
c. β-Blockers

β-blockers are beneficial both in the early management of MI and as long-

term therapy. Oral β-blockers should be initiated after the patient with
STEMI has stabilized, ideally in the first 24 hours. Long-term use of these
agents is helpful in all patients who are at risk for recurrent cardiovascular
events and who have no contraindications to their use.

d. Renin-Angiotensin System Inhibitors

Inhibitors of angiotensin-converting enzyme (ACE) decrease circulating

angiotensin II levels and increase levels of bradykinin, which in turn
stimulates production of nitric oxide. ACE inhibitors have been shown to
improve hemodynamics, functional capacity, and symptoms. They also
improve survival in patients with chronic congestive heart failure and
prevent the development of congestive heart failure in patients with
asymptomatic LV dysfunction. Patients treated with ACE inhibitors after MI
showed improved survival, with particular benefit in patients with LV
dysfunction (ejection fraction < 40%), anterior infarction, or pulmonary
congestion. This improved survival was additive to the benefits of aspirin
and ß-blockers. The mechanisms responsible for the benefits of ACE
inhibitors most likely include limitation in the progressive LV dysfunction
and enlargement (remodeling) that often occur after infarction, but a
reduction in ischemic events was also seen. Immediate intravenous ACE
inhibition with enalaprilat has not been shown to be beneficial, but oral
ACE inhibition should be started early in the hospital course. An ACE-I
 should be administered within the first 24 hours to all patients with STEMI
and LV dysfunction or heart failure unless hypotension (systolic blood
pressure < 100 mm Hg) or other contraindications, most prominently a
history of angioedema, are present. Baseline renal function should be taken
into consideration when initiating an ACE inhibitor or an angiotensin
receptor blocker (ARB), but renal failure is not an absolute
contraindication to their use. Patients should be started on low doses of
oral agents and titrated to maximally tolerated doses. STEMI patients that
are intolerant to an ACE-I should be given an ARB. ARBs have been
shown to be non-inferior to ACE inhibitors in this setting.
e. Statins

Multiple studies have shown that statin use in patients after ACS can
prevent death, recurrent MI, and stroke. Use of a high-intensity statin is
preferred and should be initiated before discharge. In patients with ACS,
high-intensity statin therapy should be given regardless of the LDL level.
Contraindications to statin use include a history of statin-induced
rhabdomyolysis or significant myopathy and/or acute liver injury, but often
patients who did not tolerate one statin will tolerate another.
f. Calcium Channel Blockers

Long-acting calcium channel blockers may be a useful secondary therapy

for recurrent myocardial ischemia but are not appropriate for first-line
treatment. Randomized clinical trials have not demonstrated that routine
use of calcium channel blockers improves survival after MI. Immediate-
release nifedipine is contraindicated in the treatment of an acute MI.
Diltiazem and verapamil are contraindicated in patients with STEMI and
LV dysfunction and heart failure.
Transfer to a facility providing a higher level of care is indicated for
patients who have persistent ischemic symptoms after MI, who develop
cardiogenic shock, who have heart failure despite aggressive therapy, or
who have recurrent ventricular fibrillation or tachycardia despite aggressive
antiarrhythmic therapy.

C. Complications
Common early complications of MI are heart failure and cardiogenic shock,
recurrent ischemia and/or infarction, and arrhythmias. Urgent cardiology
consultation should be obtained as soon as possible to assist with management and
decisions regarding advanced interventions in all patients with complications of
ACS.

1. Heart Failure and Cardiogenic Shock

Heart failure after ACS generally results from LV pump failure. Echocardiography
should be performed to evaluate LV function and to rule out mechanical
complications, and expert consultation should be sought. Consideration should be
given to evaluation for residual ischemia or restenosis or thrombosis of a recently
placed stent.
Pharmacologic treatment of heart failure should be tailored to the patient’s clinical
and hemodynamic state. Clinical evaluation can assess perfusion and intravascular
volume by characterizing patients as wet or dry and warm or cold, but
hemodynamic monitoring can be useful, especially if patients do not respond
promptly to empiric therapy because clinical assessment of cardiac output is
difficult unless patients are in frank shock. Patients with a systolic arterial pressure
>100 mm Hg and low cardiac output should be treated initially with a vasodilator,
usually IV nitroglycerin (doses of 0.3 to 1 µg/kg/min, titrated up in increments of
0.5 µg/kg/min every 10 minutes). If arterial pressure decreases or cardiac output
remains inadequate, inotropic support with dobutamine may be initiated (5
µg/kg/min) and titrated as needed. Milrinone is an alternative inotropic agent with
less arrhythmogenic effect than dobutamine, although it is often associated with
hypotension. In countries where it is available, levosimendan has shown favorable
inotropic and hemodynamic benefits, although improved outcomes have not been
demonstrated in cardiogenic shock. Intravenous loop diuretics, such as furosemide
and bumetanide should be used to reduce pulmonary congestion. Hypotension is
rarely attributable to diuretic-induced hypovolemia in this setting.

Cardiogenic shock represents the leading cause of in-hospital death after MI.
Cardiogenic shock is diagnosed clinically by hypoperfusion and hypervolemia (wet
and cold) and hemodynamically by persistent hypotension with reduced cardiac
index. Cardiac dysfunction in patients with cardiogenic shock is usually initiated by
MI or ischemia, which can then be exacerbated by hypotension. Compensatory
mechanisms that retain fluid in an attempt to maintain cardiac output may add to
the vicious cycle and further increase diastolic filling pressures. The interruption of
this cycle of myocardial dysfunction and ischemia forms the basis for the
therapeutic regimens for cardiogenic shock. Early recognition of cardiogenic shock
and timely management with revascularization is paramount to improve outcomes.

Echocardiography provides information about overall and regional systolic function,

diastolic function, and valvular disease, and can rapidly diagnose mechanical
causes of shock. Right-heart catheterization is useful to characterize hemodynamics
and to optimize therapy in unstable patients in whom clinical estimates of filling
pressures can be unreliable, and optimal filling pressures may be higher than
expected in those with LV diastolic dysfunction. Concomitant right ventricular
dysfunction is often underrecognized in patients with cardiogenic shock, and its
importance is underappreciated; right-heart catheterization is the best and most
expeditious way to assess right-sided hemodynamics and its response to therapy in
these patients. Measurement of cardiac output and mixed venous saturation can
speak to the adequacy of cardiac performance and help select patients for inotropic
and or mechanical circulatory support.

Cardiogenic shock in the setting of acute MI is an

indication for emergent revascularization (either
percutaneous intervention or coronary artery bypass
grafting).

Prompt revascularization is the only intervention that consistently reduces mortality

rates in patients with cardiogenic shock. In a randomized trial of patients with LV
failure complicating STEMI, coronary revascularization with PCI or CABG within
48 hours of presentation reduced all-cause mortality compared with optimal
medical management. As such, urgent cardiac catheterization, with transfer to a
PCI-capable institution if needed, is warranted in patients with cardiogenic shock.

Therapy with vasopressor agents may be required to maintain coronary perfusion

pressure, to break the vicious cycle of progressive hypotension with further
myocardial ischemia. Norepinephrine is the preferred first-line agent in this setting.
Inotropic agents, such as dobutamine, may be added to raise cardiac output as a
supporting measure.

Percutaneous Mechanical Circulatory Support

 Percutaneous mechanical circulatory support should
be considered in patients with ACS and shock or
impending shock, based on hemodynamic assessment.

Percutaneous mechanical circulatory support devices can increase arterial pressure

and cardiac output, reduce LV filling pressures and afterload, and support coronary
perfusion. They can provide short-term support as a bridge to recovery or to
transplantation. Mechanical therapy may be preferable to vasoactive agents in this
regard because those agents can increase myocardial oxygen demand and decrease
microvascular flow. Choices include intra-aortic balloon pumping, implantable
centrifugal pump, the axial flow pump, and extracorporeal membrane oxygenation.
A key issue in choosing among mechanical support options is right ventricular
function; some patients with both right- and left-heart failure might benefit from
initial biventricular support with the addition of right ventricular support. Invasively
derived parameters that have been shown to be useful in selecting among
mechanical support devices include the cardiac power index (CO × MAP/456) an
index of LV contractile function, and pulmonary artery pulsatility index (PAPI:
pulmonary artery pulse pressure/right atrial pressure). Trials have not shown that an
intra-aortic balloon pump can improve outcomes in patients with cardiogenic shock.
Percutaneous left ventricular assist devices provide better hemodynamics compared
with the intra-aortic balloon pump, with higher cardiac indices and mean arterial
pressures as well as lower filling pressures, but they have not been shown to
improve mortality.

2. Right Ventricular Infarction

Right ventricular infarction results in elevation of right atrial and right ventricular
filling pressures and low cardiac output. These hemodynamic abnormalities result in
characteristic clinical findings of hypotension, clear lung fields, and distended
internal jugular veins. The ECG usually reveals an inferior infarction, and an ECG
tracing of the right precordial leads should be obtained and may reveal ST-segment
elevation, especially in V4R. Initial therapy includes maintenance of right
ventricular preload with volume expansion until the blood pressure is stabilized.
Associated bradycardia or high-degree heart block may require chemical or
electrical intervention. Agents that reduce preload should be avoided, such as
morphine, nitrates, ACE inhibitors/angiotensin receptor blockers, and diuretics. If
volume expansion is inadequate to stabilize the patient, inotropic support with
dobutamine should be considered.

3. Mechanical Complications

Mechanical complications following MI include ventricular free wall rupture,

ventricular septal rupture, and acute mitral regurgitation, all of which typically
occur during the first week after infarction.

Ventricular free wall rupture is often lethal although its incidence is low (< 1%).
Risk factors include the absence of collateral flow, anterior location of the infarct,
use of corticosteroids or nonsteroidal anti-inflammatory agents, age > 70 years,
and female sex. Pseudoaneurysm with leakage may be heralded by chest pain,
nausea, and restlessness, but frank free wall rupture presents as a catastrophic
event with shock and electromechanical dissociation. Echocardiography reveals
pericardial effusion, and salvage is only possible following prompt recognition and
thoracotomy for repair.

Ventricular septal rupture presents as hypotension, severe biventricular heart

failure, and cardiogenic shock with physical findings of a pansystolic murmur and
parasternal thrill. The hallmark finding is a left-to-right intracardiac shunt (“step-
up” in oxygen saturation from right atrium to right ventricle), but the diagnosis is
most easily made with echocardiography. Rapid institution of supportive
pharmacologic measures and mechanical support is necessary. Surgical repair is the
only viable option for long-term survival, but even if done in a timely manner,
mortality remains high, ranging from 20% to 80%.

Ischemic mitral regurgitation may be seen following an inferior MI because of

compromised blood flow to the posterior papillary muscle. The typical presentation
is that of acute-onset pulmonary edema and cardiogenic shock. The murmur of
acute mitral regurgitation may be limited to early systole because of rapid
equalization of pressures in the left atrium and left ventricle or may be soft or
inaudible when cardiac output is low. Diagnosis is made by echocardiography.
Afterload reduction inotropic or vasopressor therapy may temporize by supporting
cardiac output and blood pressure, but definitive therapy is surgical valve repair or
replacement, which should be undertaken as soon as possible because clinical
deterioration can be sudden.

4. Recurrent Ischemia or Infarction

Recurrent ischemia or infarction occurs in up to 20% of patients treated with
fibrinolytic therapy for MI, whereas patients receiving primary PCI have a lower
incidence of recurrent ischemia. Ischemia after MI can be caused by residual
stenosis in the infarct-related artery, by disease in another coronary artery, or by
occlusion of a new stent. An ECG recorded during recurrent pain should be
compared with those from the index MI event. Reinfarction may be difficult to
diagnose because cardiac troponins are unreliable since levels can be elevated for 5
to 14 days and because the ECG may be evolving. If there is high suspicion for
reinfarction, cardiac catheterization should be considered regardless of cardiac
biomarker values or ECG findings. Nonischemic etiologies, such as pericarditis and
pulmonary embolism, should also be considered as potential causes of recurrent
chest pain.

Detection of reinfarction is clinically important

because it carries incremental risk for the patient.

Treatment of post-MI ischemia is similar to management of the initial MI but also

includes cardiac catheterization and reperfusion, if possible. Acute reperfusion with
PCI or coronary artery bypass graft may be required for stabilization.

3. Arrhythmias

Arrhythmias associated with ACS and reperfusion include atrial bradycardias, atrial
tachycardias, atrioventricular (AV) blocks, ventricular tachyarrhythmias, and
asystole. Hemodynamically significant atrial bradycardia or AV block in the setting
of inferior MI can be treated initially with IV atropine in a dose of 0.5 mg every 3–
5 minutes to a total dose of 3 mg while preparing for transcutaneous pacing.
Atropine rarely corrects complete heart block or type II second-degree AV block,
especially when this occurs in the course of an anterior MI. Temporary transvenous
pacing is indicated for complete heart block, bilateral bundle branch block, new or
indeterminate-age bifascicular block with first-degree AV block, type II second-
degree AV block, and symptomatic sinus bradycardia that is unresponsive to
atropine. Transcutaneous pacing should be initiated for patients who have
indications for emergent temporary pacing until transvenous pacing can be
instituted.
 Acute onset of chest pain, dysrhythmias, or
pulmonary edema – shortly after PCI – should raise
concern for acute occlusion of a new stent.

Atrial tachycardias, such as atrial fibrillation, may cause hemodynamic instability

and precipitate myocardial ischemia, or they may be clinically insignificant and
transient. Immediate cardioversion is indicated in unstable patients. Depending on
the specific arrhythmia, IV adenosine, β-blockers, diltiazem, digoxin, or
amiodarone may be effective. Careful attention must be given to contraindications
for any of these agents.

Ventricular tachycardia and ventricular fibrillation should be treated according to

current advanced cardiac life support guidelines. After defibrillation and if
indicated, amiodarone is the drug of choice in patients with an acute MI.
Antiarrhythmic drugs are not recommended as prophylaxis for ventricular
arrhythmias in the setting of acute MI. To aid in the prevention of postinfarction
arrhythmias, prompt recognition and correction of systemic precipitants (including
hypoxemia, acid-base abnormalities, and electrolyte disturbances) is recommended.

D. Special Considerations
1. Perioperative MI

Perioperative MI can occur before surgery, intraoperatively, and during the

postoperative period. The last is the most common, with the peak incidence on the
third postoperative day. Perioperative MI is often associated with atypical
presentations and may be painless; patients rarely experience classic symptoms and
signs of acute coronary syndromes, or symptoms may be masked by analgesics
and/or sedatives. New-onset or increased atrial or ventricular arrhythmia is often the
presenting finding, as is postoperative pulmonary edema. Other possible
presentations may include hemodynamic instability and respiratory distress. The
diagnosis can be sometimes confirmed with serial ECG and cardiac marker
determinations, but echocardiography can be particularly useful to identify new wall
motion abnormalities in cases with diagnostic uncertainty. Medical therapy to
decrease myocardial oxygen demand is usually the first line of therapy.
Catheterization with potential PCI should be considered as long as dual antiplatelet
therapy is feasible; fibrinolytic therapy is often contraindicated.

2. Effects of Coexisting Diseases

Many critically ill patients have more than one medical condition that may require
significant alterations in the standard therapeutic approach. Some have relative or
absolute contraindications to standard medications or procedures. Patients with
stress ulceration or gastritis may not be candidates for aspirin therapy.
Postoperative patients or those with a bleeding diathesis may not be candidates for
clopidogrel, heparin, fibrinolytic therapy, or aspirin. β-blockers should be avoided
in patients with significant ongoing bronchospasm or decompensated heart failure.
Many drugs will need dose adjustments for renal or hepatic dysfunction. Critical
illness of a non-cardiac origin may result in decreased oxygen delivery to the
myocardium and subsequent myocardial dysfunction. Recommended management
of multiple organ failure in critical illness focuses on supportive care and treatment
of the underlying disease.

3. Targeted Temperature Management After Cardiac Arrest

Neurologic injury is the most common cause of death in patients with out-of-hospital
cardiac arrest. Patients who do not follow commands or have purposeful movements
should receive targeted temperature management. Lowering the core body
temperature to between 32°C and 36°C (89.6°F and 96.8°F) for 24 hours after
cardiac arrest with appropriate supportive care can improve neurologic outcome.
Targeted temperature management is associated with an increased risk of
coagulopathy and infection.

Key Points
Acute Coronary Syndromes
The preliminary diagnosis of NSTE-ACS is based on the clinical
symptoms, assessment of risk factors for coronary artery disease, and
ECG interpretation.
A 12-lead ECG should be obtained and interpreted within 10 minutes in
patients with possible ACS.
 For patients with suspected NSTE-ACS, perform risk stratification, select
an initial management strategy, complete the diagnostic evaluation, and
use medical therapy and revascularization as appropriate.
Non–enteric-coated aspirin at a dose of 162 to 325 mg should be
administered (and chewed) as soon as possible in all patients with
suspected or diagnosed ACS.
Antiplatelet and anticoagulant agents are important interventions in all
patients with ACS.
High-risk patients (continuing ischemia, elevated troponin levels) with
NSTE-ACS may be candidates for additional therapy with an early
invasive strategy.
Oral β-blockers should be initiated in the first 24 hours for all patients
with ACS unless strong contraindications are present.
A plan for early reperfusion of patients with STEMI should be developed
based on resources available in the facility and community.
Primary PCI is the preferred reperfusion technique if it can be
performed expeditiously by experienced personnel. Fibrinolytic therapy
for reperfusion in STEMI ideally should be initiated within 30 minutes of
the patient’s arrival to the hospital if timely PCI cannot be performed.
All patients with acute MI, whether they undergo reperfusion therapy or
not, should be treated with aspirin and another antiplatelet agent, such as
clopidogrel, prasugrel, or ticagrelor.
Use of ACE inhibitors decreases the mortality rate in patients with
STEMI.
PCI is not contraindicated in patients with coma or a need for targeted
temperature management after cardiac arrest.
Patients with cardiogenic shock in the setting of acute MI should undergo
emergent revascularization.

Suggested Readings
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management of acute myocardial infarction in patients presenting with
ST-segment elevation: The Task Force for the management of acute
myocardial infarction in patients presenting with ST-segment elevation
of the European Society of Cardiology (ESC). Eur Heart J. 2018;39:
119-177.
2. Amsterdam EA, Wenger NA, Brindis RG, et al. 2014 ACC/AHA
guideline for the management of patients with non-ST-elevation acute
coronary syndromes: a report of the American College of
Cardiology/American Heart Association Task Force on Practice
Guidelines. Circulation. 2014;130(25):2354-2394.
3. Hollenberg SM. Myocardial ischemia. In: Hall J, Schmidt G, Kress J.
Principles of Critical Care. 4th ed. New York, NY: McGraw-Hill
Education; 2015:1108-1151.
4. Nikolaou NI, Welsford M, Beygui F, et al. Part 5: Acute coronary
syndromes: 2015 International Consensus on Cardiopulmonary
Resuscitation and Emergency Cardiovascular Care Science with
Treatment Recommendations. Resuscitation. 2015;95:e121-e146.
5. O’Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA
guideline for the management of ST-elevation myocardial infarction: a
report of the American College of Cardiology Foundation/American
Heart Association Task Force on Practice Guidelines. Circulation
2013;127(4):e362-e425.
6. Roffi M, Patrono C, Collet JP, et al. 2015 ESC guidelines for the
management of acute coronary syndromes in patients presenting without
persistent ST-segment elevation. Task Force for the Management of
Acute Coronary Syndromes in Patients Presenting without Persistent
ST-Segment Elevation of the European Society of Cardiology (ESC). Eur
Heart J. 2016;37(3):267-315.
7. Thygesen K, Alpert JS, Jaffe AS, et al. Fourth universal definition of
myocardial infarction (2018). J Am Coll Cardiol. 2018;72(18):2231-
2264.
Suggested Websites
1. American College of Cardiology. http://www.acc.org.
2. American Heart Association. http://www.americanheart.org.
3. European Society of Cardiology. http://www.escardio.org.
4. Global Registry of Acute Cardiac Events (GRACE).
http://www.outcomes-umassmed.org/GRACE/default.aspx.
5. National Institute for Health and Clinical Excellence.
http://www.nice.org.uk.
6. Thrombolysis Myocardial Infarction (TIMI) Study Group.
http://www.timi.org.
 Chapter 16
CARDIOVASCULAR SURGICAL
EMERGENCIES

Objectives
Identify patients who have issues with bleeding after cardiovascular
surgical (CVS) procedures including coronary artery bypass graft
(CABG) procedures, percutaneous coronary interventions (PCI), or
percutaneous arterial interventions.
Outline basic management and interpretation of information, output,
character, and quantity from chest tubes placed for purposes of
CABG.
Identify signs, symptoms, and therapeutic options for patients with
suspected cardiac tamponade status post CABG.
Identify signs, symptoms, and therapeutic options for patients with
suspected complications from insertion of intravascular
sheaths/lines/devices employed during the performance of
cardiovascular surgical procedures.
Identify signs, symptoms, and therapeutic options for patients with a
pulseless extremity.
Identify signs, symptoms, and therapeutic options for patients with
vasoplegia.
 Case Study
A 66-year-old man has recently returned from the operating room after a
CABG procedure performed immediately after an emergent cardiac
catheterization for unstable angina. He has a 40-pack per year smoking
history, poorly controlled type 2 diabetes mellitus, endogenous obesity, a
body mass index (BMI) of 35, hypertension, and gout. He arrives to the ICU
paralyzed, intubated, and ventilated through a 7.5 outer diameter
endotracheal tube (OD ETT), 23 cm from the lip, on the following settings:
assist control volume ventilation with a rate of 16, tidal volume of 500 mL,
FIO2 of 0.80, and positive end-expiratory pressure (PEEP) of 5 cm H20. He
has a heart rate of 80 beats/min sinus rhythm, and is not currently paced but
has both atrial and ventricular pacemaker wires attached to a pacemaker
generator. His temperature is 36°C (96.8°F), blood pressure is a mean
arterial pressure (MAP) of 65 mm Hg per a right radial arterial line, and
there is a pulmonary artery catheter (PAC) in place via the right internal
jugular site with good waveforms with readings of pulmonary artery pressure
(PAP) of 32/14 mm Hg. He has two peripheral 20-gauge IVs placed in each
extremity. A 30 French left chest tube and two 30 French mediastinal tubes
are all connected to separate enclosed suction systems at –20 cm H20
suction. He has an intact sternal dressing as well as a 7.5 French right
femoral artery sheath which had been placed emergently in the cardiac
catheterization suite prior to surgery.
– What additional information is needed to determine whether the
postoperative course will be uneventful?
– What possible events may contribute to the morbidity or mortality of a
procedure performed for cardiovascular disease?

I. INTRODUCTION
It is estimated that, one in four deaths are attributable to cardiovascular
disease (CVD) in the United States of America. This represented
approximately 660,000 new deaths and over 300,000 new coronary attacks.
CVD is the impetus leading to the performance of over seven million inpatient
procedures, which represented approximately 14% of all United States
medical costs in 2013 valued at an estimated $316 billion dollars (Benjamin
et al., 2017). Worldwide, CVD remains the most common factor underlying
death (Table 16-1).

Significant Events Which May Contribute to the Morbidity or

Table 16-1
Mortality of a CVD-Related Procedure

Data taken from Despotis GM, et al.6

Every surgical procedure has an intrinsic risk or inherent risk of morbidity or

mortality. The CABG procedure carries an overall mortality of about 3%. This
number includes elective, emergent, and true emergency procedures. It is
estimated that purely elective procedures have been reported to have a lower
mortality approximating 1.7%.

Risk factors for complications after a CABG procedure for CVD include:
1. Older age > 70 years
 2. Small size body
3. Prolonged CPB time
4. Increased numbers of distal anastomoses
5. Use of the internal mammary artery as a conduit for bypassing
diseased coronary vessels
6. Lower preoperative platelet counts
7. Lower body temperature post procedure, postoperative infusion of
lower intravenous volumes for fluid overload
8. Higher positive end-expiratory pressure (PEEP) during mechanical
ventilation postoperatively
9. Higher volumes of transfusion of blood products
10. Use of perioperative antiplatelet therapies, such as aspirin, and/or
P2Y12 inhibitors such as clopidogrel, prasugrel, ticagrelor,
cangrelor, or ticlopidine (Table 16-2).

Patient- and Procedural-Associated Risk Factors for Post CABG

Table 16-2
Bleeding

Abbreviations: CABG, coronary artery bypass graft surgery; CPB, cardiopulmonary bypass; PEEP,
positive end-expiratory pressure
 Significant events which may contribute to the
morbidity or mortality of a CVD-related
procedure are the history of medications used
pre- and perioperatively; medication allergies;
procedural details: number of grafts, aortic
cross-clamp time, condition of native aorta
(atherosclerotic or soft), total pump time, details
of weaning from CPB, and blood loss from drains
since transport from the operating room.

Many procedures related to CVD are invasive, frequently involve access to

venous or arterial systems, and can be accompanied by bleeding. It is
estimated that the incidence of bleeding as a complication of a CVD
procedure ranges from 2% to 7%. If bleeding accompanies a CVD
procedure, it may account for a two-to fourfold increase in overall procedural
mortality. It is important to recall that patients who have had the need for a
cardiovascular procedure are at risk for subsequent cardiovascular events
including cerebrovascular accident (CVA), myocardial infarction (MI),
congestive heart failure (CHF), and sudden death by nature of their
underlying disease process and comorbidities.
The performance of procedures to correct CVD are not infrequently fraught
with unique associated complications that may or may not involve bleeding
but are directly related to:
The procedure itself
The use of modalities employed to support the patient through the
perioperative period
Conditions that may arise independently of the cardiac procedure
 It is important to recall that patients who have
had the need for a cardiovascular procedure are
at risk for subsequent cardiovascular events
including cerebrovascular accident (CVA),
myocardial infarction (MI), congestive heart
failure (CHF), and sudden death by nature of
their underlying disease process and
comorbidities.

II. IDENTIFICATION OF PATIENTS AT RISK FOR

BLEEDING AFTER A CARDIOVASCULAR SURGICAL
PROCEDURE
One of the most common and dramatic postoperative events after a
cardiovascular surgical procedure is bleeding. The bleeding may be minor,
only requiring simple interventions such as transfusion or may necessitate
surgical reoperation in as many as 3% to 5% of all patients. Ideally the
identification of bleeding should begin with identification of the potential for
bleeding. This identification should be considered in all patients before it
occurs in the majority of cases. The classification of postoperative bleeding is
a complex issue. An overriding principle that must be applied is that as a
caregiver’s concerns for bleeding arise, it is mandatory that it is
communicated to all members of the team, including the operating surgeon. If
bleeding occurs and is unchecked, unrecognized, or underappreciated, it is
associated with a wide spectrum of events ranging from blood loss anemia,
hemodynamic instability, ventilation compromise, pericardial tamponade, and
sudden cardiac arrest. Bleeding in the post CVS patient may be subtle or
catastrophic. It may be heralded by increases in blood from the surgical sites,
venipuncture sites, and surgical drains or from the gastrointestinal tract as a
result of direct intestinal ischemia from low flow states, embolic phenomena,
or preexisting gastrointestinal disease. As previously described, various
patient and procedural factors have been associated with the appearance of
post CVS bleeding. Some factors are generic to the physiology of coagulation,
or patient-specific, and others are procedural-specific. Patient-associated
events and some procedural-related events are described in Table 16-2.

One of the most common and dramatic

postoperative events after a cardiovascular
surgical procedure is bleeding. The bleeding may
be minor, only requiring simple interventions
such as transfusion, or may necessitate surgical
reoperation in as many as 3% to 5% of all
patients.

Risk factors that can be potentially modified are the restoration of body
temperature, judicious use of intravenous fluids, blood products, and
mechanical ventilation settings. Reversal of procedural anticoagulation may
involve the use of protamine sulfate. Dosages of protamine used in reversal of
heparin should be evaluated compared with intraoperative dosages
administered, adjusted for time since administration, and checked for
inaccuracies in timing or dose to avoid attempts to reverse heparin that has
already been metabolized. One milligram of protamine neutralizes
approximately 100 units of heparin. After 2 hours of the last heparin dose,
the protamine dose should be decreased by half. Protamine is generally given
to neutralize heparin. If protamine is administered unopposed or in doses
above what is required, it is by itself an anticoagulant unless bound to
heparin.
Additional defects in coagulation should be identified. Recently the platelet
and its unique task in regulating the thrombin switch has been recognized as
holding a central position in the regulation of coagulation. Although some
patients may present with isolated congenital disorders of bleeding, the more
common scenario observed in bleeding is from a medication-related issue that
produces an acquired defect in platelets. Procedural issues related to
bleeding or the consequences of ongoing bleeding and resultant depletion of
clotting system factors may also contribute to the aggravation of postoperative
bleeding.

Bleeding is usually not due to a single

coagulation derangement but appears that most
patients undergo a progressive series of
sequential effects to their coagulation system
which, in aggregate, creates bleeding.

Bleeding is usually not due to a single coagulation derangement but appears

that most patients undergo a progressive series of sequential effects to their
coagulation system which, in aggregate, creates bleeding. Coagulation defects
acquired with extracorporeal circulation are divided into alterations of the
overall numbers of platelets, defects in platelet functionality from medications
and pump effects (generally related to reduction of coagulation factors or
pump washout), and reduction in levels of fibrinogen. See Table 16-3 for
sources and prevalence of hemostatic defects in cardiac surgery and its
integration into a diagnostic framework.

Table 16-3 Sources of Hemostatic Defects in Cardiac Surgery

Abbreviations: CRYppt, cryoprecipitate; FFP, fresh frozen plasma; MTP, massive transfusion protocol;
PAF, platelet-activating factor; PRP, platelet-rich plasma; TRAP, thrombin receptor agonist peptide
Data taken from Despotis GM, et al.6
 Careful review of preoperative medications as
well as knowledge of modalities and/or specific
reversal agents are useful to address certain
bleeding events before a series of procedural-
related factors render the patient coagulopathic.
Administration of platelets, provision of blood
products, and specific coagulation factors to
support patient-related factors should be planned
ideally with the guidance of a vascular medicine
consultant or hematologist.

Acquired platelet defects from inborn disorders of metabolism or specific

genetic conditions have been described. Careful review of preoperative
medications as well as knowledge of modalities and/or specific reversal agents
are useful to address certain bleeding events before a series of procedural-
related factors render the patient coagulopathic. Administration of platelets,
provision of blood products, and specific coagulation factors to support
patient-related factors should be planned, ideally with the guidance of a
vascular medicine consultant or hematologist (Table 16-4).

A. Identification of Bleeding
Close monitoring of chest tube initial output is imperative following any
cardiovascular invasive procedures. Early identification of a patient who is
bleeding allows for early intervention to decrease the potential for further
adverse events. Mediastinal and pleural chest tubes are placed at the
completion of surgical procedures requiring opening of the thoracic cavity.
The Birmingham Criteria describe management decisions based on
interpretation of information, output, character, and quantity from chest tubes
which had been placed at the time of CABG, or an additional cardiac
procedure such as valve replacement/repair. These criteria facilitate the
decisions surrounding timing of a patient’s return to the operating room for
bleeding or other catastrophic event. The criteria are based on a time-related
set of volumes taken from termination of the operating room event through the
postoperative period. The criteria are based on volume of bleeding from chest
drainage tubes considered against the time to accumulate the drainage.
Trigger points may vary from large volumes over a short period of time to
lesser volumes over a longer period of time.

Generally, the five criteria that have been described are:

Close monitoring of chest tube initial output is

imperative following any cardiovascular invasive
procedures.

1) The range of volumes over a given time period, specifically a drainage of

more than 500 mL for the first hour after surgery, more than 400 mL per
hour for the 2 hours following surgery, more than 300 mL per hour for the
first 3 hours after surgery, or more than 1000 mL TOTAL in the first 4
hours after surgery
2) The development of any sudden massive bleeding at any time
3) Obvious signs of cardiac tamponade
4) Excessive bleeding which does not reach volume triggers but leads to
coagulopathy or difficulty in maintaining coagulation state
5) Cardiac arrest postoperatively (Table 16-5)

Available Reversal Agents for Oral Anticoagulants and Suggested

Table 16-4
Use
Abbreviations: 4F-PCC, 4-factor prothrombin complex concentrate; aPCC, activated prothrombin
complex concentrate
Reprinted from J Am Coll Cardiol, 70(24), Tomaselli GF, et al., 2017 ACC Expert Consensus
Decision Pathway on Management of Bleeding in Patients on Oral Anticoagulants: A Report of the
American College of Cardiology Task Force on Expert Consensus Decision Pathways, 3042-3067,
Copyright (2017), with permission from Elsevier.

Table 16-5 Indications for Re-exploration after CVS

Data taken from JW Kirklin, 1986 and Karthik et al., 2004.

B. Chest Tubes Management

Evaluation of chest tubes should include the

mnemonic DOPA (Drainage, Output, Position,
Air leak).

Following initial placement, chest tubes, mediastinal and/or pleural, should be

placed to continuous wall suction moderated to achieve a desired level usually
around −20 to −40 H2O. Evaluation of chest tubes should include the
mnemonic DOPA (Drainage, Output, Position, Air leak). The consistency and
color as well as the amount of drainage should be evaluated and documented.
Monitoring the drainage system for air leaks should be done by bedside
providers at least hourly. Air leaks are present if bubbling occurs in the water
seal chamber of the drainage system. If a continuous air leak is present,
inspect the tubing and connections from the skin to the device to assess their
integrity to rule out a mechanical problem rather than a primary patient
source. The amount of drainage, color, consistency, and presence of air leak
all need to be evaluated prior to consideration of removal of a chest tube.
Drainage should be consistent with serosanguineous or serous drainage. The
amount of drainage should be approximately 20 mL/hr for the 8–12 hours
prior to removal. If an air leak is present, a chest tube should not be removed
until the air leak has resolved or the cause is identified and corrected.
Providers should become familiar with the system used at their institution
(Figure 16-1).
 Figure 16-1. Chest Drainage System

Reproduced with permission British Columbia Institute of Technology (BCIT). Download

this book for free at http://open.bccampus.ca / CC BY-SA
(https://creativecommons.org/licenses/by-sa/4.0)

C. Management of Coagulation Defects and Postoperative Bleeding

Most defects in coagulation can be addressed by the appropriate transfusion
of either fresh frozen plasma or cryoprecipitate concentrates. In certain
situations, factor-specific concentrates are available as well as specific antidote
reversal agents for medications. Earlier guidelines for administration of blood
products and coagulation factors for cardiac surgery have been published by
the National Institute of Health (NIH) as well as the American Association of
Anesthesiologists.

Most defects in coagulation can be addressed by

the appropriate transfusion of either fresh frozen
plasma (FFP) or cryoprecipitate concentrates.

In general, an infusion of 15 mL/kg of fresh frozen plasma (FFP) will raise

levels of most factor levels to >30% activity, which is sufficient for correction
of the most commonly encountered defects. Cryoprecipitate is reserved when
hypofibrinogenemia (80 to 100 mg/dL) or states of dysfibrinogenemia related
to consumption is present. Approximately 10 international units (IU) of
cryoprecipitate will increase fibrinogen levels by 50–100 mg/dL and is
thought to be equivalent to the increased volume represented by 15 mL/kg
doses of FFP. Infusion of specific factor concentrates at rates outlined in
Table 16-3 can occur every 12 to 24 hours. The administration of platelets is
guided by the symptomatology of the patient. Platelets may be infused for
patients with active bleeding and a platelet count of less than 50,000 platelets
per µL, or if there are questions as to the functional capacity of the platelets
which may have been rendered abnormal from administration of medications
to maintain patency of stents or intravascular devices. In non-bleeding
patients, platelet administration is generally unnecessary to prevent risk of
isosensitization without regard to specific platelet counts. Rarely, after the
administration of chemotherapeutic agents which may render platelets poorly
functional, prophylactic platelet infusions are necessary but not until counts
drop below 20,000 platelets per µL. In cases of massive blood loss, generally
defined as greater than one or two blood volumes, expert opinion suggests
initiation of a massive transfusion protocol (MTP) and blood products
transfused in a 1:1:1 or 1:1:2 ratio of packed red blood cells
(PRBCs):FFP:platelets. Specific medication interactions and newer reversal
agents for novel anticoagulants are found in Table 16-4. Current
recommendations by the American College of Cardiology expert opinion panel
downplay the utility of FFP in favor of novel prothrombin complex
concentrates (PCC). Sometimes there is a need for a hematology consult to
assist in management.

In cases of massive blood loss, generally defined

as greater than one or two blood volumes, expert
opinion suggests initiation of a massive
transfusion protocol (MTP) and blood products
transfused in a 1:1:1 or 1:1:2 ratio of
PRBCs:FFP:platelets.

Other interventions can be used to help control postoperative bleeding,

especially venous bleeding. Increasing the PEEP on the ventilator
theoretically should increase the intrathoracic pressure, thus causing
tamponade of the venous bleeding. However, increased pleural pressures
have been known to increase the risk of bleeding and therefore, careful
assessment of the patient must occur prior to trying this intervention.
Hypertension in cardiac surgery patients should be controlled with a goal of a
systolic blood pressure < 140 to prevent venous bleeding during the initial
postoperative period. Specific patient populations may benefit from
desmopressin (DDAVP) administration such as patients who received aspirin
within 7 days of surgery, patients with CPB times exceeding 140 minutes,
and patients with demonstrable preor perioperative platelet dysfunction.
DDAVP is an option for a patient with uremia in acute or chronic kidney
dysfunction.

III. CARDIAC TAMPONADE

Cardiac tamponade exists when fluid within or around the pericardial space
exists, compresses, and compromises the compliance of the heart chambers,
which prevents normal filling and produces a picture of obstructive shock.
Cardiac tamponade may arise from medical diseases and may have a rapid or
gradual onset. It can be caused by cancer, renal failure, chest trauma,
pericarditis, connective tissues diseases, hypothyroidism, tuberculosis, and
aortic rupture. When it occurs after CVS, it is one of the most serious
complications of cardiac surgery and the presentation is usually acute.
Symptoms include shortness of breath (if not ventilated), generalized
weakness, lightheadedness, and cough. It is a diagnosis primarily based on
clinical suspicion and the findings of hypotension, jugular venous distension,
muffled or quiet heart sounds, or a new pericardial rub. A pulsus paradoxus,
defined as a greater than 10 mm Hg difference in systolic blood pressures
taken at end expiration versus full inspiration, can occur. The pathophysiology
of cardiac tamponade can present as Beck’s triad, which is the combination of
hypotension, distended neck veins, and distant, muffled heart sounds. One,
some, or all of these symptoms may be present with cardiac tamponade. A
high suspicion for tamponade is based on history and presence of symptoms.

The diagnosis of tamponade can be suggested by specific electrocardiogram

(ECG) changes revealing low voltage or a chest radiograph that demonstrates
a flask-shaped heart shadow. Bedside ultrasound reveals a characteristic
appearance of fluid within the pericardial sac. When tamponade presents in
patients who have preexisting hemodynamic monitoring, a hallmark finding is
the equalization of right and left heart pressures. Equalization of cardiac right-
sided diastolic pressures with a reduction of left-sided heart pressures is the
most frequently observed pattern. This pattern is detected when invasive
monitoring lines, such as a pulmonary artery catheter (PAC)and arterial line,
are in place.
The severity of symptoms is dependent on the rate of fluid accumulation
within or adjacent to the heart. The pericardium of the heart is a discrete
anatomic space which usually contains 15–50 mL of fluid. If excess fluid
accumulates slowly, as in a chronic cancer patient, the normal pericardium
can stretch allowing it to accommodate up to 2 liters with relatively few
symptoms. A more rapid rise of 150–200 mL of fluid typically is seen in the
postoperative period and will produce a progressive reduction in diastolic
ventricular filling with reductions in stroke volume and cardiac output.
Despite the presence of drainage catheters in the pleural and mediastinal
spaces in the postoperative cardiac patient, blood may accumulate and cause
tamponade physiology.

A. Treatment

Generally, tamponade occurring early in the

postoperative course of a cardiac surgery patient
is best managed with a prompt return to the
operating room with reopening of the original
sternotomy or thoracotomy.

Some post-operative patients have the pericardium left unapproximated.

Despite the open nature of the pericardium, tamponade may occur.
Percutaneous maneuvers, such as catheter drainage and performance of
subxiphoid windows, have been described as a means of treatment in both
acute and more chronic presentations. Generally, tamponade occurring early
in the postoperative course of a cardiac surgery patient is best managed with a
prompt return to the operating room with reopening of the original sternotomy
or thoracotomy. Post operative cardiac tamponade occurs in 3% to 5% of
cardiac surgery patients. A pattern of early abatement of bleeding from chest
drains, followed by signs of hemodynamic compromise (tachycardia,
narrowing of pulse pressure, oliguria, and acidosis increases in inotrope
support) generally occurs. Echocardiography, which is helpful in more
chronic conditions of slowly accumulating tamponade, may not provide
sufficient information in this setting related to spectral interference from
drains, sternal wires, and obscuring of windows due to dressings or monitor
devices. Transesophageal echocardiography (TEE) is an alternative option to
view the pericardial fluid collection, cardiac chambers, and myocardial
contractility. Open drainage is preferred because collections of fluid may be
heterogeneous and contain both liquid and clotted blood. The collections may
be located posterior to the heart which further limits echocardiographic
visualization or percutaneous attempts at drainage. An additional value of
open drainage is that it allows direct visualization of potential sites of
bleeding.

A return to the operating room for bleeding is not without consequences. In

several series, a return to the operating room and reopening of either a
thoracotomy or sternotomy has been associated with increased rates of:

Perioperative stroke
Perioperative renal injury coupled with the need for postoperative
dialysis
Prolonged mechanical ventilation (>72 hours)
The need for postoperative mechanical circulation support with
assist devices
A fourfold increase in sternal wound infections
A threefold increase in pulmonary infections
Prolonged stays in the ICU
It is not surprising that a return to the operating room portends a nearly three-
time greater mortality rate than those patients who did not return to the
operating room for evaluation of suspected tamponade or bleeding.
Open drainage has been reported to be successful, with overall salvage rates
that range from as low as 50% of patients in early case series to as high as
90% of patients in more recent case series. Time to return to the operating
room is an important factor with a delay in return as a frequently cited factor
in mortality. Re-exploration is associated with an increased risk of sternal
infection in up to 2% of patients who undergo reoperation.
IV. COMPLICATIONS FROM INSERTION OF
INTRAVASCULAR SHEATHS/LINES/DEVICES FOR
CARDIAC SURGERY
Vascular access related to cardiac surgery ranges from simple peripheral
intravenous devices to large-diameter sheaths capable of providing a portal for
insertion of additional hemodynamic monitors, circulatory assist devices, or
use of CPB support. Complications from the insertion of percutaneously
inserted devices may include infection, hemorrhage, thrombosis, hemolysis,
and damage to adjacent structures. Complications related to insertion of
intravascular sheaths/lines/devices for cardiac surgery may be of minor
consequence or may lead to death.
Of the implantable devices, central venous catheters (CVCs), single or multi-
luminal, are the most common. It has been estimated that in the United States
there are approximately 15 million CVC days per year. It is estimated that as
many as two-thirds of all ICU patients have a CVC at some point in the
continuum of their care.

A. Infections
Infectious complications may arise secondary to a break in aseptic technique
during insertion, faulty technique in the use of catheters, hematogenous
seeding of catheters from abscess sites distant to the catheter, or increased
duration of use, generally related to failure to promptly remove devices that
have outlived their useful period of use. Current recommendations to
minimize the risks of infection are:

The practice of appropriate hand hygiene before insertion and

before manipulation of catheters
The employment of full head-to-toe barriers with cap, mask, sterile
gowns, and gloves for insertion
The use of chlorhexidine-based skin disinfectant with the added
caveat of allowing full drying of the agent before insertion
 Avoidance of sites prone to infection, such as the femoral site
The site of CVC insertion has been related to the presence of infectious
complications with the risk decreasing in the order of site of insertion:
subclavian (SCV) < jugular (IJV) < femoral (FV). The use of ultrasound
guidance is the standard of care and should be used to aid insertion of CVC
when available. Peripherally inserted central catheters (PICCs) appear to have
a similar risk of infection to CVC lines in several series, emphasizing the
principle of prompt removal of unnecessary devices. Aseptic techniques when
accessing central lines, as well as prompt removal of unused devices and
avoiding routine site rotation or routine line guidewire changes of existing
lines, are believed to reduce the incidence of device-related infection.

Infectious complications may arise secondary to

a break in aseptic technique during insertion,
faulty technique in the use of catheters,
hematogenous seeding of catheters from abscess
sites distant to the catheter, or increased duration
of use, generally related to failure to promptly
remove devices that have outlived their useful
period of use.

A frequently employed device in cardiac surgery is the pulmonary artery

Swan-Ganz catheter. Recent reviews suggest that complications secondary to
mispositioning, misinterpretation of waveforms, potential for creation of
structural damage to the heart, knotting, infection, fragmentation, malignant
dysrhythmias, pulmonary infarction, and rupture of the pulmonary artery are
all factors that may limit the use of this device.

B. Hemorrhage
Retroperitoneal hemorrhage is an infrequent occurrence with a rate of less
than 1% yet it is a serious complication following transfemoral access
catheterization procedures with a mortality of 7%. Survival from
retroperitoneal hemorrhage depends on prompt diagnosis and appropriate
management. The clinical presentation of retroperitoneal hemorrhage may
vary, which sometimes can lead to delayed diagnosis, hemodynamic
instability, or unrecognized compartment syndrome. Factors related to
catheter-related retroperitoneal hemorrhage include:
Access above the inguinal ligament
Puncture or through and through needle arterial access leading to
vessel disruption
Avulsion or blind advancement of guidewire/sheath into small
arterial side branches

The three main management strategies are conservative medical management,

percutaneous endovascular intervention, or surgical vascular surgery
intervention. Conservative medical management includes volume resuscitation
with isotonic fluid, serial determinations of hemoglobin/hematocrit, and
transfusion of blood products as needed. If the patient becomes
hemodynamically unstable, has signs or symptoms of shock, or worsening
acidosis or coagulopathy escalation for percutaneous endovascular
intervention or vascular surgery, consultation is needed.

With advancements in technology, complications with the use of larger size

arterial catheters and sheaths are dependent on the size of the device relative
to the size of the arterial vessel insertion site. Devices with larger diameters
are more likely to reduce or occlude distal flow in vessels, if:

Placed in smaller diameter vessels

Vessels are affected with peripheral vascular disease
Patients are of smaller stature
 Factors related to catheter-related
retroperitoneal hemorrhage include access above
the inguinal ligament, puncture or through and
through needle arterial access leading to vessel
disruption, and avulsion or blind advancement of
a guidewire/sheath into small arterial side
branches.

Intra-aortic balloon pumps (IABP), temporary ventricular assist devices, or

veno-arterial extracorporeal membrane oxygenation (ECMO) may result in the
development of distal ischemia, embolization, tissue loss, or permanent nerve
injury. A well-documented complication of an IABP is the development of a
foot drop from peroneal nerve palsy in survivors.

C. Treatment
Treatment is best directed at prevention of complications by appropriate
training of individuals performing procedures. All procedures should involve
documenting the risks and benefits and sharing anticipated outcomes with
patients.

V. EARLY CARDIAC ARREST IN THE POSTOPERATIVE

CARDIAC SURGERY PATIENT
A rare, but deadly serious complication in a postoperative cardiac surgery
patient is cardiac arrest. Estimates of occurrence of cardiac arrest after
cardiac surgery fall between 0.7% and 5.2% of all patients who undergo a
cardiac operation. Most occur relatively early in the postoperative course, with
50% occurring in the first 3 hours and 84% in the first 8 hours following
surgery. This would imply that most of these arrests are witnessed because all
postoperative patients are closely monitored in an ICU setting with a trained
team immediately available. In most cases, an exact etiology for the arrest is
frequently not discovered due to the retrospective nature of investigations of
arrests and the inherited limitations with such reviews. Most retrospective
reviews have focused on the identification of a pre-arrest deterioration in
physiology and stress the benefit of early recognition of potentially reversible
etiologies prior to the arrest.
The correctible causes listed as precursors to arrest generally include:
Malignant dysrhythmias
Hemorrhage-induced hypovolemia
Cardiac tamponade
Hypoxia
Electrolyte abnormalities
Tension pneumothorax
Failure of pacing devices or wires
Ongoing graft occlusion ischemia

Ventricular fibrillation (VF) is the cause of 25% to 50% of arrests attributable

to malignant dysrhythmias in the immediate postoperative period, with the
next most common causes of arrests related to cardiac tamponade and major
bleeding.
The actual figures for patient survival after a perioperative arrest is unknown.
The reported range of survivors is from 5% to 70%. Most figures for survival
after arrest approximate 50% whether the resuscitation occurs with an open
or closed chest.

The correctible causes listed as precursors to

arrest generally include malignant dysrhythmias,
hemorrhage-induced hypovolemia, cardiac
tamponade, hypoxia, electrolyte abnormalities,
 tension pneumothorax, failure of pacing devices
or wires, and ongoing cardiac ischemia.

Early defibrillation without CPR, chest compressions coupled with

defibrillation as needed, attempts at high-level pacing prior to performance of
compressions, rapid opening of the chest at the bedside in the ICU, or “scoop
and run” (rapid return to operating room) techniques (Figure 16-2) to allow
opening of the chest in the operating room have all been suggested.
Proponents of rapidly opening the chest propose early identification of
correctable causes such as bleeding or tamponade which may be altered
successfully. In the few reports that address this action, survivors of
successful resuscitation are largely reported to be discharged neurologically
intact.
 Figure 16-2. Algorithmic Schema for Treatment of Early
Postoperative Arrest

A. Treatment
As mentioned previously, cardiac arrest in the postoperative cardiac surgery
patient differs significantly from the typical out-of-hospital cardiac arrest
scenario for which advanced cardiac life support (ACLS) was designed.
Patients are in monitored conditions and have a wide spectrum of associated
data, not the least of which are a complete history, frequent and concurrent
laboratory values, and readily available resuscitative equipment. Although
there is still controversy surrounding the proper treatment of cardiac arrest in
the postoperative cardiac surgery patient, the Society of Thoracic Surgeons
recently adopted an expert consensus statement advocating for early
defibrillation, minimizing external CPR, and rapid reopening of the chest.
The first step in the treatment of the arrest is to identify the rhythm and
determine whether it will respond to defibrillation. In the case of ventricular
fibrillation (VF) or pulseless ventricular tachycardia (VT), rapid defibrillation
is the preferred treatment. It is generally believed that external CPR is not
needed if defibrillation can be provided in less than 1 minute, a goal that
should be generally obtainable in a modern ICU setting. Unlike traditional
ACLS, defibrillation should proceed with three shocks before proceeding to
external CPR. Studies have shown that this stacked shock strategy has
improved Return of Spontaneous Circulation (ROSC), improved 24-hour
survival, and improved survival to hospital discharge.

If the patient remains in VF/VT following three shocks, a bolus dose of 300
mg IVP amiodarone is recommended. This is consistent with ACLS
guidelines. If VF/VT persists, it is unlikely that additional defibrillation will be
effective and at this point, external CPR should begin as a bridge to re-entry
sternotomy. External CPR is largely ineffective in cases of cardiac tamponade
or bleeding, two of the more common causes of postoperative cardiac surgery
arrest. This objective finding has led to the conclusion to withhold
compressions prior to defibrillation, based on reports of myocardial injury,
sternal and rib fractures, damage or avulsion of grafts, lung injury, disruption
of implanted prosthetic valves, and hemorrhage caused by CPR which invokes
the concept of “primum non nocere” (first, do no harm) in choosing the route
to avoid potential complications. External CPR may be necessary, but should
be performed cautiously, targeting a rate of 100–120 bpm and an SBP of 60
mm Hg on the arterial line.

The first step in the treatment of the arrest is to

identify the rhythm and determine whether it will
respond to defibrillation. In the case of
ventricular fibrillation (VF) or pulseless
 ventricular tachycardia (VT), rapid defibrillation
is the preferred treatment.

Another unique quality of the postoperative cardiac surgery patient is the

common presence of epicardial pacing wires. Most patients following cardiac
surgery will have epicardial pacing wires placed before leaving the operating
room and they will be connected to an external pacemaker device. In the case
of patients with arrests arising from asystole or severe bradycardia, pacing via
this device should be initiated immediately. If the patient does not have
epicardial pacing wires in place or if they fail to work properly, external
pacing should be attempted. As with VF/VT arrests, it is acceptable to delay
external CPR for up to 1 minute in order to allow attempts to pace the heart.
If pacing remains unsuccessful at this point, external CPR should be initiated,
again as a bridge to re-entry sternotomy.

In cases of apparent pulseless electrical activity (PEA), and if the patient is

being paced, the pacemaker should be turned off to ensure that the PEA is
not actually an underlying VF/VF. Additional considerations, such as the
presence of tension pneumothorax or large hemothorax, should be considered
in PEA arrests. The position of the endotracheal tube should be confirmed to
ensure that it has not been displaced.

In cases of apparent PEA, and if the patient is

being paced, the pacemaker should be turned off
to ensure that the PEA is not actually an
underlying VF/VF. Additional considerations,
such as the presence of tension pneumothorax or
large hemothorax, should be considered in PEA
arrests.
Administration of epinephrine is standard practice in ACLS. It is difficult to
separate the effects of bolus epinephrine from continuous infusion of inotrope-
vasopressors frequently used in the perioperative period. The Society of
Thoracic Surgeons (STS) guidelines acknowledge, however, that epinephrine
may be useful in smaller doses (50–300 mcg) in certain situations but
cautions that it should only be given under the guidance of experienced
clinicians and not as part of a protocol.
Re-entry sternotomy should ideally be performed by or under the guidance of
a cardiac surgeon and definitive repair of cardiac defects causing arrest is
beyond the scope of this course. However, immediate opening of the chest to
evacuate cardiac tamponade or provide internal cardiac massage may be a
life-saving temporizing measure until a cardiac surgeon is available. Current
STS guidelines suggest that properly trained intensivists, including advanced
practice providers, may safely perform the procedure in emergency situations.
In general, postoperative arrests mirror that of nonoperative-associated arrests
and guidelines stress prompt defibrillation and immediate uninterrupted high-
quality chest compressions.

VI. THE PULSELESS EXTREMITY IN THE

POSTOPERATIVE CARDIAC SURGERY PATIENT
Individuals with coronary artery disease (CAD) are frequently afflicted with
peripheral arterial disease (PAD). The similarities in risk factors for CAD and
PAD are mirrored with that for cerebrovascular disease. This association
assumes a major role when interventions for CAD involve procedures that
require canalization of extremity arterial supply for diagnostic or therapeutic
purposes because insertion of support devices may produce undesired side
effects including limb ischemia, cerebrovascular embolization, or bleeding.
The pulseless extremity in the postoperative cardiac surgery patient is a
surgical emergency and frequently associated with the need for additional
interventions. Extremity vascular-related complications are not limited to the
arterial system. Ischemic limb complications can be classified into those
associated with a direct intervention in the afflicted limb such as the insertion
of either a venous or arterial catheters and those in which a previously present
or undisclosed insufficiency is unmasked by alterations in cardiac output or
the use of vasopressor agents in the perioperative period.

The pulseless extremity in the postoperative

cardiac surgery patient is a surgical emergency
and frequently associated with the need for
additional interventions. Extremity vascular-
related complications are not limited to the
arterial system.

Recent estimates of deep vein thrombosis (DVT) occurrence in the

postoperative CABG patient range from 10% to 48% with an average value of
20%. The incidence of pulmonary embolus may be as high as 10% in this
population and is thought to be related to reluctance of early anticoagulation
use in the perioperative period, immobility imposed by monitoring, and
ventilator assist devices as well as inflammatory changes produced by CPB
itself. Venous complications may lead to short-term or long-term disability
related to chronic venous insufficiency. A rare complication of venous
thrombosis is phlegmasia cerulea dolens which, if untreated, can progress to
venous gangrene of an extremity.
Arterial complications may present as a result of unresolved cardiogenic
shock in the postoperative period or may be a result of the need for higher
doses of vasopressors to sustain goals for mean arterial pressure. Arterial
complications have a wide range of presentations and are reported to appear
in 10% to 70% of patients who have varying degrees of shock, low flow,
and/or require insertion of intravascular support devices such as IABP,
ventricular support devices, or ECMO cannulae. Patients who develop
complications after device insertion often have a high prevalence of historic
risk factors generally associated with PAD and include preexisting
hypertension, diabetes mellitus, hyperlipidemia, and smoking. Arterial
insufficiency after CABG is associated with higher mortality. There is a
disease-related effect, with an increased risk of mortality in those patients
afflicted with diabetes mellitus versus the non-diabetic, 58% versus 34%.
It is felt that in addition to the presence of risk factors contributing to PVD
already mentioned, size discrepancies of arteries with respect to the size of
support catheters may have a role. When time permits, care should be taken
to perform a thorough vascular examination prior to the contemplation of or
insertion of cardiovascular support devices. The upper extremity is not
immune to ischemia because brachial artery access has also been associated
with distal vascular complications.

A. Treatment
Emphasis should be placed on obtaining an accurate pre-insertion history and
conducting a physical examination with attention to documentation of a
thorough neurologic examination and noting condition of the extremities prior
to insertion of devices. Coordination of goals and expectations with all team
members for hemodynamic variables, acceptable ranges of vasopressors, and
vigilance in monitoring limb perfusion in sites of insertion of monitoring lines
or assist devices will also reduce this complication.
The hallmarks of physical examination are often referred to as the six “Ps”:
pain, paresthesia, pallor, pulselessness, paralysis, and the ominous
appearance of poikilothermia. Once the complication of a pulseless limb
occurs, the time to treatment is critical. Of the reported signs, paresthesia
appears to be an early sign. Reliance on Doppler pulses or delay in
consultation is dangerous. Misinterpretation of Doppler signals may give a
false sense of security with signals appearing as a result of a water hammer-
type phenomenon. Options for therapy include removal of the device, local
anticoagulation or lytic therapy, or thrombectomy from either an urgent
interventional radiographic or open vascular surgical consultation.

VII. VASOPLEGIA
Vasoplegia, a term resulting from the combination of the Latin root words
vaso for vessel or container and plegia or stroke, is a syndrome characterized
by a low mean arterial blood pressure and a high cardiac index in the face of
adequate cardiac filling pressures. It has been described in a diverse
spectrum of conditions including cardiac and non-cardiac surgery, sepsis,
neuroaxial anesthesia, trauma, burns, and pancreatitis.
Vasoplegia is most commonly described as a complication of CPB, with a
reported incidence of between 5% and 25%. It is characterized by significant
hypotension, a mean arterial pressure < 60, normal or high cardiac outputs,
and low systemic vascular resistance (SVR) despite treatment with fluids and
vasopressors. Once the syndrome develops, afflicted patients are at increased
risk for death and other major complications following cardiac surgery with
mortality as high as 25% in those patients in whom the condition lasts longer
than 48 hours postoperatively.

Multiple risk factors have been described that may predict vasoplegia in the
postoperative cardiac patient (Table 16-6). The exact pathogenesis remains
unclear but is thought to involve activation of the contact, coagulation, and
complement systems with resultant activation of leukocytes, platelets, and
endothelial cells. This causes release of intracellular contents including
bradykinin and other substances affecting the vascular tone.

Table 16-6 Multiple Risk Factor Categories for Vasoplegia

The treatment of vasoplegia relies primarily on recognition of its presence and

the use of support in the form of vasopressors which exhibit primarily alpha-1
effects. If present, vasoplegia presents and is associated with hypotension,
refractory to treatment, and mortality may be as high as 25%. The link to
nitric oxide-related vasoactive substances has prompted treatment with
methylene blue in order to reverse refractory hypotension, but at present
conclusive evidence is lacking.

Vasoplegia is most commonly described as a

complication of CPB, with a reported incidence
of between 5% and 25%. It is characterized by
significant hypotension, a mean arterial pressure
< 60, normal or high cardiac outputs, and low
systemic vascular resistance (SVR) despite
treatment with fluids and vasopressors.

Key Points
Cardiovascular Surgical Emergencies
Coronary artery bypass grafting carries an overall mortality of
about 3%, including elective, emergent, and true emergency
procedures.
Risk factors for complications after a CABG procedure could be
patient- or procedure-dependent.
Most patients who have postoperative bleeding sustain a
progressive series of sequential hits to their coagulation system
which, in aggregate, creates the bleeding.
In general, most defects in coagulation can fortunately be
addressed by the appropriate transfusion of either fresh frozen
plasma or cryoprecipitate concentrates.
Platelet administration is guided by the symptomatology and may
be infused for patients with active bleeding and a platelet count
greater than 50,000 platelets per µL or if there are questions as to
the functional capacity of the platelets. In non-bleeding patients,
platelet administration is generally unnecessary and rarely
administered.
In massive blood loss, initiate a massive transfusion protocol
(MTP): transfuse in 1:1:1 or 1:1:2 ratio of PRBCs:FFP:platelets.
Prothrombin complex concentrates (PCCs) may be used instead of
FFP after consultation with experts in vascular medicine or
hematology.
Cardiac tamponade exists when fluid within or around the
pericardial space exists and compresses and compromises the
compliance of the heart chambers. This prevents normal filling and
produces a picture of obstructive shock.
Criteria for emergent re-exploration after CABG include increasing
chest tube drainage, sudden massive bleeding, tamponade
physiology signs, and cardiac arrest.
The risks of intravascular device placement cannot be
underestimated, and devices should be promptly removed at the
earliest point in postoperative care.
Vasoplegia is a syndrome characterized by a low mean arterial
blood pressure and a high cardiac index in the face of adequate
cardiac filling pressures. It is treated with fluids and vasopressor
agents.
In all instances in which consultation is requested, it is mandatory
that communication to all members of the team, especially the
operating surgeon and attending cardiology staff, be directly and
personally accomplished and recorded in the patient record.
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surgery in nonagenarians: a 10-year experience. Ann Thorac
Surg. 2003;75(4):1215-1220.
2. Benjamin EJ, Blaha MJ, Chiuve SE, et al. Heart disease and
stroke statistics-2017 Update: A report from the American Heart
Association. Circulation. 2017;135(10):e146-e603.
3. Bradley SM, Liu W, Chan PS, et al. Defibrillation time intervals
and outcomes of cardiac arrest in hospital: retrospective cohort
study from Get With The Guidelines-Resuscitation registry. BMJ.
2016;353:i1653.
4. De Laria GA, Tyner JJ, Hayes CL, Armstrong BW. Heparin-
protamine mismatch. A controllable factor in bleeding after open
heart surgery. Arch Surg. 1994;129(9):944-950; discussion 950-
951.
5. Despotis G, Avidan M, Eby C. Prediction and management of
bleeding in cardiac surgery. J Thromb Haemost. 2009;7 Suppl
1:111-117.
6. Frojd V, Jeppsson A. Reexploration for Bleeding and Its
Association With Mortality After Cardiac Surgery. Ann Thorac
Surg. 2016;102(1):109-117.
7. Garmo C, Bajwa T, Burns B. Physiology, Clotting Mechanism, in
Stat Pearls. 2018, Stat Pearls Publishing. Treasure Island (FL).
8. Karthik S, Grayson AD, McCarron EE, Pullan DM, Desmond MJ.
Reexploration for bleeding after coronary artery bypass surgery:
risk factors, outcomes, and the effect of time delay. Ann Thorac
Surg. 2004;78(2):527-534; discussion 534.
 9. Klein AA, Collier T, Yeates J, et al. The ACTA PORT-score for
predicting perioperative risk of blood transfusion for adult cardiac
surgery. Br J Anaesth. 2017;119(3):394-401.
10. La Par DJ, Isbell JM, Mulloy DP, et al. Planned cardiac
reexploration in the intensive care unit is a safe procedure. Ann
Thorac Surg. 2014;98(5):1645-1651; discussion 1651-1652.
11. Link MS, Berkow LC, Kudenchuk PJ, et al. Part 7: Adult
Advanced Cardiovascular Life Support: 2015 American Heart
Association Guidelines Update for Cardiopulmonary Resuscitation
and Emergency Cardiovascular Care. Circulation. 2015;132 (18
Suppl 2):S444-464.
12. Lopes CT, Brunori EHFR, Santos VB, et al. Predictive factors for
bleeding-related reexploration after cardiac surgery: A
prospective cohort study. Eur J Cardiovasc Nurs.
2016;15(3):e70-e77.
13. McQuilten ZK, Crighton G, Brunskill S, et al. Optimal Dose,
Timing and Ratio of Blood Products in Massive Transfusion:
Results from a Systematic Review. Transfus Med Rev.
2018;32(1):6-15.
14. Nascimento B, Goodnough LT, Levy JH. Cryoprecipitate therapy.
Br J Anaesth. 2014;113(6):922-934.
15. Nearman H, Klick JC, Eisenberg P, Pesa N. Perioperative
complications of cardiac surgery and postoperative care. Crit
Care Clin. 2014;30(3):527-555.
16. O’Grady NP, Alexander M, Burns LA, et al. Summary of
recommendations: Guidelines for the Prevention of Intravascular
Catheter-related Infections. Clin Infect Dis. 2011;52(9):1087-
1099.
17. Practice Guidelines for blood component therapy: A report by the
American Society of Anesthesiologists Task Force on Blood
Component Therapy. Anesthesiology. 1996;84(3):732-747.
18. Rushing GD, Yuh DD. Primary Coronary Artery Bypass Surgery,
in Johns Hopkins Textbook of Cardiothoracic Surgery, Yuh DD,
et al, Editors. 2014, McGraw-Hill Education: New York, NY.
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Resuscitation of Patients Who Arrest After Cardiac Surgery. Ann
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Suggested Websites
1. https://accesssurgery.mhmedical.com/content.aspx?
sectionid=80030289&bookid=1340&jumpsectionID=8003035
7&Resultclick=2 Accessed: July 19, 2018
2. Copyright © 2018 McGraw-Hill Education. All rights reserved. In
https://accesssurgery.mhmedical.com/content.aspx?
sectionid=80030289&bookid=1340&jumpsectionID=8003035
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Education.
 Chapter 17
MANAGEMENT OF LIFE-
THREATENING ELECTROLYTE
AND METABOLIC DISTURBANCES

Objectives
Review the emergent management of severe electrolyte disturbances.
Recognize manifestations of acute adrenal insufficiency and initiate
appropriate treatment.
Describe the management of severe hyperglycemic syndromes.

Case Study
A 65-year-old man with altered mental status is brought into the emergency
department by his son. His son states the patient has been increasingly weak
for the past 3 days. He adds that he has been having multiple episodes of non-
bloody diarrhea with decreased appetite. Further history reveals the son has
yet to install an air conditioning unit in the patient’s room at home even
though it is the middle of summer. The patient is unable to provide additional
information because of his confusion. His initial vital signs are as follows:
blood pressure of 104/66 mm Hg, heart rate of 111 beats/min, respiratory
rate of 18 breaths/min, oxygen saturation level of 99% on room air, and
temperature of 36.9ºC (98.4°F). Examination findings include an awake
Caucasian male not oriented to place, time, or person. He appears clinically
dehydrated with dry mucous membranes and poor skin turgor with tenting.
The electrocardiogram shows frequent premature ventricular contractions.
– What risk factors does this patient have for electrolyte disturbances?
– Which electrolyte abnormalities might contribute to his presentation?
– How would you initiate the evaluation and treatment of this patient?

I. INTRODUCTION
Electrolyte and metabolic disturbances are common in critically ill and injured
patients. These abnormalities alter physiologic function and contribute to
morbidity and mortality. The most common life-threatening electrolyte and
metabolic disorders in critically ill patients are disturbances in potassium,
sodium, calcium, magnesium, phosphate, and glucose levels. With early
recognition and treatment of these abnormalities, potentially life-threatening
complications may be avoided and outcomes improved.

II. ELECTROLYTE DISTURBANCES

Electrolyte disturbances result from an underlying disease process or
iatrogenic causes. It is important to seek the cause of the abnormality, as well
as to treat the electrolyte change itself. Many clinical manifestations are not
specific to a particular electrolyte change and may be the result of multiple
abnormalities. The urgency of treatment depends on the clinical circumstances
rather than the absolute electrolyte concentration. All severe electrolyte
abnormalities require frequent reassessment during correction.

A. Potassium
Potassium is primarily an intracellular cation that is essential for maintenance
of the electrical membrane potential. Its normal range is 3.5–5.0 mEq/L
(3.5–5.0 mmol/L). Most potassium (95% to 98%) is found intracellularly and
the remainder is present in the extracellular compartment. Potassium plays an
important role in maintaining cellular function in excitable tissues. Alterations
in this cation primarily affect the cardiovascular, neuromuscular, and
gastrointestinal systems.

1. Hypokalemia

Hypokalemia (potassium level < 3.5 mEq/L [< 3.5 mmol/L]) is a common
electrolyte disorder. It results from renal or extrarenal losses, transcellular
shifts, and decreased intake (Table 17-1). Life-threatening clinical
manifestations of hypokalemia primarily involve the cardiac and
neuromuscular systems. Dysrhythmias (ventricular and supraventricular,
conduction delays, sinus bradycardia), electrocardiogram (ECG) abnormalities
(U waves, QT-interval prolongation, flat or inverted T waves), muscle weakness
or paralysis, paresthesias, ileus, abdominal cramps, nausea, and vomiting are
common manifestations.

Table 17-1 Causes of Hypokalemia

Always consider the possibility of

hypomagnesemia when significant hypokalemia
exists.
Treatment of hypokalemia is aimed at correcting the underlying cause and
administering potassium (Figure 17-1). Discontinuing offending drugs (if
possible), correcting hypomagnesemia and other electrolyte disturbances, and
correcting alkalosis should be completed as part of the treatment process.
Because potassium is primarily an intracellular ion, an estimated deficit cannot
be calculated from serum values. Therefore, administration must be titrated
against periodic reassessment of the serum levels. Infusion of 20 m Eq (20
mmol) potassium in 100-mL fluid over 1 hour, with additional doses
administered sequentially, is recommended to avoid potential complications
with more concentrated solutions. This concentration must be administered
through a central line, although more dilute solutions can be administered
peripherally. The infusion rate can be slowed after life-threatening symptoms
resolve. Concentrations and rates may vary by institutional policy. Serum
potassium levels must be monitored at frequent intervals during repletion (ie,
every 3–4 hours during initial replacement). If acidemia is present, correct the
potassium level before correcting the pH because potassium shifts
intracellularly as the pH increases.

2. Hyperkalemia
Hyperkalemia (potassium levels > 5 mEq/L [> 5mmol/L]) is very common in
the critical care setting and most often results from renal dysfunction or
overzealous replacement. Other causes of hyperkalemia are listed in Table 17-
2. Pseudohyperkalemia may result from a white blood cell count >
100,000/mm3, a platelet count > 600,000/mm3, or secondary to
phlebotomy technique resulting in hemolysis. Pseudohyperkalemia is a
potential cause of hyperkalemia and should be ruled out prior to
commencement of treatment, especially if the measured potassium level is not
consistent with a previous trend without an obvious disease process to explain
the elevation.
 Figure 17-1. Treatment of Hypokalemia

Table 17-2 Causes of Hyperkalemia

 Hyperkalemia with significant ECG changes,
such as widened QRS and sine wave, mandates
immediate therapy.

In the evaluation of a patient with hyperkalemia, a complete medical history

and physical examination and an accurate reconciliation of patient medication
therapy are vital. Clinical manifestations of hyperkalemia relate primarily to
the heart and muscular system (Figure 17-2). Arrhythmias, heart block,
bradycardia, diminished conduction and contraction, ECG abnormalities (eg,
diffuse peaked T waves, PR interval prolongation, QRS widening, diminished
P waves, sine waves), muscle weakness, paralysis, paresthesias, and
hypoactive reflexes are common manifestations.

Treatment of hyperkalemia involves the recognition and treatment of

underlying diseases, the removal of offending drugs, the limitation of
potassium intake, and the correction of acidemia or electrolyte abnormalities.
Any serum potassium level > 6 mEq/L (6 mmol/L) should be addressed, but
the urgency of treatment depends on the clinical manifestations and ECG
findings. Options for treating hyperkalemia are summarized in Table 17-3.
Serial serum potassium levels, continuous cardiac monitoring, and serial ECG
tracings should be obtained during evaluation and treatment.
 Figure 17-2. Electrocardiographic Effects of Hyperkalemia

Two rhythm strips showing the electrocardiographic effects of hyperkalemia. A, peaked T

waves and widened QRS complex. B, sine wave pattern.

Table 17-3 Options for Treating Hyperkalemia

B. Sodium
Disorders of sodium and water balance are common in critical illness.
Multiorgan failure, fluid therapy, and the numerous therapies administered to
patients admitted to the ICU can interfere with the different mechanisms that
maintain total body sodium and water homeostasis. Sodium is the principal
osmolyte in the extracellular fluid and determines the size of the extracellular
volume. Sodium functions as the primary determinant of blood osmolality and
is involved in the regulation of extracellular volume. Abnormalities in
circulating sodium primarily affect neuronal and neuromuscular function.

When discussing osmolality and tonicity, the osmolality of a solution is

determined by the numbers of solutes per kilogram. Plasma (serum) osmolality
can be calculated by freezing point depression or using the following formula:

2 (Na) [mEq/L] + Glucose (mg/dL)/18 + BUN (mg/dL)/2.8 Normal value:

275–295 mOsm/kg H2O

The difference between measured osmolality and calculated osmolality is <

10 mOsm/kg H2O. Water moves freely between the intracellular and
extracellular spaces based on the osmotic gradient with the osmolality of both
compartments being virtually identical. It is important to remember that
sodium is the major determinant of plasma tonicity. Tonicity is the relative
concentration of solutes dissolved in solution which determine the direction
and extent of diffusion

Thirst mechanism and antidiuretic hormone (ADH) tightly control osmolality.

ADH stimulates reabsorption of water within the collecting ducts of the kidney.
Increases in tonicity produce stimulation of thirst and ADH. Disorder in
osmolality reflects impaired water homeostasis and pathologic abnormalities of
these mechanisms.

1. Hyponatremia

By definition, hyponatremia is a serum sodium concentration below 135

mEq/L (135 mmol/L). Pseudohyponatremia, a spurious form of iso-osmolar
hyponatremia, may occur in the presence of severe hyperlipidemia,
hyperproteinemia, or hyperglycemia when the sodium concentration is
measured by flame photometry. Serum osmolality determines true
hyponatremia. A serum osmolality value of 280–295 mOsm/kg indicates
pseudohyponatremia as a result of hyperlipidemia or hyperproteinemia. A
serum osmolality value of greater than 295 mOsm/kg indicates hyperglycemia
or the use of mannitol as the cause of low serum sodium levels. True
hyponatremia is indicated when the serum osmolality value is less than 280
mOsm/kg.
If serum osmolality rules out hyperglycemia or mannitol as the source of
hyponatremia and that true hyponatremia is present, the volume status of the
patient needs to be evaluated. Clinical presentation, along with urine
osmolality and urine sodium, are used to determine volume status. Fractional
excretion of sodium is an additional value that can aid in determination of
volume status. A urine sodium level of < 100 mOsm/kg indicates a low solute
level from primary polydipsia, low sodium intake, or beer potomania. A urine
sodium level > 100 mOsm/kg indicates a disturbance in sodium/water
balance. Hypovolemia, euvolemia, or hypervolemia is determined using the
clinical diagnosis and presentation. Review of the medication administration
record needs to be completed to identify any medications that could affect
sodium-water balance needs. Urine sodium and fractional excretion of sodium
(FENa) values narrow the underlying cause of the hyponatremia to correctly
manage the disorder and correct the sodium level.
Figure 17-3. Diagnostic Approach to the Etiology of Hyponatremia

Abbreviations: FENa, fractional excretion of sodium; SIADH, syndrome of inappropriate

antidiuretic hormone

Adrenal insufficiency should be ruled out in

patients with euvolemic and hypovolemic
hyponatremia.
Clinical manifestations of hyponatremia involve the central nervous system
(CNS) and muscular system and include disorientation, decreased mentation,
irritability, seizures, lethargy, coma, nausea/vomiting, weakness, and
respiratory arrest. Treatment requires identifying the type of hyponatremia,
treating the underlying disease, removing offending drugs, and improving the
circulating sodium level. Hypovolemic hyponatremia usually responds to
intravascular volume repletion (ie, with normal saline). As volume is replaced,
the release of ADH is appropriately suppressed and the kidneys begin to
excrete free water. Hypervolemic hyponatremia is usually not severe and
improves with successful treatment of the underlying condition.

Euvolemic hyponatremia is almost always secondary to elevated levels of

ADH. Diagnosis is facilitated by determining urine osmolality before treatment
(especially with diuretics) to compare with a calculated serum osmolality. If the
hyponatremia is acute or the patient is symptomatic, the serum sodium level
should be increased by restricting free-water intake, increasing free-water
clearance with loop diuretics, and replacing intravascular volume with normal
saline (154 mEq/L [154 mmol/L]) or hypertonic 3% saline (513 mEq/L [513
mmol/L]).

Hypertonic saline is indicated for treatment in the presence of severe

symptoms, such as seizures, coma, or impending respiratory arrest. The goal
of therapy in this situation is to remove free water and not sodium. The
increase in serum sodium should be controlled, and although the precise rate
of increase is controversial, the serum sodium increase should be limited to
approximately 6 to 8 mmol/L in the first 24 hours. However, one option is to
accelerate the rate of serum sodium elevation early in the treatment course in
the presence of life-threatening symptoms, such as seizures, and then slow the
rate of increase after resolution of the symptoms with a proper strategy to
minimize a potential demyelination lesion as a result of a unplanned rapid
correction. When hypertonic saline is used in symptomatic patients, 1
mmol/kg sodium chloride should be infused initially (3% saline contains ~0.5
mmol/mL). The same amount can be administered in incremental doses to a
maximum of 3 to 5 mmol/kg or until symptoms resolve. Alternatively, the
change in serum sodium expected after administering 1 liter of 0.9% normal
saline can be estimated by using the following formulas:
The sodium concentrations of various infusates are listed in Table 17-4. The
formulas presented previously do not take into account other fluid gains (ie,
tube feeds or continuous medication infusions) and losses (ie, urine output),
and therefore, should serve only as guides to intervention. Serum sodium
levels should be monitored at frequent intervals during therapy for
hyponatremia, at least every 6 hours. When serum sodium is greater than 125
to 130 mEq/L (125 to 130 mmol/L), restriction of free water alone allows for
slower return of the sodium level to normal.

Do not use vasopressin antagonists in patients

with severe neurologic symptoms and do not co-
administer with hypertonic saline.

Correction of the serum sodium level that is too rapid may result in CNS injury
(ie, osmotic demyelinating syndrome), particularly in the setting of chronic
hyponatremia. Osmotic demyelinating syndrome rarely occurs in patients
whose serum sodium is greater than 120 mEq/L (120 mmol/L). Symptoms of
demyelination are typically seen after initial improvement in mentation. In 1 to
7 days following a hasty reversal of chronic hyponatremia, patients may
develop focal motor deficits, respiratory insufficiency, and progressive loss of
consciousness. Patients at greatest risk for osmotic demyelinating syndromes
are those with malnutrition, hypokalemia, alcohol abusers, elderly women, and
burn patients. If hyponatremia is chronic and the patient is asymptomatic,
regardless of the magnitude of hyponatremia, free-water restriction alone may
be sufficient to allow for slow return of serum sodium to normal.

Table 17-4 Sodium Characteristics of Selected Infusates

Although controversial, vasopressin receptor antagonists, such as conivaptan
and tolvaptan, are available for use in the management of hyponatremia.
These agents should not be used in the management of acute hyponatremia
and expert consultation should be sought before their use. They inhibit
resorption of water via their action on the V2 receptor of the kidney and result
in a slow rise in the serum sodium level. Vasopressin receptor antagonists can
cause hypotension and volume depletion and therefore should be avoided in
patients with hypovolemia. After a vasopressin receptor antagonist is
administered, serum sodium levels should be monitored frequently (every 4
hours) because of concerns for rapid sodium correction and neurologic
sequelae (specifically, demyelination). To prevent over-correction, avoid using
vasopressin antagonists in combination with hypertonic saline. Once an
increase of 6 to 8 mmol/L is achieved, consider replacing free water (orally or
intravenously) to match urine output and prevent an excessive rise in sodium
levels.

2. Hypernatremia

Hypernatremia (sodium > 145 mEq/L [145 mmol/L]) indicates intracellular

volume depletion with a loss of free water that exceeds sodium loss. Causes of
hypernatremia are listed in Table 17-5.

Table 17-5 Causes of Hypernatremia

The clinical manifestations of hypernatremia relate to CNS and muscle
function. Manifestations of hypernatremia include altered mentation, lethargy,
seizures, coma, and muscle weakness. Polyuria suggests the presence of
diabetes insipidus or excess salt and water intake.

Treatment focuses on correcting the underlying cause of hypernatremia.

Nearly all patients with hypernatremia require free-water repletion. The water
deficit can be estimated by using the following equation:
Water Deficit (L) = 0.6 (0.5 for women) × weight (kg) [(measured Na/normal
Na) – 1]

Example: Water deficit of a 70-kg man with sodium measurement of 160

mEq/L (mmol/L)
0.6 × 70 [(160/140) – 1]
42 [1.14 – 1]
42 × 0.14 = 5.88 L water deficit
A portion of the free-water deficit should be replaced initially at a speed
commensurate with the severity of symptoms, and the patient should be
reevaluated for subsequent replacement frequently (monitor sodium levels
every 6 hours). Regardless of the serum sodium level, if the patient shows
signs of hypovolemic shock (eg, hypotensive, orthostatic, or significantly
tachycardia), administer normal saline until the intravascular volume is
corrected. When the patient is hemodynamically stable, replete the remaining
water deficit with 5% dextrose in water, 0.45% NaCl, or 0.2% NaCl with 5%
dextrose. To estimate the change in serum sodium expected after
administering 1 liter of fluid, use the same formulas as for hyponatremia:
In stable patients, water may be replaced via the enteral route (ie, nasogastric
tube). In the rare patient with extreme sodium overload, sodium may be
removed with loop diuretics or dialysis (provided intravascular volume is
adequate). Administration of aqueous vasopressin or desmopressin should be
considered for patients with central diabetes insipidus.

Rapid correction of serum sodium can result in

cerebral edema and neurologic injury.

Sodium concentrations should be measured frequently during treatment, and

therapy should be adjusted for optimal correction of the sodium level. If
hypernatremia developed over a period of hours, reducing the serum sodium
by 1 mEq/L/h (1 mmol/L/h) is appropriate. In hypernatremia of longer or
unknown duration, a slower rate of correction (0.5 mEq/L/h [0.5 mmol/L/h])
is recommended. Increasing free-water intake in maintenance fluids allows for
a slow return to normal sodium levels.

C. Other Electrolyte Abnormalities

1. Calcium

Calcium is the most abundant mineral in the body, comprised of 50% active
ionized calcium and 50% calcium bound to albumin in extracellular fluid. It is
required for muscle contraction, nerve impulse transmission, hormone
secretion, blood clotting, cell division, cell motility, and wound healing.
Effective calcium levels in a seriously ill patient are best assessed by using
ionized calcium measurements, if available. Total serum calcium is directly
related to serum albumin whereas ionized calcium is inversely related to
serum albumin. In general, for each increase or decrease in serum albumin of
1 g/dL, the serum calcium increases or decreases by 0.8 mg/dL (0.2 mmol/L).
However, the relationship between albumin and serum calcium is less reliable
in critically ill patients.
a. Hypocalcemia

Hypocalcemia (total calcium < 8.5 mg/dL [< 2.12 mmol/L], ionized
calcium < 4 mg/dL [1 mmol/L]) is common in critically ill patients
and results from impairment of the parathyroid and/or vitamin D
systems (Table 17-6). Cardiovascular abnormalities, the most
common clinical manifestations of hypocalcemia in critically ill
patients, include hypotension, bradycardia, arrhythmias, heart failure,
cardiac arrest, digitalis insensitivity, and QT interval and ST-segment
prolongation. Neuromuscular manifestations include weakness,
muscle spasm, laryngospasm, hyperreflexia, seizures, tetany, and
paresthesias.

Table 17-6 Causes of Hypocalcemia

Treatment is aimed at correcting the underlying disease process and

any concomitant electrolyte abnormalities, and administering calcium.
Mild hypocalcemia is well tolerated, and aggressive treatment may
result in tissue injury (especially during ischemic and septic states). If
the hypocalcemia is severe (ionized calcium < 4 mg/dL [1 mmol/L])
or if the patient is symptomatic, administer 100 mg calcium
intravenously over 5 to 10 minutes (3–4 mL of 10% calcium chloride
or 10 mL of 10% calcium gluconate), followed by calcium in the
amount of 0.3 to 2 mg/kg/h. Calcium preparations vary in their
content of elemental calcium: 1 g of 10% calcium chloride contained
in 10 mL has 272 mg of calcium; 1 g of 10% calcium gluconate
 contained in 10 mL has 90 mg of calcium. When the circulating
calcium concentration is stable, calcium may be replaced via the
enteral route (ie, 500–1,000 mg every 6 hours).
Monitor ionized or total calcium levels frequently during treatment,
and adjust repletion to maintain calcium in the lower normal range so
as not to suppress parathyroid gland function. If calcium replacement
alone fails to maintain the circulating calcium level, consider
administration of vitamin D and confirm normal magnesium levels.
Adverse effects of calcium administration include hypercalcemia,
bradycardia, nausea/vomiting, flushing, and tissue calcium
precipitation.

b. Hypercalcemia
The most common causes of hypercalcemia (total calcium > 11
mg/dL [> 2.75 mmol/L], ionized calcium > 5.21 mg/dL [1.3
mmol/L]) are the result of calcium release from bone (Table 17-7).
The clinical manifestations of hypercalcemia relate primarily to the
cardiovascular and neuromuscular systems and include hypertension,
cardiac ischemia, arrhythmias, bradycardia, conduction
abnormalities, digitalis toxicity, dehydration, hypotension, weakness,
depressed mentation, coma, seizures, and sudden death.
Gastrointestinal manifestations include nausea/vomiting, anorexia,
abdominal pain, constipation, pancreatitis, and ulcer disease.
Nephrogenic diabetes insipidus with polyuria may occur and
contribute to volume depletion. Renal stones, nephrocalcinosis, and
renal failure may also be encountered.

Table 17-7 Causes of Hypercalcemia

 Treatment of hypercalcemia is aimed at controlling the underlying
disease, rehydrating the patient, and lowering the calcium level. The
circulating calcium level frequently needs to be lowered while the
primary disease is being evaluated and treated. Intravascular volume
should be restored with normal saline to ensure adequate tissue
perfusion and renal blood flow (urine output 2–3 mL/kg/h). Saline
also decreases renal tubular calcium reabsorption. Once adequate
volume status is secured, diuresis with a loop diuretic further
increases calcium excretion. Serum potassium and magnesium levels
should be monitored and low levels corrected. In patients with renal
failure, pulmonary edema, or life-threatening hypercalcemia, calcium
levels may be lowered with dialysis. After initial stabilization, therapy
with calcitonin and bisphosphonates can be considered.

2. Phosphorus
Phosphate is important in cellular energy metabolism. Hypophosphatemia
(phosphate < 2.5 mg/dL [0.81 mmol/L]) results from transcellular shifts,
renal loss, gastrointestinal loss, or inadequate intake (Table 17-8). Phosphate
depletion primarily affects the neuromuscular and central nervous systems.
Clinical manifestations include muscle weakness, respiratory failure,
rhabdomyolysis, paresthesias, lethargy, disorientation, obtundation, coma, and
seizures. Other possible complications include impaired renal tubular function,
impaired pressor response, hepatic dysfunction, immune dysfunction,
impaired protein synthesis, hemolysis, impaired platelet function, and
impaired oxygen off-loading from hemoglobin.

Treatment of hypophosphatemia consists of controlling the underlying disease,

removing offending drugs, correcting electrolyte abnormalities, and replacing
phosphate. Phosphate levels < 1 mg/dL (< 0.32 mmol/L) associated with
symptoms are considered life-threatening and require immediate treatment.
For emergency treatment, administer phosphate at 0.6 to 0.9 mg/kg daily
intravenously. When circulating levels are stable, maintenance replacement of
phosphate is 1,000 mg/day intravenously plus excess estimated losses (ie, in
urine or stool). Phosphate may be administered as potassium phosphate (93
mg/mL phosphate, 1.1 mmol/mL potassium) or sodium phosphate (93
mg/mL). Enteral administration of phosphate is preferred in patients with
serum phosphate levels > 1.0 to 1.5 mg/dL (> 0.32–0.48 mmol/L).

Table 17-8 Causes of Hypophosphatemia

Serum phosphate should be monitored during repletion and therapy adjusted

to achieve a circulating level of 3 to 4 mg/dL (0.97–1.29 mmol/L). Adverse
effects of phosphate administration include hyperphosphatemia, hypocalcemia,
tissue calcium precipitation, renal injury, and diarrhea (enteral phosphate).

Hyperphosphatemia is uncommon in critical illness except with renal failure.

Increased bone metabolism secondary to tumors or increased gut absorption
also may cause hyperphosphatemia. Symptoms are similar to those of
hypocalcemia: ventricular arrhythmias, prolonged QT interval, seizures,
paresthesias, and muscle cramps. Hyperphosphatemia is treated with
intravenous calcium and enteral phosphorus binders. Dialysis may be required
with renal failure.

3. Magnesium
Magnesium is important to the body for energy transfer and electrical stability.
Causes of hypomagnesemia (magnesium < 1.8 mg/dL [< 0.75 mmol/L]) are
listed in Table 17-9.

Table 17-9 Causes of Hypomagnesemia

Clinical manifestations of hypomagnesemia overlap those of hypokalemia and
hypocalcemia, including cardiovascular abnormalities (ie, QT-interval
prolongation, arrhythmias, vasospasm, myocardial ischemia), neuromuscular
abnormalities (eg, weakness, tremor, seizures, tetany, obtundation, coma), and
electrolyte abnormalities (eg, hypokalemia, hypocalcemia).
Treatment of hypomagnesemia consists of addressing the underlying disease,
discontinuing problematic drugs, correcting concomitant electrolyte
abnormalities, and replenishing magnesium. For emergency treatment (ie,
arrhythmias), administer 1 to 2 g magnesium sulfate intravenously over 5 to
10 minutes. The agent can be administered over a longer interval (10–60
minutes) in less urgent situations. Depending on the clinical situation,
subsequent intravenous replacement ranges from 1 to 2 g magnesium sulfate
every 4 to 6 hours. Once serum levels stabilize, intravenous maintenance
doses are 0.1 to 0.2 mmol/kg daily (1 g magnesium sulfate = 8 mmol).
Maintenance magnesium may be administered enterally. The dose should be
reduced if renal failure is present. Magnesium levels should be monitored
during repletion. Deep tendon reflexes can be used to assess for
hypermagnesemia during replacement (ie, decreased at serum level 4–5
mg/dL [1.65–2.06 mmol/L]).

Hypermagnesemia is uncommon in critical illness but may be seen with renal

failure or shifts in magnesium from intracellular fluid as a result of soft-tissue
injury as with crush injuries, burn trauma, and rhabdomyolysis. Hyporeflexia,
lethargy, and apnea may result. Treatment consists of administration of
intravenous calcium, diuretic administration, and dialysis in severe cases.

III. METABOLIC DISTURBANCES

 Case Study
A 54-year-old woman is admitted to the general medicine floor (day 3) with
cellulitis of her left lower extremity. Her medical history is significant for
diabetes mellitus (Type 2) and rheumatoid arthritis, and her home medications
include metformin, methotrexate, and prednisone. During this admission, she
has been started on antimicrobial therapy and insulin glargine. Her home
methotrexate and prednisone are on hold to help with healing of her infection.
The emergency response team is called because of a new finding of altered
mental status, respiratory rate of 22 breaths/min, heart rate of 140 beats/min,
blood pressure of 84/42 mm Hg, and temperature of 37.2°C (98.9°F). A
complete blood count and basic metabolic panel are unremarkable. She is
given a 2-L fluid bolus of lactated Ringer and started on 10 µg/min of
norepinephrine and remains hypotensive.
– What metabolic disorder may contribute to this patient’s new onset
hypotension?
– What interventions should be considered?
– What laboratory tests could confirm this diagnosis?

A. Acute Adrenal Insufficiency

Acute adrenal insufficiency in the critically ill patient, also known as critical
illness-related corticosteroid insufficiency (CIRCI), may result from preexisting
or previously undiagnosed chronic disease of the adrenal glands or
hypothalamic-pituitary axis, or acute conditions affecting these endocrine
organs (Table 17-10). Patients with chronic disease may develop acute
adrenal insufficiency precipitated by infection or other stressors. In addition,
functional impairment during serious illness may result from relative or
absolute insufficiency of glucocorticoid production, which usually reverses with
recovery from the illness. Relative adrenal insufficiency occurs when cortisol
response is normal or high, but is reduced relative to the severity of illness.
 Electrolyte abnormalities are less likely with
acute adrenal insufficiency compared with
chronic adrenal insufficiency.

Lack of specific signs and symptoms of acute adrenal insufficiency makes for a
challenging early diagnosis in the critically ill population. Clinical
manifestations consistent with acute adrenal insufficiency include weakness,
nausea and vomiting, abdominal pain, tachycardia, and orthostatic
hypotension. A diagnostic clue is hypotension refractory to volume
resuscitation. Suggestive laboratory findings may include eosinophilia,
hyponatremia, hyperkalemia, acidosis, and hypoglycemia. Acute adrenal
hemorrhage may cause abdominal, flank, or back pain. Clinical and laboratory
manifestations overlap significantly with manifestations of other common
critical illnesses, such as sepsis.

Table 17-10 Etiologies of Adrenal Insufficiency

Important clues for possible adrenal insufficiency in critically ill patients are
vasopressor-dependent states, failure to respond to appropriate fluid
administration, fever without an apparent source, and a discrepancy between
the expected disease severity and the patient’s condition.

Hydrocortisone also provides some

mineralocorticoid effects.
The value of a single test for hypothalamic-pituitary-adrenal axis function is
limited. Either a random cortisol level of < 10 µg/dL or a stimulation test
may be used to diagnose CIRCI. With the cosyntropin stimulation test,
clinicians may use the change in cortisol of less than 9 µg/dL 60 minutes after
a 250-µg cosyntropin dose as suggestive of a diagnosis of adrenal
insufficiency. Current recommendations call for administration of less than
400 mg of hydrocortisone per day for 3 or more days. Improvement in
hemodynamic status after administration of hydrocortisone was previously an
important physiologic indicator, but laboratory testing is now preferred.
Although corticosteroid therapy is frequently weaned by reducing the dose
over a period of 3–5 days, no specific recommendations for weaning exist and
many trials did not wean therapy.

B. Hyperglycemic Syndromes
1. Diabetic Emergencies

HHS develops over days to weeks and results in

greater dehydration than does DKA, which
usually evolves in < 24 hours.

Serious metabolic complications of diabetes mellitus result from a relative or

absolute lack of insulin coupled with increased production of counter-
regulatory hormones such as glucagon, catecholamines, cortisol, epinephrine,
and others. Life-threatening hyperglycemic syndromes include diabetic
ketoacidosis (DKA) and hyperglycemic hyperosmolar state (HHS). These
syndromes differ in the severity of dehydration and degree of acidosis (ketosis)
but share many clinical manifestations and therapeutic interventions. In
addition, patients may manifest components of both syndromes. Table 17-11
lists characteristics that may distinguish the syndromes, but considerable
variability is possible. Although DKA and HHS may be the initial presentation
of diabetes mellitus, the most common precipitating factors are infection and
medication noncompliance. Other precipitants include corticosteroid use,
myocardial infarction, stroke, alcohol abuse, pancreatitis, trauma, and
pregnancy.

Table 17-11 Characteristics of Hyperglycemic Syndromes

The corrected serum sodium concentration

[measured sodium + 0.016 × (serum glucose-100
)] should be used to assess the severity of
dehydration.

Clinical manifestations result from hyperglycemia in both syndromes and from

excess ketone production in DKA. Hyperglycemia causes hyperosmolality,
osmotic diuresis, fluid and electrolyte loss, dehydration, and volume depletion.
Ketones, specifically beta-hydroxybutyrate and acetate, are responsible for the
metabolic acidosis and can be measured indirectly by the anion gap. Clinical
features of both hyperglycemic syndromes may include weakness,
dehydration, polyuria, polydipsia, tachycardia, hypotension, anorexia,
nausea/vomiting, and ileus. Abdominal pain, hyperpnea (Kussmaul
respirations), and fruity odor to the breath are more characteristic of DKA,
whereas altered mental status (ranging from lethargy to coma) and
dysrhythmias are more common in HHS. Laboratory investigation may reveal
hyperglycemia, hyperosmolality (more common in HHS), glucosuria, anion
gap metabolic acidosis (DKA), hyperkalemia (when acidemia is present) or
hypokalemia and hypophosphatemia (after insulin therapy is initiated), lactic
acidosis, leukocytosis, and azotemia. Serum sodium concentrations may be low
as a result of translocation of water to the extracellular space. An elevated
serum sodium concentration suggests severe dehydration.

An initial rapid evaluation of the patient with a possible hyperglycemic

condition should include assessment of mental status, degree of dehydration
(vital signs, orthostatic changes, urine output), and presence of infection.
Laboratory studies should include complete blood count, electrolytes, renal
function, glucose (plasma or fingerstick), urine or serum ketones, and arterial
blood gas (venous pH can be used as a substitute). An electrocardiogram
should be obtained to evaluate for ischemia and changes caused by electrolyte
abnormalities. If infection is suspected, appropriate cultures are indicated.

The goals for treatment of hyperglycemic syndromes are to restore the fluid
and electrolyte balance, provide insulin, and identify precipitating factors. The
initial management of DKA and HHS is outlined in Table 17-12. Volume
deficits correlate with the severity of hyperglycemia and are usually greater in
HHS. Urine output should be maintained at 1 to 3 mL/kg/h to ensure
adequate tissue perfusion and clearance of glucose.
The intravenous route for insulin administration is the most reliable and
easiest to titrate. Because of the short half-life of intravenous insulin, a
continuous infusion is necessary with serial monitoring of the glucose and
electrolyte concentrations. Smaller doses of insulin may be adequate in HHS.
In the case of DKA, insulin infusion should be continued until the removal of
beta-hydroxybutyrate and acetone, as measured by normalization of the anion
gap or normalization of beta-hydroxybutyrate levels. Normalization of the
anion gap usually occurs many hours after normalization of the serum glucose
levels.

Glucose concentrations should be monitored

every 1–2 hours.
Glucose-containing fluids may be started earlier than recommended if blood
glucose cannot be monitored frequently. When glucose and/or serum
osmolality are controlled, acidosis has cleared, and the patient is stable,
subcutaneous insulin may be administered; an insulin sliding scale of regular
and longer-acting preparations can be started and should overlap for 1 to 2
hours with discontinuation of the insulin infusion.

Be aware that bicarbonate therapy in addition to

insulin will lower the serum potassium
concentration.

Insulin and correction of acidosis shifts potassium intracellularly and may lead
to precipitous drops in serum potassium levels. Oral potassium replacement
can be considered if nausea and vomiting are not present. Potassium and
other electrolyte levels should be monitored frequently (especially in the first 6
hours) until levels stabilize and acidosis is resolved.

Table 17-12 Initial Management of Hyperglycemic Syndromes

Abbreviations: DKA, diabetic ketoacidosis; HHS, hyperglycemic hyperosmolar state

Acidosis is well tolerated by patients with DKA, and bicarbonate therapy is

controversial. No benefit has been found when bicarbonate is administered to
DKA patients with a pH of 6.9 to 7.1, and fluid and insulin therapy results in
rapid improvement in pH. Bicarbonate administration may be considered if
the arterial pH is < 6.9 (give 100 mmol bicarbonate over 1 hour to increase
pH > 7). Do not attempt to normalize blood pH with bicarbonate because
acidosis resolves as ketones are metabolized.

2. Hyperglycemia in Critical Illness

Hyperglycemia is common in diabetic and nondiabetic patients with critical

illness and may be the result of stress hormones, inflammatory mediators,
glucocorticoid therapy, excessive nutritional calories, decreased activity, and
other mechanisms. Significant hyperglycemia is associated with poor wound
healing, impaired immune function, increased inflammation, endothelial
dysfunction, and other adverse effects leading to increased illness and death.
Early studies of tight glucose control (80–110 mg/dL, 4.4–6.1 mmol/L)
suggested benefit in a surgical population, but this target has been difficult to
achieve in subsequent studies without increasing the risk for severe
hypoglycemia. In addition, in multiple subsequent trials, no consistent
reduction in mortality was observed with intensive control of glucose levels.
Some recent studies of tight glycemic control have actually demonstrated
increased mortality associated with higher rates of hypoglycemia.
In critically ill patients, insulin therapy should be initiated for persistent
hyperglycemia (blood glucose level > 150 mg/dL). Once it has been initiated,
a glucose level of 140–180 mg/dL (7.8–10 mmol/L) with the avoidance of
hypoglycemia is recommended. Intravenous insulin infusions are the preferred
method to achieve and maintain control. During intravenous insulin therapy,
frequent monitoring of blood glucose is essential to minimize the risk of
hypoglycemia (blood glucose < 70 mg/dL), and achieve optimal control.

Patients with renal dysfunction require lower

rates of insulin infusions.

The ability to provide adequate nursing support and monitoring may affect the
blood glucose goals chosen. Different types of blood sampling and glucose
measurement methods may also yield different results. The institution’s
protocol for blood sampling, insulin infusion, and glucose management targets
should be followed to achieve consistency and minimize the risk of
hypoglycemia.

Key Points
Management of Life-Threatening Electrolyte and
Metabolic Disturbances
In the presence of life-threatening dysrhythmias or paralysis
associated with hypokalemia, administer potassium chloride, 20
mmol/h, through a central venous catheter.
If hyperkalemia-associated ECG abnormalities are present,
administer calcium chloride or calcium gluconate intravenously over
5 to 10 minutes, then consider shifting potassium intracellularly
with 50% dextrose and regular insulin intravenously, inhaled β-
agonists, and/or sodium bicarbonate.
In symptomatic euvolemic hyponatremia, limit the increase in
serum sodium to 6 to 8 mmol/L in the first 24 hours. Correction of
serum sodium that is too rapid may result in CNS injury.
Patients with hypernatremia and hemodynamic instability should
have normal saline administered until intravascular volume is
corrected. Subsequently, replace water deficit with 5% dextrose in
water, 0.45% NaCl, or 0.2% NaCl with 5% dextrose. Enteral
replacement with water is an effective strategy in stable patients.
Emergent treatment with a glucocorticoid is indicated in patients
with critical illness-related corticosteroid insufficiency (CIRCI)
diagnosed by random plasma cortisol or the results of the
cosyntropin stimulation test.
A glycemic target of 140–180 mg/dL is appropriate for most
hospitalized patients to provide clinical benefits with a reduced risk
of hypoglycemia.
The goals of treatment in hyperglycemic syndromes are to restore
the fluid and electrolyte balance, provide insulin, and identify
precipitating factors.
In diabetic ketoacidosis, insulin infusion should be continued until
the ketosis and acidosis have resolved. Glucose-containing fluids
 should be administered to prevent hypoglycemia during insulin
infusion.
Maintain the glucose between 250 and 300 mg/dL (13.9–16.7
mmol/L) in hyperglycemic hyperosmolar syndrome until the plasma
osmolality is < 315 mOsm/kg and the patient is alert.
Potassium should be added to the fluid therapy for hyperglycemic
syndromes as soon as serum potassium is recognized to be < 5
mmol/L and urine output is adequate.
A protocol of blood sampling, insulin infusion, and target glucose
levels should be followed to avoid hyperglycemia and minimize
hypoglycemia in critically ill patients.

Suggested Readings
1. American Diabetes Association. Diabetes care in the hospital:
standards of medical care in diabetes – 2020. Diabetes Care.
2020;43(Suppl 1):S193-S202.
2. Annane D, Pastores S, Rochwerg B, et al. Guidelines for the
diagnosis and management of critical illness related corticosteroid
insufficiency (CIRCI) in critically ill patients (Part I): Society of
Critical Care Medicine and European Society of Intensive Care
Medicine 2017. Crit Care Med. 2017;45:2078-2088
3. Annane D, Pastores S, Rochwerg B, et al. Guidelines for the
diagnosis and management of critical illness related corticosteroid
insufficiency (CIRCI) in critically ill patients (Part II): Society of
Critical Care Medicine and European Society of Intensive Care
Medicine 2017. Crit Care Med. 2018;46:146-148.
4. Berl T. Vasopressin antagonists. N Engl J Med. 2015;372:2207-
2216.
 5. Brown GR, Greenwood JK. Drug- and nutrition-induced
hypophosphatemia: mechanisms and relevance in the critically ill.
Ann Pharmacother. 1994;28:626-632.
6. Charron T, Bernard F, Skrobik Y, et al. Intravenous phosphate in
the intensive care unit: more aggressive repletion regimens for
moderate and severe hypophosphatemia. Intensive Care Med.
2003;29:1273-1278.
7. Gennari FJ. Disorders of potassium homeostasis: hypokalemia and
hyperkalemia. Crit Care Clin. 2002;18:273-288.
8. Jacobi J, Bircher N, Krinsley J, et al. Guidelines for the use of an
insulin infusion for the management of hyperglycemia in critically
ill patients. Crit Care Med. 2012;40:3251-3276.
9. Kamel KS, Wei C. Controversial issues in the treatment of
hyperkalemia. Nephrol Dial Transplant. 2003;18:2215-2218.
10. Noronha JL, Matuschak GM. Magnesium in critical illness:
metabolism, assessment, and treatment. Intensive Care Med.
2002;28:667-679.
11. Tzamaloukas AH, Malhotra D, Rosen BH, et al. Principles of
management of severe hyponatremia. J Am Heart Assoc.
2013;2(1):e005199. Available at:
http://jaha.ahajournals.org/content/2/1/e005199.long. Accessed
October 5, 2015.
12. Verbalis JG, Goldsmith SR, Greenberg A, et al. Hyponatremia
treatment guidelines 2007: expert panel recommendations. Am J
Med. 2007;120:S1-S21.

Suggested Website
Society Critical Care Medicine. http://www.SCCM.org/Guidelines
 Chapter 18
MANAGEMENT OF SPECIAL
POPULATIONS

Objectives
Review the epidemiology, risk factors, classification, and treatment of
pulmonary embolism.
Recognize the risk factors for venous thromboembolism (VTE).
Review ICU management and complications related to patients
undergoing bariatric surgery.
Review postoperative management and complications in organ-specific
transplant patients.
Understand the risks and benefits of immunosuppressive therapy, as
well as vital adverse effects of immunosuppressive drugs and drug-drug
interactions.

Case Study
A morbidly obese 56-year-old man presents with progressive shortness of
breath at rest and fatigue 2 days after undergoing a laparoscopic Roux-en-Y
gastric bypass complicated by significant intraoperative splenic bleeding. While
walking in the hall, the patient had a worsening of shortness of breath and loss
of consciousness. The patient regained consciousness. Examination revealed
tachycardia and his SpO2 was noted to be decreased at 88% on room air. Past
medical history was unremarkable, and social history revealed him to be a
nonsmoker with no substance abuse. The physical examination was consistent
with sinus tachycardia, tachypnea, and stable blood pressure. Additional
physical examination findings were unremarkable except for serosanguinous
drainage from a surgical drain in the left upper quadrant. The patient became
more dyspneic and desaturated and required 100% supplemental oxygen.
Serum troponin was elevated at 1.14ng/mL, as was the proBNP at 1144
ng/mL. A venous Doppler scan was positive for deep vein thrombosis in the left
common femoral vein. The patient was started on an unfractionated heparin
drip after the calculated bolus. An attempt for catheter-directed intervention to
extract the right atrial thrombus and intrapulmonary artery thrombolysis was
aborted because of the presence of patent ductus arteriosus. Twelve hours after
achieving therapeutic anticoagulation, the nursing staff noted an increasing
amount of blood coming from the surgical drain.
– Is this finding concerning?
– Would it change the approach to this patient?
– What are your alternative options?

I. INTRODUCTION
Certain populations of surgical patients are more prone to specific
complications or have unique problems due to the type of surgery performed.
Although all surgical patients can develop venous thromboembolism,
populations such as the morbidly obese are at higher risk. The morbidly obese
patient, the post-operative bariatric surgery patient and the solid organ
transplant patient are all susceptible to distinct problems that if missed can
cause increased morbidity and mortality.

II. PULMONARY EMBOLISM (PE)

A. Epidemiology/Incidence
Venous thromboembolism (VTE) is the third most common cardiovascular
disorder after myocardial infarction and stroke. VTE is a common disease with
an incidence of approximately 0.5 to 1.5 per 1000 per year inhabitants. The
incidence of nonfatal VTE in the United States is nearly 900,000 events
occurring annually. Reported incidence rates for PE ± deep vein thrombosis
(DVT) and leg DVT alone range from 29 to 78 and 45 to 117 per 100,000
person-years, respectively (51.4% DVT, 28.2% PE, and 20.5% PE+DVT).
The total annual number of VTE remains underestimated because certain
percentages of acute pulmonary emboli remain undiagnosed and not suspected
until after patient death. Silent PE develops in about 40% to 50% of patients
with DVT. Overall, VTE incidence may be higher in African Americans and
lower in Asians and Native Americans. The overall age-adjusted incidence rate
is higher for men (130 per 100,000) than women (110 per 100,000;
male:female sex ratio is 1.2:1). The incidence increases among both sexes with
age.

Approximately one-half are related to a current or recent hospitalization. VTE

attack rates (2005– 2010) did not change despite near universal in-hospital
VTE prophylaxis, possibly the result of short prophylaxis duration. It is
reported that the median duration of hospitalization was 3 days, and the
median duration of in-hospital prophylaxis was 70 hours. A total of 75% of
VTE events occurred after hospital discharge, with a 19.5-day median time to
VTE.

The incidence of recurrent VTE is 33% within the first 10 years from the
initial episode, with the peak incidence within the first 6 to 12 months.
Distribution by recurrent VTE event type was DVT 57.4%, PE 26.4%, and
PE+DVT 16.2%. Independent predictors of recurrence include increasing
patient age, body mass index (per 10 kg/m2), male sex, active cancer,
neurologic disease with leg paresis, thrombophilia, persistent elevated D-dimer
among patients with unprovoked or idiopathic VTE, and possibly residual vein
thrombosis (Table 18-1). Several reversible factors are associated with reduced
risk of recurrence of VTE among women, such as pregnancy or the postpartum
state, oral contraceptive use, hormone therapy, and gynecologic surgery.

Table 18-1 Independent Risk Factors for Increased Mortality from VTE
VTE carries a high mortality. The mortality rate for acute PE exceeds 15% in
the first 3 months after diagnosis and surpasses that of myocardial infarction.
The Centers for Disease Control (CDC) reported approximately 600,000 to
1,000,000 PE-related deaths per year in the United States. The incidence of
sudden death as the presentation of PE is 25%. The risk of early death among
PE patients is 18-fold higher compared with patients with DVT alone (Table
18-2). PE is an independent predictor of mortality for up to 3 months from the
initial event. Survivors of PE are at risk for chronic thromboembolic pulmonary
hypertension. High mortality could be related to low clinical suspicion, failure
to identify the high-risk population, inadequate prophylaxis, missed diagnosis
of severe PE, and insufficient therapy.
Provoked VTE indicates that there was an identifiable risk factor for the VTE;
on the contrary, unprovoked VTE indicates that there was no risk factor
identified.

Predictor Factors for Reduced Survival from PE at Time of

Table 18-2
Presentation
B. Risk
The risk of thromboembolism among surgical patients is either surgery or
patient-related (Table 18-3). Surgery-related factors include infection,
mobilization, dehydration, and duration and type of surgery. Colorectal surgery
had the highest incidence of a thromboembolic event compared with other
abdominal surgeries. The incidence of VTE with minor abdominal surgery is
relatively low, on average 0.1% to 0.6%. Conversely, major abdominal surgery
carries a high risk of 0.8% to 1.7%. Laparoscopic surgery carries a low risk for
DVT of 0.03% and 0.02% for fatal PE. Obese patients who undergo bariatric
surgery have traditionally been categorized as a high risk for VTE, with PE
being one of the most common causes of postoperative death. It is important to
mention that these are the non-lower extremities orthopedic, non-oncologic, or
trauma surgeries, which usually carry the highest risk of VTE in the
postoperative period. Duration of surgery for more than 3.5 hours carries a
high risk for thromboembolic events regardless of the type of anesthesia.
General anesthesia is associated with a higher risk for DVT than spinal or
epidural anesthesia.

Table 18-3 Patient-Related Risk Factors for VTE

Abbreviation: ASA, American Society of Anesthesiologists

Hospitalization for medical illness and hospitalization for surgery account for
almost equal proportions of VTE (22% and 24%, respectively). Active cancer
accounts for nearly 20% of all incidents of VTE. The risk appears to be higher
for patients with cancer of the brain, pancreas, ovary, colon, stomach, lung,
kidney, and bone, and in patients with distant metastases.

C. Classification
Pulmonary embolus is classified based on angiographic thrombus burden,
hemodynamic effect, right ventricular (RV) strain, and pulmonary
hypertension. The clinical classification reflects the severity of the pulmonary
emboli and the associated in-hospital or 30-day related mortality risk. The
classification has significant implication in the diagnostic and therapeutic
interventions and includes:
Massive pulmonary emboli
Submassive pulmonary emboli
Low-risk pulmonary emboli
Massive pulmonary emboli are defined as acute PE with:
Sustained hypotension (systolic blood pressure 90 mm Hg for at
least 15 minutes or requiring inotropic support)
Shock not due to a cause other than PE
 Arrhythmia
Hypovolemia
Sepsis
Left ventricular (LV) dysfunction
Pulselessness
Persistent profound bradycardia (heart rate 40 beats/min with signs
or symptoms of shock)
Massive PE carries a high 90-day mortality rate for patients with acute PE and
systolic blood pressure 90 mm Hg at presentation. Risk of death is estimated to
be 30% to 50%.

Submassive PE is defined as hemodynamically stable PE with RV dysfunction

detected on physical examination, electrocardiography, cardiac biomarkers,
echocardiography, and chest computed tomography (CT). It is further
subdivided into low-intermediate and high-intermediate risk depending on
evidence of signs of RV dysfunction and cardiac biomarkers. Either one or
none will be present in low-risk intermediate submassive pulmonary emboli. It
carries a 15% to 20% 30-day mortality.

Low-risk PE carries a low mortality with an average of ≤1%. It still has

significant rates of morbidity and mortality that are functions of older age and
comorbidities. It is defined as an acute PE in a normotensive patient with
normal biomarker levels and no evidence of RV dysfunction on imaging.

D. Diagnosis
1. Clinical Picture

A high clinical suspicion of PE is essential to properly diagnose PE in a timely

fashion because the clinical signs and symptoms are nonspecific. PE can be an
incidental finding on radiologic imaging or at autopsy. The clinical signs and
symptoms of confirmed PE are:

Dyspnea 50%
 Pleuritic chest pain 39%
Substernal chest pain 39%
Signs of DVT 24%
Cough 23%
Fever 10%
Hemoptysis 8%
Syncope 6%
Unilateral leg pain 6%

The physical examination is often unremarkable. Hypoxemia is present in only

60% of the patients, and PaCO2 can be normal, decreased, or elevated.
Hypercapnia is often present in patients with limited pulmonary reserve.
Alveolar-arterial oxygen gradient is normal in 20%.

The chest radiographic findings are neither sensitive nor specific for PE.

2. Electrocardiogram
Electrocardiogram (ECG) patterns suggestive of PE and indicative of RV strain
are (Figure 18-1):

New right bundle-branch block

S wave in lead I, Q wave in lead III, or an inverted T wave in lead
III
New T-wave inversion in leads V1 through V4
New-onset atrial fibrillation
 Figure 18-1. ECG Pattern Suggestive of Pulmonary Emboli

Sinus tachycardia, S1T3Q3, T inversion in V1-3, and late transition in lateral leads. Image
courtesy of Bushra Mina, MD

3. Echocardiography
Echocardiography is essential in the assessment of PE severity.
Echocardiographic findings in submassive and massive pulmonary emboli are
(Figure 18-2):

RV dilatation and hypokinesis

The ratio of the RV end-diastolic area to the LV diastolic area
exceeds the upper level of normal (0.6)
Interventricular septal flattening with paradoxical septal motion
Tricuspid regurgitation and evidence of pulmonary hypertension
Diastolic LV impairment with a small difference between the LV
area during diastole and systole
 McConnell sign (akinesia of the mid RV free wall and hyperkinesia
of the apical wall)
Lack of collapse of the inferior vena cava during inspiration

Figure 18-2. Echocardiographic Findings of Submassive and

Massive PE

ECHO revealed dilatation of both the right atrium and ventricle with bulging of the
interventricular septum into the left ventricle. There is a thrombus on the tricuspid valve.
Image courtesy of Bushra Mina, MD

4. Biomarkers

Biomarkers of myocardial injury and dysfunction have a prognostic factor.

Elevated troponin I and T were associated with 4.26-fold increased odds of
overall mortality. Elevated brain natriuretic peptide (BNP) and N-terminal pro-
BNP (> 6 ng/mL) have odds ratios for short-term mortality of 9.51 (95% CI:
3.16 to 28.64) and 5.74 (95% CI: 2.18 to 15.13), respectively. The odds of
mortality from PE are increased with a combination of markers. Elevated
troponin and NT-pro-BNP were found to stratify normotensive patients with PE
more accurately with PE-related 30-day mortality exceeding 30%. A
combination of cardiac troponin I 0.1 ng/L and RV/LV 0.9 on
echocardiography identified a subgroup with an all-cause 30-day mortality of
38%.

5. Radiographic Studies

CT scan angiography is the modality of choice for confirming the diagnosis of

PE (Figure 18-3). In patients with a low or intermediate clinical probability of
PE, a negative CT had a high negative predictive value for PE (96% and 89%,
respectively), whereas this was only 60% in those with a high pre-test
probability. Conversely, the positive predictive value of a positive CT was high
(92% to 96%) in patients with an intermediate or high clinical probability, but
much lower (58%) in patients with a low pre-test likelihood of PE.

Figure 18-3. Computed Tomography Scan of Chest with IV Contrast

A. RV dilated with RV:LV ratio >1 with bowing of the interventricular septum into the left
ventricle. B. Dilatation of the pulmonary artery diameter with increase in the PA:ascending
aorta ratio. C. Saddle embolus into the right main pulmonary arteries.
Image courtesy of Bushra Mina, MD
 CT scan angiography is the modality of choice for
confirming the diagnosis of PE.

The size of the pulmonary artery in comparison with the ascending aorta is
indicative of underlying pulmonary hypertension. That dilatation of the RV in
contrast to the LV with an RV/LV ratio of ≥ 1 with deviation of the
interventricular septum to the left is indicative of RV strain and has a poor
prognostic implication.

6. Scoring System

Clinical scores can predict the probability and adverse outcomes/severity

independent of imaging or biomarker. Wells score (Table 18-4), Revised
Geneva score, and pulmonary embolism severity index (PESI/simplified PESI
scores) (Table 18-5) are validated clinical prediction scores to aid in the
assessment of the clinical probability of underlying PE.

Table 18-4 Simplified Wells Score

 Table 18-5 Simplified PESI Score

Abbreviation: PESI, pulmonary embolism severity index

E. Treatment
1. Segmental and Subsegmental Pulmonary Embolism

Treatment strategies depend on the hemodynamic effect of PE. For PE without

shock or any evidence of RV strain, such as in cases on segmental and
subsegmental PE, treatment consists of anticoagulation either with
unfractionated heparin (UFH) or low-molecular-weight heparin (LMWH) with
conversion to oral anticoagulation either with warfarin or non-vitamin K-
dependent direct oral anticoagulants (DOACs). No evidence suggests that bed
rest has any beneficial effect on these patients’ clinical outcomes.
New evidence supports the outpatient treatment of segmental or subsegmental
hemodynamic stable PE with DOACs. The duration of therapy for provoked PE
is 3 months and unprovoked is 6 months. Treatment for a more extended
period is not recommended, providing that the underlying risk no longer exists.
2. Submassive Pulmonary Embolism
Treatment of intermediate low-risk submassive PE is hospitalization and
anticoagulation with UFH or LMWH with consideration for early discharge on
oral agents. Existing evidence does not support primary reperfusion treatment
either with catheter-directed intervention or systemic thrombolysis. The
duration of anticoagulation is 3 months in provoked PE and 6 months for
unprovoked PE.
Treatment of intermediate high-risk submassive PE is anticoagulation and
consideration for rescue reperfusion. Full-dose systemic thrombolysis should be
considered if there are signs of hemodynamic decompensation. Catheter-
directed intervention or surgical pulmonary embolectomy are alternative rescue
interventions, especially if there is a bleeding risk or contraindications for
systemic thrombolysis (Table 18-6). The duration of treatment is a total of 3
months, but an extended period might be recommended.

Table 18-6 Contraindications for Systemic Thrombolytics

Approved thrombolytics are:

Streptokinase 250,000 IU as a loading dose over 30 min, followed
by 100,000 IU/h over 12–24 h or accelerated regimen: 1.5 million
IU over 2 h
Urokinase 4400 IU/kg as a loading dose over 10 min, followed by
4400 IU/kg/h over 12–24 h or accelerated regimen: 3 million IU
over 2 h
 rtPA 100 mg over 2 h or 0.6 mg/kg over 15 min (maximum dose 50
mg)

3. Massive Pulmonary Embolism

Hemodynamic support and mechanical ventilation

are indicated in the initial management of massive
PE.

Treatment of massive PE requires a multidisciplinary team approach. Patients

are admitted to intensive care units (ICU). Hemodynamic support and
mechanical ventilation are indicated in the initial management of massive PE.
Patients will require vasopressors to maintain adequate blood pressure and
tissue perfusion. Inotropic support might be necessary for acute right heart
failure. Primary reperfusion should be initiated urgently. Primary reperfusion
treatment, mainly systemic thrombolysis, is the treatment of choice.
Intravenous UFH should be administered to these patients as the preferred
mode of initial anticoagulation. Catheter-directed intervention should be an
option in experienced centers. Extracorporeal membrane oxygenation (ECMO)
might be required. Surgical pulmonary embolectomy is indicated if systemic
thrombolysis is contraindicated or fails to stabilize the hemodynamic status.
Treatment for unprovoked PE is indefinite after the first 3 months of treatment,
depending on the risk factors and bleeding risks. In these patients, periodic
reassessment based on the risk of thromboembolic event and bleeding risk for
the withdrawal of anticoagulant treatment is recommended (Figure 18-4).
 Figure 18-4. Treatment Algorithm for Pulmonary Emboli

Inferior vena cava filters are recommended if anticoagulation is contraindicated

or there is recurrence of VTE despite proper anticoagulation. The retrievable
filter should be removed once anticoagulation is initiated. The incidence of late
complications of retrievable filters is 10% as a result of filter migration, tilting
or deformation, penetration of the cava wall by filter limbs, the fracturing of the
filter and embolization of fragments, and thrombosis of the device.
The recurrence rate of VTE after discontinuation of treatment is approximately
2.5% per year after provoked PE compared with 4.5% per year after
unprovoked PE. Recurrence rates may be higher, up to 10%, in the first year
after withdrawal of anticoagulant treatment.

F. Prophylaxis
Prophylaxis is indicated for surgical patients with the encouragement of early
mobility. Bimodal prophylaxis is indicated in high-risk patients with
pharmacologic and mechanical agents. Pharmacologic agents include low-dose
unfractionated heparin, LMWH, fondaparinux, adjusted-dose vitamin K
antagonist, and aspirin. Apixaban, dabigatran, or rivaroxaban can be an
alternative. An intermittent pneumatic compression device (IPCD) is indicated
in all patients. Risk stratification for VTE is based on both patient- and
procedure-specific risk factors. Specific models for risk stratification exist, such
as Rogers and Cabrini scores. The American College of Chest Physicians
published (Antithrombotic Therapy and Prevention of Thrombosis, 9th ed:
Evidence-Based Clinical Practice Guidelines) recommendations for VTE
prophylaxis in surgical patients (Table 18-7, Table 18-8). All bariatric surgery
patients are at risk of VTE, with 30% of postoperative death due to PE.
Bariatric patients will have at least a Caprini score of at least four and,
therefore, be at least at moderate risk or higher. Low-dose aspirin or
fondaparinux can substitute LMWH or low-dose unfractionated heparin if
heparin is contraindicated. It is not recommended to use inferior vena cava
filters as primary prophylaxis. Also, periodic venous ultrasonography
surveillance is not recommended. VTE prophylaxis regimes are listed in Table
18-9.

Table 18-7 VTE Prophylaxis in Abdominal and Pelvic Surgical Patients

Abbreviations: LMWH, low-molecular-weight heparin; LDUH, low-dose unfractionated heparin; IPC,

intermittent pneumatic compression.

Table 18-8 VTE Prophylaxis in Trauma Patients

Abbreviations: LMWH, low-molecular-weight heparin; LDUH, low-dose unfractionated heparin; IPC,
intermittent pneumatic compression.

Table 18-9 Prophylaxis Regimens in Surgical Patients

Abbreviation: Cr CI, Creatinine clearance

VTE prophylaxis should be initiated 2 hours postoperatively except when

contraindicated. In spinal and neurosurgical procedures, postoperative
chemoprophylaxis is often delayed 24–48 hours. The duration of prophylaxis
is 7–10 days and can extend up to 12 days. An extended period of prophylaxis
is indicated if risk factors persist. VTE prophylaxis should be discontinued
temporarily for certain surgical procedures or other invasive interventions.
LMWH can be discontinued 12 hours before the procedure and can be
restarted 2 hours postoperatively and after removal of epidural catheters.
III. ICU MANAGEMENT OF THE BARIATRIC SURGERY
PATIENT

Case Study
A 61-year-old woman with morbid obesity (BMI 43) is admitted with severe
community-acquired pneumonia. Medical history includes diabetes mellitus,
essential hypertension, obstructive sleep apnea, and hypercholesterolemia.
Surgical history includes biliopancreatic bypass, caesarean section, and carpal
tunnel release. Preoperative medication included metformin 500 mg daily,
atenolol 25 mg daily, and rosuvastatin 10 mg daily. The patient uses BiPAP at
bedtime. Of note, since her bariatric surgery 9 months ago, she has lost 90 lb.
– How would the patient’s morbid obesity or a history of bariatric surgery
change the approach to this patient?

A. Treatment
To provide high-quality care for the bariatric surgery patient, it is crucial to
have the staff trained in caring for these patients and for the facility to have the
necessary appropriate equipment. Standard equipment such as beds,
stretchers, wheelchairs, blood pressure (BP) cuffs, IV catheters, as well as
imaging devices (CT/MRI scanners) may not accommodate these patients. ICU
admission criteria include:
Body mass index (BMI) greater than 60
A requirement for continuous cardiac monitoring
Severe obstructive sleep apnea (OSA)
Refractory diabetes mellitus
Intraoperative complication, ie, bleeding, cardiac or respiratory
event
1. Cardiac/Hemodynamic Monitoring
The indication for the use of invasive catheters (central venous catheters,
arterial lines) is the same as the non-bariatric surgical patient. Because of
altered anatomy, placement of central catheters should be performed with
ultrasound guidance. The length of standard central catheters and needles may
not be adequate (Figure 18-5). Noninvasive BP cuffs should be of the
appropriate size. There can be a spurious elevation of 10–50 mm Hg systolic if
the cuff is too small.

Figure 18-5. Inadequate Length of Central Venous Catheter in

Morbidly Obese Patient

Image courtesy of Mary Jane Reed, MD

Vascular access via two peripheral lines is usually adequate. If the ICU stay is
extended, a dual lumen peripherally inserted central cathether is
recommended.
2. Respiratory
Bariatric patients are at high risk for pulmonary complications because of the
high incidence of OSA or obesity hypoventilation syndrome (OHS), which can
be present in up to 70% of bariatric surgery patients. These patients also have
a small diameter upper airway. Pulmonary compliance is reduced as a result of
a non-compliant chest wall and restrictive lung disease because of truncal
obesity. When mechanical ventilation is required, the tidal volume should be
6–8 mL/kg ideal body weight (IBW). Plateau pressures need to be maintained
below 30 cm H2O if possible. Increasing positive end-expiratory pressure
(PEEP) will improve compliance in part by increased recruitment and
decreasing atelectasis. Starting with 10 cm H2O of PEEP in an obese patient
may prevent atelectrauma.

Extubation should be provided as soon as appropriate. The difficulty of

intubation should be noted before extubation. Extubation to noninvasive
positive-pressure ventilation (NIPPV) can reduce reintubation rates.

Noninvasive ventilation (NIV) can be used effectively in these patients. No

evidence exists that positive pressure ventilation from NIV increases the risk of
leakage from the anastomosis site. If patients use NIV at home, they should be
encouraged to bring their device to the hospital, unless oxygen supplementation
is required. This improves comfort and effectiveness compared with hospital-
provided units.
Early tracheostomy is recommended if intubation and the need for mechanical
ventilation are expected to be prolonged. This improves patient comfort and
may reduce complications from prolonged intubation. Expertise in
tracheostomy in the morbidly obese is helpful because redundant tissue and
thick adipose tissue may overlie the trachea, requiring submental
panniculectomy and specialized tracheotomy tubes.

3. Nutrition
 Critically ill post-bariatric surgery patients should
receive thiamine and folate before glucose.

Most patients begin an oral diet the day or evening of bariatric surgery.
Patients with significant delay of appropriate enteral nutrition should have
parenteral nutrition begun. Nutritional deficiency is common among bariatric
surgery patients because of malabsorption, and adequate dietary
supplementation is required. Micronutrient deficiencies often present in
patients who have had malabsorption surgery and significant weight loss.
Ensuring that these patients have thiamine and folate before significant
amounts of glucose should be considered because Wernicke’s-like syndrome
has been described in these patients. Other micronutrients such as copper,
vitamin D, and zinc may also be deficient. B12 levels should also be obtained.

4. Analgesia
Pain assessment scales should guide the goal of pain management. Pain
management should be according to a protocol-based approach with a stepwise
approach. Opiates should be avoided because of the risk of respiratory
depression, delirium, ileus, and immunosuppression. Epidural analgesia, as
well as the use of acetaminophen and ketamine, could be adjunct to opioids.
Neuropathic pain medication, such as gabapentin, can be used. Avoid NSAIDs
because of their risk profile and association with marginal ulceration of
anastomosis.

5. Glycemic Control

Glycemic control in critically ill postoperative patients has been well studied.
The optimal glucose control level is 140–180 mg/dL and not below 70 mg/dL.
Many bariatric patients postoperatively require less insulin than prior to surgery
as a result of weight loss, decreased oral intake, and change in insulin
resistance.

6. Medication Dosing
Bariatric patients have a large volume of distribution for lipophilic drugs and
increased clearance of hydrophilic drugs. This finding requires adjusting the
doses of commonly used medications in the ICU. Drugs are dosed based on
ideal body weight (IBW), total body weight (TBW), or dosing weight (DW),
sometimes referred to as adjusted body weight (ABW).

Up to a 30% higher dose of enoxaparin may be

needed for prophylaxis in the morbidly obese
patient, but the ideal dose is unknown.

IBW is used to calculate digoxin, beta-blockers, penicillins, cephalosporins,

acyclovir, glucocorticoids, H2 blockers, atracurium, vecuronium, fentanyl,
midazolam, lorazepam, morphine sulfate, and phenytoin. TBW is used to
calculate the dose of succinylcholine, heparin, enoxaparin, and vancomycin.
DW is used to calculate the dose of aminoglycosides.

B. Complications of Bariatric Surgery

To address and treat the complications associated with bariatric surgery, one
should understand that this field is a dynamic one, and the procedures,
instruments, techniques, and technology are continually changing. There are
two categories of procedures: volume restrictive and nutrient malabsorptive
procedures (Table 18-10, 18-11, 18-12).

Table 18-10 Postoperative Complications of Bariatric Surgery

Table 18-11 Laparoscopic Gastric Banding Complications

Table 18-12 Sleeve Gastrectomy (SG) Complications

Roux-en-Y Gastric Bypass (RYGB)

RYGB is a restrictive procedure with a malabsorptive component. This

procedure has the risk of “dumping syndrome,” which is a constellation of
symptoms, including flushing, tachycardia, and weakness (Figure 18-6).

Sleeve Gastrectomy (SG)

SG is a restrictive procedure without a malabsorptive component. Leakage and
bleeding from a long staple line can occur (Figure 18-7).

Biliopancreatic Diversion with Duodenal Switch (BPD/DS)

BPD/DS is a procedure that has both restrictive and malabsorptive properties.
There is more malabsorption, especially of protein and fat-soluble vitamins
(Figure 18-8).
Intragastric Balloon (IGB)

IGB is a purely restrictive tool placed endoscopically. Nausea, vomiting, reflux,

balloon migration, perforation of stomach and/or intestine are all known
potential complications. Because the balloon is usually filled with blue dye, the
presence of urine that is blue should prompt the patient to seek medical
attention because the deflated balloon has the potential to migrate and cause an
intestinal obstruction.

Gastric Band (GB)

GB is a purely restrictive procedure that has decreased in use in the last
decade because results have not been sustainable. Reflux, erosion, and
slippage causing obstruction can occur (Figure 18-9).

Figure 18-6. RYGB

Reproduced with permission American Society for Metabolic and Bariatric Surgery.
https://asmbs.org/. Accessed January 15, 2020.
Figure 18-7. Gastric Sleeve

Reproduced with permission American Society for Metabolic and Bariatric Surgery.
https://asmbs.org/. Accessed January 15, 2020.
Figure 18-8. Biliopancreatic Diversion (BPD/DS)

Reproduced with permission American Society for Metabolic and Bariatric Surgery.
https://asmbs.org/. Accessed January 15, 2020.
 Figure 18-9. Gastric Band

Reproduced with permission American Society for Metabolic and Bariatric Surgery.
https://asmbs.org/. Accessed January 15, 2020.

1. Anastomotic Leak

A sustained pulse of 120 beats per minute in the

early postoperative bariatric surgery patient
should be investigated.

Leaks usually occur within 2 weeks of the procedure. The signs and symptoms
are often subtle, with a lack of abdominal findings on clinical examination.
Typical signs of peritonitis and sepsis may be absent. This lack of clinical
findings is, in part, a result of body habitus and pain management. The most
common signs are tachypnea and tachycardia. A low-grade fever is also
common. These patients are often assessed for PE and or other respiratory
complications because of the presenting signs and symptoms. The diagnosis is
made after a contrast study or CT scan. If there is difficulty in obtaining an
imaging study and there is a high index of suspicion and worsening
hemodynamics, reoperation should be performed immediately. The treatment
is irrigation, drainage, broad-spectrum antibiotics, and placement of a
percutaneous drain and an enteral feeding tube in the OR. Because the
diagnosis is often difficult, these patients should undergo CT pulmonary
angiography with oral contrast abdominal and pelvic CT.

2. Hemorrhage

Most bleeding occurs at the staple line or anastomosis. This problem is often
the result of the inability of the staple line to compress a small vessel.
Tachycardia is a common sign followed by melena. Most episodes resolve
without the need for intervention. Transfusion of blood products and reversal of
anticoagulation is done if needed. If there is an ongoing transfusion
requirement, endoscopic evaluation is recommended. If there is hemodynamic
instability or bleeding not amenable to endoscopic therapy, surgery is
recommended.

3. Venous Thromboembolism

Making the diagnosis of VTE can be difficult. Imaging requires appropriate

machines to support the patient’s weight. If there is a high suspicion of PE and
a delay or inability to obtain an imaging study, anticoagulation should be
started immediately. This is usually done with heparin since it can be stopped,
and the anticoagulation effect dissipates quickly if bleeding occurs. If there is a
contraindication to anticoagulation, an IVC filter should be placed to decrease
the risk of further clot embolization. Risk factors for VTE and PE are included
in Table 18-13.

Table 18-13 Risk Factors for VTE and Fatal PE

4. Acute Myocardial Infarction (MI)

The risk of acute MI is approximately 0.2%. The risk increases with a history
of coronary artery disease (CAD). Bariatric patients have known risk factors for
CAD. Their risk decreases over time after surgery as their comorbidities
improve.

5. Respiratory Failure/Pneumonia

The risk for respiratory failure and pneumonia following bariatric surgery is
0.25% to 0.6%. The risk for pneumonia is increased by a history of congestive
heart failure, chronic obstructive pulmonary disease (COPD), bleeding
disorders, tobacco use, increasing age, and open versus laparoscopic
procedure. The risk for respiratory failure is increased in patients with COPD,
previous percutaneous coronary intervention, diabetes mellitus, increased age,
prolonged anesthesia, and an open versus laparoscopic procedure. Early
ambulation, abdominal pain control, and incentive spirometry have been shown
to decrease the incidence of respiratory failure.

IV. TRANSPLANT ICU

Case Study
A 55-year-old man with a significant history of COPD undergoes bilateral lung
transplantation. The donor was cytomegalovirus (CMV) negative, and the
recipient is CMV positive. The surgery is performed without the use of
cardiopulmonary bypass, no complications, and minimal reported blood loss.
The patient is transported to the ICU on mechanical ventilation of volume
control with a tidal volume of 6 mL/kg, FIO2 of 0.7, and PEEP of 8 cm H2O
with an arterial SpO2 of 95%. The following treatments are initiated via
nasogastric tube: prophylactic antimicrobials vancomycin and cefepime,
valganciclovir, itraconazole, and immunosuppressive drugs tacrolimus and
mycophenolate mofetil. IV methylprednisolone and inhaled amphotericin are
administered. The patient’s last pulmonary artery occlusion measurement
before discontinuation of the pulmonary artery (PA) catheter 4 hours
postoperatively was 6 mm Hg. Six hours after surgery, the patient requires
increased FIO2, and peak and plateau pressures on the ventilator have
increased. He has developed a low-grade fever of 38°C (100.4°F) but remains
hemodynamically stable. A chest radiograph is obtained (Figure 18-10).
– Is this finding concerning?
– How does the surgical history change the approach to this patient?
 Figure 18-10. Chest Radiograph of COPD Patient Six Hours After
Uneventful Bilateral Lung Transplant

A. Diagnosis and Management of Organ-specific Postoperative

Complications
Since the 1960s, surgical techniques, as well as immunosuppressive therapy
for allograft rejection, have improved in solid organ transplantation. Survival
time has increased, and antimicrobial treatment has helped decrease infection.
In recent decades, kidney and pancreas transplant patients do not necessarily
require a stay in the ICU. However, transplant institutions may still want the
recipient to be observed for at least 24 hours. The lung, liver, and heart
continue to remain a challenge because of their respiratory and hemodynamic
risk intraoperatively and postoperatively. Depending on how these patients do
early postoperatively affects their long-term outcome. Recognizing common
illnesses and syndromes that come with transplant is vital because missing
diagnoses such as infection, acute rejection, or allograft dysfunction can result
in death.
1. Heart Transplant
Primary indications for heart transplant include coronary artery disease,
valvular heart disease, congenital heart disease, and dilated cardiomyopathy.
The median range of survival has reached 11 years. The most common causes
of death from heart transplants are allograft rejection, infections, vasculopathy,
and malignancies such as lymphoma.
Intraoperatively, a transesophageal echocardiogram is performed. If tricuspid
regurgitation (TR) is seen intraoperatively, an echocardiogram within 24 hours
is warranted. Depending on the severity of the TR, a donor tricuspid valve may
be considered. Pericardial effusions are common postoperatively and are only
drained if hemodynamic instability occurs. The transplanted heart cannot
respond to hypovolemia with reflex tachycardia because of denervation, so
adequate preload is necessary to maintain blood pressure and stroke volume.
In conjunction, intravenous fluids are used frugally, and diuresis is aggressively
administered intraoperatively and postoperatively. In cases where the left
ventricle needs assistance with cardiac output, inotropes such as dobutamine or
milrinone are used.

Complications of heart transplant are detailed here.

a. Primary Heart Graft Failure

Primary graft failure accounts for 20% to 40% of deaths in the early
postoperatively period. Failure of the graft typically occurs when the
demands of the new heart are unable to respond to that of its new
circulatory environment. Severe graft failure is described as low
cardiac output and high filling pressures.

b. Right Ventricular Failure and Pulmonary Hypertension

Patients who have pulmonary hypertension perioperatively might

experience RV failure. Usually, this can be controlled with
isoproterenol in reducing RV afterload. If pulmonary hypertension is
not resolving and causing hemodynamic instability, intravenous
nitroglycerine, nitroprusside, and prostaglandin E1 may be used. A
vasopressor might be needed because these agents are potent general
 vasodilators. Inhaled nitric oxide (iNO) can be used as a selective
pulmonary vasodilator, thus reducing intrapulmonary shunting.
Sildenafil has also been used in pulmonary hypertension that remains
persistent.

c. Left Ventricular Failure

LV failure results from reperfusion injury in patients who have had
greater than 5 hours of cold ischemic time. Weeks to years post-
transplant, LV failure can result from myocarditis, acute rejection,
allograft CAD, and allograft dysfunction.

d. Rejection

In heart transplant patients, rejection is typically asymptomatic,

making it challenging for the clinician. Within the first 30 days, there
is still a 7% death rate from rejection. Clinical symptoms are
nonspecific, including hypotension, fatigue, fever, and congestive heart
failure. Endomyocardial biopsies are performed weekly within the first
30 days. In chronic rejection typically months to years later,
accelerated CAD will manifest itself clinically presenting as dyspnea.
More than 50% of patients develop CAD in 5 years.

2. Lung Transplant

Patients who primarily have COPD and interstitial pulmonary fibrosis (IPF)
receive lung transplantation. Patients may receive a single lung transplant or a
double lung transplant. Patients with cystic fibrosis receive double lung
transplants to avoid the various multidrug-resistant organisms that colonize the
native lungs.

Certain factors need to be acknowledged in lung transplant patients.

Lung-protective ventilation is recommended postoperatively, and
high airway pressures should be avoided.
Patients will have pulmonary artery catheters for evaluation of
hypoxia if present.
 Recipients are taken off invasive mechanical ventilation quickly to
help decrease ventilator-associated pneumonia.
Patients with lung transplants also have apical and basal chest tubes.
Basal chest tubes remain longer to help relieve ongoing pleural
effusions, usually 5 to 7 days.
Fluid management tends to be difficult in lung transplant because patients can
have a systemic inflammatory response from cardiopulmonary bypass, primary
graft dysfunction, and sepsis. When this occurs, patients will develop
noncardiogenic pulmonary edema which remains a challenge for the new lung
and also makes it challenging to suppress edema because of disrupted
lymphatic drainage. Minimizing fluids postoperatively is recommended.

Complications of lung transplants are detailed here.

a. Primary Graft Dysfunction (PGD)

The International Society of Heart and Lung Transplant (ISHLT)

developed a grading system to help identify primary graft dysfunction.
The presence of diffuse infiltrates involving the lung allografts are
revealed on a postoperative chest radiograph. PaO2/FIO2 (P/F ratio) is
used to identify the grade of severity: Grade 1 (PF ratio>300), Grade
2 (PF ratio 200–300), and Grade 3 (PF ratio<200). Furthermore,
other causes of PGD need to be ruled out, such as pneumonia,
rejection, cardiogenic pulmonary edema, and pulmonary venous
outflow obstruction. The clinician should be aware of ischemic time,
donor lung pathology, and time for lung reperfusion because these are
major risk factors for PGD.

As mentioned earlier, fluid is generally avoided in lung transplant

patients. When PGD is confirmed, a negative fluid balance helps
reduce symptoms. In cases of severe hypoxia and PGD, iNO has been
used to improve oxygenation; however, no controlled studies have
shown any mortality benefit. Furthermore, in PGD that is refractory to
invasive mechanical ventilation and iNO, prostaglandin E1 (PGE1) has
shown to improve reperfusion injury. Because PGE1 is a nonselective
vasodilator, it may hasten a decline in ventilation/perfusion matching
in the lung. If therapy continues to show no improvement in PGD,
extracorporeal life support (ECLS) is used during this stage of severity.

b. Rejection

Hyperacute rejection rarely occurs because recipient and donor

antihuman leukocyte antigen antibodies are performed before
transplant. Acute rejection occurs after the first week up to the first
year. Clinically, patients have low-grade fevers, negative cultures,
perihilar infiltrates, hypoxemia, airway inflammation, and an elevated
white blood count. Acute rejection is treated with pulse
methylprednisolone 10–15 mg/kg for the first 3 to 5 days and then
continued for 2 to 3 weeks with a tapering dose.

c. Bleeding

Even though blood may not be seen in chest tube drainage, a drop in
hemoglobin is concerning and remains one of the reasons patients may
return to the operating room. Bleeding has not been shown to increase
mortality perioperatively.

d. Airway Complications
Bronchial necrosis, endobronchial infections, exophytic excessive
granulation tissue formation, tracheobronchomalacia, bronchial
fistulas, and bronchial stenosis remain challenging to the clinician.
Bronchial necrosis and endobronchial infections can occur earlier in
the postoperative period. Necrosis may occur because of the
interruption of blood supply from the bronchial artery at the site of
anastomosis. The new lung then only relies on blood supply from
pulmonary artery collaterals. Clinical findings of bronchial necrosis are
persistent air leak, lung collapse, difficult to extubate, subcutaneous
emphysema, pneumomediastinum, and pneumothorax. Treatment
involves visualizing anastomosis via bronchoscopy and CT scan to
evaluate for possible surrounding air or infection.

Chronic lung allograft dysfunction (CLAD) remains a long-term

complication with poor outcomes. CLAD has an obstructive-type
 disease pattern termed bronchiolitis obliterans syndrome (BOS), and a
restrictive pattern termed restrictive allograft syndrome (RAS) or
restrictive CLAD (rCLAD). Risk factors that have been identified for
the two pathologies include CMV, gastroesophageal reflux disease
(GERD), and episodes of acute rejection. Treatment involves the use of
bronchodilators, steroids, treatment of GERD, and adjustments in
immunosuppressive therapy.

3. Pancreatic Transplant
Pancreatic transplant is usually performed with either kidney or at times with
small bowel transplant. Pancreatic transplantation is performed in patients who
have diabetes mellitus without nephropathy. It should be of note that
intraoperatively, pancreatitis and allograft edema are common because of
reperfusion. Typically, diuretics are given to help alleviate edema and assist in
microvascular perfusion. Therefore, it is essential to know whether osmotic
diuresis helped with edema because if it did not, allograft function requires
vigilant monitoring postoperatively.
Graft dysfunction is a complication of pancreatic transplants. The two most
common causes of graft failure are rejection and thrombosis. The bleeding risk
is lower in pancreatic transplant patients compared with other solid organs, and
therefore intraoperatively, low-dose systemic heparin is administered to
decrease thrombosis.
If a patient is experiencing ileus, fever, and abdominal pain, pancreatitis then
pancreatic ischemia should be considered. Because amylase levels will be
elevated postoperatively, the levels cannot be correlated with the severity of
pancreatitis. However, if there is a rapid rise in amylase and lipase and
requirements for exogenous insulin increase, graft ischemia or necrosis should
be evaluated. Rejection ultimately needs the confirmation of a biopsy, and
thrombosis is evaluated through the means of ultrasonography.

In patients who have pancreatic transplants with exocrine drainage through the
bladder, rejection is suspected when urine amylase levels drop significantly. In
males, the risk of urethritis is higher than in females. Bladder infection and
metabolic acidosis can also occur. Metabolic acidosis is usually the result of
losing bicarbonate in the urine. These patients also can become dehydrated
early in the postoperative course.

4. Liver Transplant

Most liver transplant patients are monitored in the ICU. The first 72 hours are
essential to frequently assessing hemodynamics using ultrasonography or
through invasive monitoring. In the postoperative period, monitoring levels of
hemoglobin are crucial for evaluating signs of bleeding. Patients may continue
to be in a hyperdynamic circulatory state postoperatively given a history of
portal hypertension. This finding can be challenging because it may mimic
sepsis with increased cardiac output and decreased systemic vascular
resistance. Cautions must be taken to not under resuscitate or over resuscitate
the transplanted patient.
Graft function is monitored every 6 hours focusing on values of total bilirubin,
lactate, glucose, international normalized ratio (INR), transaminases, and levels
of potassium. Urine output and core body temperature are measured on an
hourly basis. Decreased urine output, consistent rise in INR, lactate,
transaminases, and inability to regulate normal body temperature are signs of
inadequate allograft function. INR is usually elevated immediately
postoperatively and should start to return to normal within 24 hours if the graft
is properly functioning. Transaminases typically rise within the first 48 hours
and begin to normalize a few days after. Bilirubin may take longer than other
values before it starts to normalize but do be aware of drastic changes that may
occur. A Doppler scan of the liver is performed within the first 24 hours to
assess hepatic vein and artery flow.

Liver transplant patients should be extubated as soon as adequate graft

function is evident. Furthermore, hemodynamic status and pain should be well
controlled. Early nutrition is initiated to help decrease metabolic stress.
There are surgical and medical complications to a liver transplant.

a. Surgical Complications

Primary graft nonfunction is the failure of the liver graft, which is seen
early in the postoperative period. Consistently elevated transaminases,
INR and bilirubin, lactate, and worsening acidosis should raise
concern for graft failure after acute infection, acute rejection, and
hepatic vein or artery thrombosis have been ruled out. Although the
complication of primary graft nonfunction is between 3% and 5%, the
mortality is higher than 20%.

Vascular complications, such as thrombosis, occur early compared

with stenosis or pseudoaneurysm, which occurs in later stages. Hepatic
artery thrombosis is second to primary graft nonfunction as the most
significant complication early in the postoperative period. Diagnosis
can be challenging because some patients may not experience pain,
whereas others may quickly have a drastic rise in transaminases to
fulminant liver failure.
Immediate Doppler ultrasonography should be used, followed by
potential arteriography or exploratory laparotomy at the discretion of
the surgeon. Portal vein thrombosis occurs less frequently, clinically
presenting as worsening ascites or variceal bleeding. Portal vein
thrombosis is diagnosed by liver ultrasonography and if found early,
thrombectomy and revision of anastomosis can be effective.

Bile leak is another major complication that occurs in about 15% of

liver transplant patients. Patients may show signs of abdominal
discomfort and fever. Suspicion should rise when abdominal pain is
not resolving, and fever cannot be explained. Although
ultrasonography may reveal a fluid collection, ultimately,
cholangiography is definitive for diagnosis. Many bile leaks typically
need abdominal exploratory laparotomy and washout.
In some cases, endoscopic stenting has shown success. Strictures and
bilomas are later complications. Strictures usually present at the site of
the anastomosis clinically revealing overt cholestasis or cholangitis.
Based on the severity of the stricture, balloon dilation may be
successful. In other cases, retransplantation may be required.

b. Medical Complications

i. Sepsis
Bacterial infections are more common than fungal and mostly
arise from biliary leaks or deep surgical spaces within the
abdomen. Aside from the surgical site as a potential source of
infection, other possible sources of infections should be
explored as well, such as indwelling catheters (Foley, central
venous).

ii. Neurologic Complications

Clinical studies have reported rates of 8.3% to 47% for

neurologic complications. The most common include
encephalopathy, brain hemorrhage, and seizures. Patients
who are encephalopathic before liver transplantation carry a
higher risk of neurologic complications. Seizures are the
second most common complication known to be a
consequence of various factors stemming from metabolic
disturbances, infection, stroke, or drug toxicity.
Immunosuppression-related complications may reveal as
headaches, confusion, myoclonus, delirium, and lowering the
seizure threshold. Central pontine myelinolysis occurs in
about 1% to 3.5% of patients after rapid correction of
hyponatremia. Posterior leukoencephalopathy is a rare and
severe manifestation activated by neuronal loss and reactive
astrocytosis, usually the result of calcineurin inhibitors.

iii. Respiratory Complications

Transient pulmonary edema from sepsis or systemic
inflammatory response syndrome (SIRS) may occur early in
the postoperative period. Pneumonia is also common. Most
pulmonary infiltrates are noncardiogenic pulmonary edema
originating from abdominal sepsis. Pleural effusions are
common on the right side postoperatively. As mentioned
earlier, early extubation is vital, and if prolonged more than 7
to 10 days, tracheostomy should be considered. Patients with
hepatopulmonary syndrome (HPS) have been reported to
require a longer length of stay, primarily because of
 pulmonary vascular shunting causing hypoxemia. Pleural
effusions are common after liver transplantation and tend not
to cause respiratory compromise.

iv. Cardiovascular Complications

Transplanted liver patients classically present with

hyperdynamic circulation resulting in increased cardiac index
and low blood pressure. If a patient has a history of
portopulmonary hypertension with high cardiac output, this
tends to resolve post-transplant. In cases of low cardiac
output, clinicians should evaluate volume status, bleeding, or
stunned myocardium in the setting of SIRS or sepsis. Serial
lactate measurement and echocardiography can assist in the
hemodynamic management of these patients. In the acute
setting postoperatively, colloid fluids, such as 5% albumin,
are preferred for resuscitation. Albumin helps to maintain
fluid balance, especially in liver transplant patients who tend
to have hypoalbuminemia. Transplant surgeons should be
made aware of patients’ hemodynamics, especially when
difficult to control with volume resuscitation.

v. Renal Complications

Renal complications vary widely in regard to post-liver

transplant. Acute kidney failure ranges anywhere from 27% to
67%. At the discretion of the transplant surgeon, treatment
typically includes renal replacement therapy and potential
adjustments in immunosuppressive therapy that may be
contributing to acute renal failure.

5. Kidney Transplant
Renal transplant patients typically do not need to go to the ICU postoperatively
unless there is a concern for hemodynamic instability and respiratory
complications. Immediate postoperatively, volume status needs to be monitored
closely along with laboratory values (specifically including electrolytes,
complete blood count), chest radiograph, and ECG. Renal ultrasonography is
performed immediately after surgery.

Strict input and output are a crucial factor in managing patients

postoperatively. It is imperative to keep patients heading toward a positive fluid
balance considering the new kidney is in diuresis and there are insensible
losses, which may average anywhere from 500–1000 mL/day. Patients should
be kept toward a higher systolic blood pressure ≥ 150 mm Hg. If hypotension
occurs, patients should be resuscitated with isotonic fluids.
Complications for a kidney transplant are detailed here.

a. Bleeding

If patients continue to be hypotensive with a decrease in hematocrit

and experience abdominal pain, evaluation for intra-abdominal
bleeding is warranted. If there are any drains or ureteral stents placed,
the output should be monitored, and color change should be
immediately reported to the surgeon. The output from drains is
serosanguinous in the first few days. Therefore, if gross blood or any
other change is noted, caution should be taken.

b. Graft Dysfunction
Graft thrombosis, arterial or venous, can occur in the first 72 hours.
Venous thrombosis presents with hematuria and pain. Diagnosis is
established by ultrasonography. Arterial thrombosis usually results in
graft loss. Clinically there is an abrupt drop in urine output, with
ultrasonography confirming the diagnosis. Renal artery stenosis can
also occur but typically occurs a few months to 2 years later.

c. Urologic Complications

Urinary leaks occur early in the postoperative period. Symptoms

present as tenderness over the graft site, fever, decreased urine
output, and a rising creatinine. Analysis of drain output is sent for
creatinine to confirm leakage. More substantial leaks require surgical
repair.
6. Small Bowel Transplant

Small bowel transplant patients may be challenging because few specific

markers are available to help guide management postoperatively. Clinicians
need to be cognitive of specific laboratory findings and conduct regular
physical examinations to determine whether the graft is functioning properly.
Ostomy output, lactate, hyperkalemia, and metabolic acidosis are valuable in
assessing the graft. In these patients, volume depletion occurs because of
inflammation and primarily a lack of absorption from the transplanted small
bowel. Fluid resuscitation is challenging because, as with the pancreas where
diuresis and fluid restriction may be considered, the transplanted small bowel
also tends to be edematous. Therefore, in those instances, albumin 5% or
albumin 25% is preferred for volume resuscitation.

Rejection is a complication of small bowel transplant. Rejection typically can

occur within the first 30 days of transplantation. A biopsy is the gold standard
for diagnosing rejection. In centers that perform small bowel transplants,
endoscopies are conducted twice a week for the first month post-transplant.
Patients who receive an intestinal transplant have significantly low albumin
levels and are subject to malnutrition. If, for any reason, patients remain
nothing by mouth for more than 3 days, it is preferred that nutrition is
provided parenterally. Rejection is treated with adjustments in
immunosuppression, corticosteroids, and plasmapheresis. Plasmapheresis is
given postoperatively within the first 24 hours in patients who have elevated
levels of donor-specific circulating antibodies.

B. Immunosuppressive Therapy

Many common drugs affect immunosuppressive

levels, so pharmacy consultation is suggested
before introducing new drugs.
Immunosuppression therapy is the mainstay treatment of transplanted patients.
Transplant surgeons decide what kind of regimen their patients are prescribed.
The primary intent in administering immunosuppression is to help prevent
rejection of the transplanted organ. Typically, a corticosteroid, calcineurin
inhibitors, and antiproliferative agents are used as immunosuppression agents.
Moreover, monoclonal antibodies are used when a patient is resistant to
steroids or to help decrease the effects of calcineurin inhibitors.

1. Corticosteroids
Methylprednisolone and prednisone are the steroids used in
immunosuppression. Significant adverse effects to be aware of entail
hyperglycemia, hypokalemia, metabolic alkalosis, myopathy, mood changes,
hypertension, gastritis, encephalopathy, and increased the risk of infection.

2. Calcineurin Inhibitors

Interleukin-2 (IL-2) inhibitors, cyclosporine and tacrolimus, can be monitored

via serum levels. However, be advised that serum levels may not correlate with
the severity of the adverse effects depicted in patients. Both drugs are known to
have nephrotoxicity and neurotoxicity as adverse effects with cyclosporine
having less neurotoxicity than tacrolimus. Clinicians should remember to avoid
low magnesium levels in patients taking calcineurin inhibitors because it may
intensify neurotoxicity. Neurotoxic adverse effects are broad, ranging from
headaches, tremors, seizures, delirium, cognitive impairment, dysarthria,
posterior reversible encephalopathy syndrome to coma. Nephrotoxicity
incidence and severity with cyclosporine increase with dose and duration of the
medications and can occur even at traditional therapeutic drug serum levels.
Patients who experience nephrotoxicity from cyclosporine and tacrolimus may
be treated with sirolimus. Sirolimus blocks cytokine stimulation through mTOR
inhibition without affecting calcineurin activity and prevents proliferation of T-
lymphocytes and reduces antibody production. Sirolimus has been known to
cause a higher incidence of hepatic artery thrombosis after liver
transplantation, can delay wound healing, and may cause angioedema.

3. Antiproliferative Agents
Antimetabolite purine synthesis inhibitors include mycophenolate mofetil and
azathioprine. Myelosuppression, electrolyte abnormalities, and gastrointestinal
symptoms such as ileus, vomiting, diarrhea, and ulcers are common adverse
effects. Azathioprine is used when patients are intolerant of the gastrointestinal
adverse effects of mycophenolate mofetil.

4. Monoclonal Antibodies

Monoclonal antibodies consist of basiliximab and muromonab-CD3.

Basiliximab blocks IL-2 receptors to inhibit activation of T-lymphocytes while
muromonab-CD3 first activates T cells, which tends to exacerbate systemic
inflammation.

5. Antimicrobials
Immunosuppressive therapy places patients at risk for infection and neoplasm.
Aside from immunosuppressive therapy post-transplant, all patients are started
on trimethoprim-sulfamethoxazole (TMP/SMX, Bactrim™) for Pneumocystis
jirovecii (PCP) prophylaxis. Depending on the history of the patient and
previous exposure, patients may also be started on antivirals for prophylaxis
against cytomegalovirus (CMV) and Epstein-Barr virus (EBV), hepatitis C virus
(HCV), and hepatitis B virus (HBV). Patients who have received an organ from
a seropositive donor remain at high risk, especially if the patient is
seronegative. Furthermore, in the first month postoperatively, patients are at
risk for nosocomial bacterial infections. Once the full effect of
immunosuppressive therapy takes effect, which is typically between 1 to 6
months, opportunistic infections are more common. TMP/SMX substantially
prevents infections such as PCP, Listeria monocytogenes, Toxoplasma gondii,
and Nocardia species susceptible to sulfa. However, clinicians need to be
cognizant of fungi, Aspergillus, Cryptococcus, Trypanosoma cruzi, and
strongyloidiasis that may occur. Beyond 6 months, patients tend to have a
lower risk of opportunistic infections because patients are at lower doses of
immunosuppression.

C. Management of Adverse Effects of Therapy

In all transplanted patients, the most worrisome complication is rejection and
failure of the graft. Adverse effects of immunosuppressive therapy and
complications of surgery can affect the quality of life for these patients. This
makes it imperative to identify complications sooner.

Ultimately, imaging, physical examination, and serum markers allow the

clinician to recognize complications. Furthermore, immunosuppressive therapy
can cause significant toxicity if combined with a medication that is either an
inhibitor or inducer of liver cytochrome P-450 enzyme system. CYP3A4 is an
isoenzyme involved in liver metabolism, and cyclosporine and tacrolimus are
CYP3A4 substrates. Antifungals such as fluconazole, posaconazole,
itraconazole, and voriconazole are potent CYP3A4 inhibitors.

If toxicity occurs, doses are adjusted at the discretion of the transplant team.
Immunosuppressive therapy is rarely stopped because of higher risks of
rejection. When acute rejection is confirmed by biopsy, immunosuppressive
therapy may be adjusted for higher doses. Antilymphocyte antibodies have
been shown to have a higher success rate in the treatment of acute rejection
compared with steroids.

Key Points
Management of Special Populations
Venous thromboembolism (VTE) is the third most common
cardiovascular disorder. Approximately one-half are related to
current or recent hospitalization.
The mortality rate for acute PE exceeds 15% in the first 3 months
after diagnosis.
Early and late complications of bariatric surgery are uncommon and
often difficult to diagnose.
Anastomotic leak occurs most often during the first week of surgery.
Leaks can present as respiratory failure.
 Nutritional deficiencies are common after bariatric surgery.
Knowledge of the anatomic changes associated with each operation
is essential to understanding possible complications.
Diagnosis and management of organ-specific postoperative
complications are essential in treating transplant patients.
Immunosuppression therapy is the mainstay treatment of
transplanted patients to prevent transplanted organ rejection.
Corticosteroid, calcineurin inhibitors, and antiproliferative agents are
used as immunosuppression agents. Monoclonal antibodies are used
when a patient is resistant to steroids or to help decrease the effects
of calcineurin inhibitors.

Suggested Readings
1. Antithrombotic Therapy for VTE Disease. CHEST Guideline and
Expert Panel Report. Chest. 2016;149(2):315-352.
2. Prevention of VTE in Nonorthopedic Surgical Patients
Antithrombotic Therapy and Prevention of Thrombosis, 9th ed:
American College of Chest Physicians Evidence-Based Clinical
Practice Guidelines. Chest. 2012;141(2 Suppl):e227S–e277S.
3. Konstantinides SV, Torbicki A, Agnelli G, et al. 2014 ESC
guidelines on the diagnosis and management of acute pulmonary
emboli. Eur Heart J. 2014;35(43):3033-3080.
4. Diaz GC, Wagener G, Renz JF. Postoperative care/critical care of
the transplant patient. Anesthesiol Clin. 2013;31(4):723-735.
5. Feltracco P, Barbieri S, Galligioni H, Michieletto E, Carollo C, Ori
C. Intensive care management of liver transplanted patients. World
J Hepatol. 2011;3(3):61-71.
6. Lau C, Patterson G, Palmer S. Critical care aspects of lung
transplantation. J Intensive Care Med. 2004;19(2):83-104.
7. Ma IT, Madura JA. Gastrointestinal Complications after Bariatric
Surgery. Gastroenterol Hepatol (N Y). 2015;11(8):526-535.
8. Pagalilauan GL, Limaye AP. Infections in transplant patients. Med
Clin North Am. 2013;97(4):581-600.
9. Pham P-TT, Pham P-CT, Danovitch GM. The acute care of the
transplant recipient. In: McKay DB, Steinberg SM, eds. Kidney
Transplantation: A Guide to the Care of Kidney Transplant
Recipients. New York: Springer; 2010:207-235.

Suggested Websites
1. Metabolic and Bariatric Surgery Accreditation and Quality.
https://www.facs.org/quality-programs/mbsaqip
2. American Society of Transplantation. https://www.myast.org/
3. American Society of Metabolic and Bariatric Surgery
www.asmbs.org
 Chapter 19
SURGICAL SOFT-TISSUE
COMPLICATIONS AND
URGENCIES

Objectives
Identify a healthy, healing wound.
Recognize wound dehiscence and infection.
Recognize and manage necrotizing soft-tissue infection (NSTI).
Recognize and manage compartment syndrome.

Case Study 1
A 58-year-old man sustained trauma to his leg while working on his boat. He
presented to the hospital with a painful open wound on the inferior portion of
his leg. The patient was found to have a tibial fracture and he underwent
closed fixation of the fracture. On postoperative day 2, he developed
worsening pain. The skin along the surgical site became increasingly
edematous. By postoperative day 3, erythema of the affected leg was
increasing. He soon became persistently febrile, and the leg began to harden.
– Is this finding concerning?
– What distinguishes a normal wound from a complicated wound?
 – What are the critical first steps in managing a wound complication?

Case Study 2
A 63-year-old man fell in the bathroom where he was found by a neighbor
after almost 24 hours. At the hospital, he was found to have cervical spine
fractures and minor head trauma. He was taken for cervical discectomy and
fusion and was brought to the intensive care unit intubated, with a right
internal jugular central venous catheter and a right radial arterial line. Over
postoperative day zero, his right hand began to swell. His hand was elevated,
and compresses were applied. By postoperative day 1, the edema of the hand
had worsened and the arterial line was removed. The edema began to affect
the distal portion of the forearm, and the affected area began to harden.
– What are the signs and symptoms of compartment syndrome?
– What are the critical first steps in managing compartment syndrome?

I. INTRODUCTION
Surgical wound infections are one of the most common adverse events in
hospitalized surgical patients. Surgical site infections are classified as
superficial incisional, deep incisional, and organ/space infections. These
infections occur within 30 days of the surgery. Physical examination remains
the most essential and reliable approach to diagnosis. Local examination
findings of pain, swelling, erythema, purulent drainage, and wound
dehiscence all suggest possible surgical site infections. However, not all
surgical site infections may present this way.

II. POSTOPERATIVE WOUND CARE

For most operations, wound care is either straightforward or nonexistent
because the skin is typically closed and covered with an occlusive dressing for
the first 48 hours. However, this can vary significantly for emergency cases or
those wounds associated with a significant amount of contamination. The
location of the incision can frequently give information about what operation
was performed and, therefore, what to expect postoperatively (Figure 19-1)
(Table 19-1).

Figure 19-1. Common Incision Locations and Associated

Operations

Table 19-1 Common Incision Locations and Associated Operations

* A complete midline incision (laparotomy) is occasionally performed if additional exposure is needed
or the exact location of surgery is unknown preoperatively, such as in trauma.

A. Diagnosis
When caring for a postoperative patient, it is important to know what
operation was performed, the length of the procedure, and the degree of
contamination. The type of surgery can help predict the expected
postoperative course and potential complications (eg, elevated liver enzymes
are to be expected after liver resection, but could be problematic after a
routine colectomy). More prolonged operations are associated with a higher
likelihood of fluid or electrolyte disturbances, and operations with more
contamination are associated with more frequent wound complications and
increased risk of postoperative infections. The Centers for Disease Control
and Prevention (CDC) has directed that each surgical procedure have a
wound classification assigned (Table 19-2).

Table 19-2 CDC Wound Classifications

Reproduced with permission Onyekwelu I, Yakkanti R, Protzer L, Pinkston CM, Tucker C, Seligson D.
Surgical Wound Classification and Surgical Site Infections in the Orthopaedic Patient. J Am Acad
Orthop Surg Glob Res Rev. 2017;1(3):e022. Copyright © 2017 The Author(s). Published by Wolters
Kluwer Health, Inc. on behalf of the American Academy of Orthopaedic Surgeons.

As the wound classification increases, the risk of surgical site infections (SSI)
or organ space infections increases as well. Although most incisions are
covered with an occlusive dressing for 24–48 hours postoperatively, as the
wound classification increases, it becomes more likely that the wound will not
be closed at the time of operation.

The healing of a surgical wound takes place by one of three mechanisms. For
most operations, the tissues of a clean incision are reapproximated with
sutures, which is referred to as healing by primary intention. If there is
significant contamination of the wound, only the deep layers will be closed,
and the superficial layers will be allowed to heal by the formation of
granulation tissue and wound contraction. This is referred to as healing by
secondary intention. Although it takes longer, the risk of wound infection is
significantly lowered. A combination of these two techniques involves placing
sutures at the time of the operation, leaving the wound open for several days,
and then closing the wound by tying the sutures. This is referred to as
delayed primary closure or healing by tertiary intention.
B. Management
1. Phases of Wound Healing
The healing of any wound, surgical incisions included, follows a predictable
pattern of phases that can be characterized by the types of cells present and
the predominant activity of those cells. Although these phases overlap in their
duration, they follow a consistent linear pattern, and derangement in any
stage will prevent the re-establishment of tissue integrity. These phases are as
follows:
Inflammatory Phase
Proliferative Phase
Maturation Phase

The healing process begins with the initial injury. As tissues and blood vessels
are disrupted, the extracellular matrix and collagen are exposed, allowing for
platelet aggregation. Platelets then release a variety of active substances that
promote the formation of a fibrin clot. After the wound becomes hemostatic,
local tissue factors and platelets promote vasodilation and increase capillary
permeability. This allows for the influx of inflammatory cells (predominantly
neutrophils) and fluid, which causes the wound to become erythematous,
edematous, and warm. The neutrophils mainly facilitate the phagocytosis of
bacteria and removal of dead tissue, and, in experimental models, do not
seem to be critical to wound healing. After 2–3 days, macrophages will
become the predominant inflammatory cell and help to facilitate matrix
deposition, angiogenesis, and tissue remodeling by the release of cytokines
and tissue growth factors. Macrophages may be the most important cell
involved with healing because of the aforementioned effects, and they will
remain until the wound has completely healed.

The proliferative phase of wound healing is characterized by the influx of

endothelial cells and fibroblasts, which outnumber inflammatory cells by
approximately postinjury day 4. By day 5–7, there is no longer a large
population of inflammatory cells remaining in the wound. Type III collagen is
being replaced by type I collagen, and for the next 2–3 weeks, angiogenesis,
the formation of granulation tissue and wound contraction, will take place.

The final phase of wound healing (maturation/remodeling) begins around 3–4

weeks and will persist for months. At this point, collagen cross-linking will
take place and, even though collagen is continuing to be synthesized, it is
being broken down at almost the same rate that it is being created.
Vascularity will also decrease during this phase until an acellular and
avascular scar is formed. See Table 19-3 for factors that can impair wound
healing.

Table 19-3 Factors That Can Impair Normal Wound Healing

2. Wound Dressings

The most common postoperative wound dressing is an occlusive dressing that

prevents a clean wound from being exposed to bacteria until epithelization
takes place at about 24–48 hours. In general, these dressings should be left
in place unless an early postoperative wound infection is suspected (erythema,
excess drainage, fevers, etc.). Surgeries associated with large or chronic
wounds can be managed with a variety of different dressing types. The ideal
dressing maintains a moist environment, removes excess exudate, does not
cause further damage to the wound with removal, protects the wound from
further trauma, is impermeable to bacteria, requires infrequent changes,
conforms to the wound easily, minimizes pain, and is cost-effective. A list of
common dressings and their potential advantages/disadvantages are listed in
Table 19-4.

Dressings are frequently forgotten in critically ill

patients and left in place for too long. These
wounds should be periodically inspected,
especially in the setting of unexplained fevers. In
general, simple dressings that are saturated,
bloody, or covering a wound with suspicious
drainage can safely be removed, the wound
inspected, and replaced with a clean dressing.

Table 19-4 Common Wound Dressings

* Gauzes are typically soaked in saline to prevent wound desiccation. However, they can also be soaked
in antimicrobial solutions such as povidone-iodine or Dakin’s solution.
Data taken from Fonder MA, et al. Treating the chronic wound: A practical approach to the care of
nonhealing wounds and wound care dressings. J Am Acad Dermatol 2008;58(2):185-206.

3. Surgical Drains

The management and purpose of surgical drains and tubes are frequently
overlooked by treating physicians who are not part of the surgical team that
placed them. Part of any surgical sign out should include a description of any
drains or tubes including the location of the drain (subcutaneous vs. deep
organ space), the purpose of the drain (remove excess fluid vs. monitor for
changes in output), the proper care of the drain (active vs. passive), and
things that would be concerning (increased output, decreased output, change
in the appearance of output, etc.). Also, instructions should be given for what
to do if the drain comes out: is it an emergency, or can it be safely left out?
This should be clarified even for common drains like a nasogastric tube or
indwelling bladder catheters. For instance, there may be a risk of injury by
replacing a nasogastric tube in a patient with a fresh esophageal anastomosis,
and a indwelling catheter may be protecting a bladder repair or ureteral
anastomosis in the case of renal transplant.
The following is a description of different types of drains and their typical
purpose (Figure 19-20):
a. Jackson-Pratt (JP): These are radiopaque silicone or PVC tube drains
that can be either round, flat, or multi-channeled. They are commonly
attached to a bulb suction device that provides active suction. Their location
typically dictates what function they are supposed to perform. Placed in the
subcutaneous tissues of the neck, breast, extremities, or near surgical
incisions, they are primarily for drainage of excess thin exudates that could
potentially create a seroma. Placed intra-abdominally or intra-thoracically,
they can serve to drain exudate or monitor for changes in output (eg,
sudden production of bile or succus could indicate an anastomotic leak).
b. Blake: These are radiopaque silicone drains with four channels
surrounding a solid core. They are typically attached to a bulb suction
device and are placed in similar locations and for the same purposes as JP
drains. There usually is a manufacture mark that indicates the most distal
extent of draining channels and should remain at or below the level of the
skin.
c. Davol/Hemovac: These drains are similar in structure to JP and Blake
drains, although they are typically larger and attached to an evacuator that
is spring-loaded and can hold a larger volume (~400 mL). They are
commonly used in neurosurgical or orthopedic procedures for the control of
exudate and bleeding.
d. Sump drain: Sump drains typically have three lumens that allow for the
application of suction, installation of fluids, and an air vent. They generally
are allowed to drain by gravity to a collection bag and are placed intra-
abdominally to facilitate the removal of large volumes of thicker exudates.
e. Malecot: This is a latex drain tipped with a splayed, mushroom-shaped tip
that drains by gravity to a collection bag. It is typically placed in the urinary
system as a nephrostomy tube or enterally. Enterally, its function is for
diversion of intestinal contents or to allow access for feeding.
f. Abdominal wound VAC: This is a temporary abdominal closure device
that provides an egress for abdominal exudates and as an occlusive barrier
to prevent contamination of an open abdominal wound. Careful attention
should be paid to output because a significant amount of fluid can be lost
through an open abdominal incision.
g. T-tube: This tube, traditionally placed into the bile duct, is also used to
create controlled fistulae after duodenal or esophageal perforations. They
serve to either protect a biliary anastomosis or provide egress for
obstruction (eg, choledocholithiasis or malignancy). They can either be
allowed to drain by gravity or attached to a suction device (eg, bulb
suction).
h. Cholecystostomy tube: This drain is placed directly into the gallbladder
to allow for the egress of bile when cholecystectomy cannot be immediately
performed. It can be placed surgically or percutaneously, often transversing
liver parenchyma.
i. Tube thoracostomy: These drains come in a variety of sizes from a pigtail
drain (8–14F) used for pneumothorax to a large 36F silicone tube placed
for the evacuation of a hemothorax associated with trauma. They are
connected to a three-chamber drainage device that allows for the collection
of output (collection chamber), prevents the reflux of air into the pleura
(water-seal chamber), and prevents the application of excessive suction
(suction chamber) that could injure the lung. While active bubbling in the
suction chamber simply indicates that suction is being applied, bubbling in
the water-seal chamber indicates air is being removed from the pleural
space. Active suction assists with the evacuation of air, but typically does
little for the egress of fluid because the amount of suction applied is usually
low (~20 cm H2O). Fluid often needs to drain by gravity. After
pneumonectomy, chest tubes are not typically placed to suction because it
can cause acute mediastinal shift.
j. Penrose: These drains are flat, flexible open system drains that provide
egress of fluids and prevent premature closure intentional sinus tract.
Replaced mainly by closed drain systems mentioned previously, Penrose
drains are still used in selected situations and resource-limited
environments. Penrose drains need to be secured to prevent both egress out
of the wound but also inadvertent advancement and loss into the wound.

Figure 19-2. Types of Surgical Drains

III. WOUND DEHISCENCE

Wound dehiscence is a surgical complication that refers to the partial or
complete disruption of one or multiple layers of surgical wound closure. It
ranges in severity from the partial separation of the skin to complete fascial
disruption and evisceration of abdominal viscera. While this is an infrequent
problem, especially in young, healthy patients, the risk increases with age or
systemic illness.
A. Diagnosis
One of the most important aspects of diagnosing wound complications is
identifying those patients that are at increased risk. Systemic factors that can
potentially lead to dehiscence include those that contribute to delayed wound
healing (eg, diabetes mellitus, sepsis, immunosuppression, malignancy,
nutritional deficiencies) and those that increase intra-abdominal pressure (eg,
obesity, ileus, coughing). Ascites can also contribute by both increasing intra-
abdominal pressure and by the constant leakage of fluid through the incision,
preventing reapproximation of the wound, and providing a route for infection
to develop. Technical factors associated with the closure (ie, suture selection
and placement of sutures) can also increase the risk of dehiscence. However,
this information cannot typically be assessed once the wound has been closed.
In reality, it is usually a combination of factors that contribute to wound
disruption, and special attention should be paid in those patients at higher
risk. Interventions aimed at reducing these risk factors (NG tube for ileus,
abdominal binder for obesity or coughing, preoperative nutritional
optimization, etc.) are more desirable than dealing with the complication.

While new serosanguinous drainage from a

wound could be nothing more than a
subcutaneous fluid collection, it could also
herald fascial dehiscence, which could progress
to evisceration. Prompt surgical consultation is
warranted.

Although it can occur at any time, dehiscence usually takes place

approximately 7 days after the initial operation when the tensile strength of
the wound is at its lowest. The earliest sign of dehiscence is typically the
egress of serosanguinous fluid or discharge from a previously dry incision.
However, it can also present as the sensation of “something popping” while
coughing or sudden evisceration. In the case of thoracic incisions, this can
also manifest as air leaking from the wound or paradoxical chest wall
movement. However, the dehiscence of thoracic incisions is less common
because the surrounding ribs typically support the incisions, and there is less
pressure from underlying viscera. If the skin of the wound has separated, the
integrity of the fascial closure can be tested by gently probing the wound with
a cotton-tip applicator.

B. Management
At a basic level, the management of dehiscence is reclosing the wound,
especially if it is in the early postoperative period. The degree of dehiscence
will also dictate the treatment and the urgency of intervention. If the
underlying fascia is intact and the dehiscence is limited to the skin, these
wounds can usually be treated with packing alone. However, if all of the
wound layers have been compromised, it typically requires urgent
reoperation.
Abdominal laparotomy incisions with fascial dehiscence should be stabilized
with an abdominal binder and returned to bed to prevent progression to
evisceration. At this point, the patient should be returned to the operating
room, and the surgeon will typically open the wound and re-do the fascial
closure. Frequently, the skin is also left open to prevent wound infection, and
the wound either packed with saline-soaked gauze or a negative pressure
wound therapy device is applied. In the event of complete evisceration, the
patient should be returned to bed, the viscera covered with a saline moistened
sterile non-adherent dressing and the patient prepared for emergent return to
the operating room. No attempt should be made to return the bowel to the
abdominal cavity outside of the operating room. If there is only partial
dehiscence and there is significant contamination of the wound from infection
or the patient is a poor surgical candidate, it may be prudent to avoid
reoperation. In this case, the skin closure should be maintained, the incisions
should be supported with a binder or corset, and a resulting incisional hernia
is to be expected. However, even small defects can serve as a site of bowel
herniation and incarceration that can potentially complicate this approach.
 If fascial dehiscence results in the evisceration of
abdominal contents, the most important thing to
do preoperatively is return the patient to bed and
keep the viscera moist with sterile towels.

Sternal wounds require special attention because they are almost uniformly
caused by infection and require urgent debridement and reapproximation to
prevent sternal nonunion or more serious mediastinal infection. With the
exception of significant sternal osteomyelitis, most sternal wounds can be
effectively reclosed. However, they will occasionally require mediastinal
irrigation or closure with a pectoralis major flap.

IV. NECROTIZING SOFT-TISSUE INFECTON (NSTI)

Necrotizing surgical site infections differ from milder infections in that they
involve deep fascial and muscle compartments. Necrotizing soft-tissue
infection is a destructive infection that tracks along superficial fascia.
Presentation is often one of cellulitis; affected tissue will have a “wooden-
hard” induration, and severe pain that may seem disproportionate to physical
examination. Skin may have bullous lesions, necrosis, or crepitus, suggestive
of gas within the tissue. Patients often will have fever and as the infection
progresses may develop hemodynamic instability that can result in organ
failure and ultimately death if not treated promptly and correctly. While
surgical site infections rarely occur in the first 48 hours after surgery, when
surgical site infections occur within the first 48 hours, they are often due to
Streptococcus pyogenes or Clostridioides species. Common organisms are
Streptococcus pyogenes, Staphylococcus aureus, Vibrio vulnificus, or
Aeromonas hydrophila but surgical site infections can also be polymicrobial.

A. Background
Skin and soft-tissue infections (SSTIs) include infections of the superficial or
deeper structures of the skin and surrounding tissues. They range from non-
necrotizing SSTIs, which include superficial infections (impetigo, erysipelas,
cellulitis) and purulent types (simple and complex abscesses, furuncles, and
carbuncles). The severity can range from mild to severe depending on the
extent of progression and presence of systemic response. Necrotizing SSTIs
(NSTIs) may involve the dermis in cases of necrotizing cellulitis, superficial
and deeper fascia as well as subcutaneous fat in cases of necrotizing fasciitis,
and the muscle layer in cases of myonecrosis. Fournier’s gangrene is a NSTI
confined to the genital area, including the perineum, scrotum, penis, or vulva.
Severe NSTIs typically have signs and symptoms of sepsis or septic shock.
Bullae, skin sloughing and necrosis are concerning signs of deeper infection.
Without appropriate control of the source, NSTIs can quickly progress and
are associated with increased morbidity and mortality. (Table 19-5)

Table 19-5 Skin and Soft-Tissue Structures and Associated Syndromes

B. Epidemiology and Risk Factors
The overall incidence of cellulitis is estimated to be 24.8/1000 patient-years.
Conversely, the incidence of necrotizing fasciitis is less common with an
incidence of 0.04/1000 patient-years, although this does not include other
forms of NSTIs and is limited to Streptococcus pyogenes. The overall rates of
NSTIs have reported to be increasing, which are purported to be the result of
increasingly resistant organisms. According to Surgical Infection Society
clinical practice guidelines, the mortality remains high for these patients
(mean 23.5%, range 7% to 70%). However, a more recent evaluation
reported an average mortality rate of 14% (range 9% to 22%), which may
reflect improved mortality with modern care focusing on early initial
debridement, repeated debridement to obtain adequate source control, early
and appropriate antimicrobials, and supportive care. Based on several
evaluations, one major factor associated with increased mortality rates is the
delay to surgical debridement. Other clinical factors associated with increased
mortality includes age 50 years and greater, increased involvement of body
surface area, lactic acidosis, hypotension, organ dysfunction at admission,
immunocompromised state, and a white blood cell count greater than
30,000/mm3. Although true risk factors are not well known, reported risk
factors for NSTI, methicillin-resistant Staphylococcus aureus (MRSA), and
community-acquired MRSA (CA-MRSA) are included in Table 19-6.

Table 19-6 Risk Factors Associated with NSTI, MRSA, and CA-MRSA
Abreviations: NSTI, necrotizing soft-tissue infection; MRSA, methicillin-resistant Staphylococcus
aureus; CA-MRSA, community-acquired methicillin-resistant Staphylococcus aureus

C. Diagnosis
1. Clinical Presentation and Physical Examination
Early diagnosis is paramount in minimizing morbidity and mortality for
patients with NSTI. Clinical presentation represents a major challenge for the
diagnosis because of nonspecific complaints, such as nonspecific pain,
gastrointestinal symptoms (ie, nausea, vomiting, diarrhea), and influenza-like
symptoms. In addition, physical examination findings may only consist of mild
local erythema and may be difficult to distinguish from cellulitis. Other
clinical manifestations for necrotizing fasciitis include soft-tissue edema,
erythema, severe pain, tenderness, fever, and skin bullae and necrosis. Bullae
and necrosis are often late signs (Figure 19-3). Patients may, however,
present with the absence of fever by self-administration of antipyretics,
absence of cutaneous manifestations, attributing pain to an injury or
procedures, or attribute systemic manifestations to other causes, such as
nausea, vomiting, and diarrhea. Therefore, recognition and diagnosis may be
challenging. In an evaluation of missed diagnosis of NSTI by primary care or
emergency room physicians, patients were misdiagnosed as having
musculoskeletal pain (40%), influenza (20%), gastroenteritis (13%),
hemorrhoids (6%), gout (6%), first-degree burn (6%), and varicella (6%).
 Figure 19-3. Examples of Necrotizing Soft-Tissue Infection

Images courtesy of Mary Jane Reed, MD

2. Laboratory and Imaging

According to surgical clinical guidelines, some clinical features may be

strongly suggestive of a NSTI. These may include pain disproportionate to
physical examination findings, tense edema, bullae, skin ecchymosis or
necrosis, cutaneous anesthesia, progression despite antimicrobial therapy, and
signs of systemic toxicity. Systemic signs may range from leukocytosis greater
than 14 × 109/L, serum sodium level less than 135 mEq/L, blood urea
nitrogen level greater than 15 mg/dL, to septic shock requiring vasopressors.
A rapidly progressive soft-tissue infection should strongly be considered to be
a NSTI. Scoring systems have been evaluated and suggested to aid in the
diagnosis of NSTI. The most extensively studied is the Laboratory Risk
Indicator for Necrotizing Fasciitis (LRINEC) score, which includes C-reactive
protein levels, white blood cell count, hemoglobin, serum sodium, serum
creatinine, and serum glucose. A score of 6 or greater was found to have a
sensitivity, specificity, positive predictive value, and negative predictive value
of 90%, 95%, 92%, and 95%, respectively. While the original study was
promising, more recent studies have not replicated these findings and a score
of less than 6 cannot rule out the diagnosis of NSTI (Table 19-7).

Table 19-7 Laboratory Risk Indicator for Necrotizing Fasciitis (LRINEC) Score

Reproduced from Wong CH, Khin LW, Heng KS, et al. The LRINEC (Laboratory Risk Indicator for
Necrotizing Fasciitis) score: A tool for distinguishing necrotizing fasciitis from other soft tissue infections.
Crit Care Med. 2004;32(7):1535-41. Copyright © 2004 by the Society of Critical Care Medicine and
Lippincott Williams & Wilkins.
Imaging may aid in the diagnosis and should be considered when the
diagnosis is undetermined by clinical history or physical examination findings.
Plain radiographs may only be helpful if gas is present, which only occurs in
approximately one-third of patients, thus providing low sensitivity. Although
there is no gold standard, either computed tomography (CT) or magnetic
resonance imaging (MRI) may be useful in the detection of soft-tissue gas;
however, an MRI may be difficult to obtain under an emergent situation in
addition to the increased cost and limited availability. CT imaging is more
sensitive for the presence of soft-tissue gas and inflammatory changes (up to
80%), but may not be specific for NSTI. Alternatively, ultrasound may aid in
the diagnosis for those unstable patients to differentiate cellulitis from
necrotizing fasciitis. Furthermore, imaging may be useful to identify other
potential diagnoses, such as abscesses. Although diagnostic studies have
possible utility for the diagnosis of NSTI, direct examination in the surgical
setting may be required to make a definitive diagnosis, thus emphasizing the
need for early surgical consultation and a very low threshold for surgical
exploration. Delays in diagnosis and treatment of these infections may be
associated with significant mortality and morbidities, further elevating the
importance of early diagnosis and surgical management.

3. Microbiology
Type I infections are the most common type of NSTI, accounting for at least
85% to 90%. These infections generally have a mixture of aerobic and
anaerobic organisms, including gram-positive, gram-negative, and anaerobic
pathogens that typically arise from a chronic, indolent source and spread
along a fascial plane. A type II infection is the second most common type,
and typically include gram-positive aerobic pathogens, including
Streptococcus species and CA-MRSA. These pathogens are known to be
virulent related to their toxin production. A type III infection is a
monomicrobial infection caused by other gram-positive or gram-negative
species, such as Clostridioides or Bacillus species. Other types of
monomicrobial NSTIs include water-borne pathogens, such as Vibrio
vulnificus and Aeromonas hydrophila. Patients with liver disease, including
alcoholic cirrhosis, chronic hepatitis, and hemochromatosis, may be
predisposed or higher risk for Vibrio infections. Another type of
monomicrobial infection that typically involves the rhino-orbital-cerebral
passages or paranasal sinuses should be strongly considered for Mucor or
Rhizopus infections. Patients with increased risk include those with
immunosuppression, diabetes mellitus, iron overload, and recent treatment
with deferoxamine. Other types of fungal infections are not typical for NSTI,
but may still occur.

D. Management
1. Early Surgical Debridement

Clinical deterioration in a patient with NSTI

should prompt immediate reevaluation of wounds
for need of further emergent surgical
debridement.

An early surgical consultation is paramount for the management of patients

with NSTI. Immediate surgical debridement is considered the cornerstone of
therapy while adjunctive therapies are also necessary, including appropriate
empiric antimicrobials and supportive care. A delay in surgical debridement
and inadequate debridement is associated with worse outcomes, including
increased risk of mortality. Subsequent debridement is likely necessary with
the second exploration within a 24- to 48-hour period. In addition, these
patients receive an average of four total debridements to achieve source
control. Amputations may be necessary when a limb is not viable or not
expected to be functional. Diverting colostomies may be needed for
Fournier’s gangrene to prevent soiling of the perineum. Once source control
is achieved and no further debridements are necessary, skin grafts and/or
flaps or use of wound vacuum-assisted closure (VAC) may be used.

2. Initial Resuscitation
Initial resuscitation is critical for these patients, especially for those with
severe systemic symptoms and shock. Fluid resuscitation is needed to replace
intravascular volume, initial management of hypotension, and optimizing
blood volume to maintain tissue perfusion. Crystalloids, including normal
saline or balanced crystalloids, such as Plasmalyte or lactated Ringer solution,
are typically considered first-line for initial fluid resuscitation. Packed red
blood cell transfusions may be needed for patients with significant blood loss
during the surgical procedure or anemia from hemolysis caused by toxin
production. Other blood products, such as platelets and fresh frozen plasma,
are not routinely needed and should be reserved for those with significant
thrombocytopenia and coagulopathy, respectively. For patients presenting in
septic shock, after adequate fluid resuscitation, vasopressor therapies may be
needed to maintain adequate mean arterial pressure greater than 65 with
norepinephrine and vasopressin or epinephrine considered first- and second-
line therapies, respectively. Multiorgan failure is common in patients with
NSTI and additional therapies may be necessary.

3. Antimicrobial Therapy

Empiric antimicrobial therapy should be broad to include the likely pathogens

involved and should be initiated promptly. Clinical guidelines for patients
presenting with sepsis and septic shock suggest initiation of antimicrobials
within 1 hour of presentation. The likely pathogens may differ based on the
clinical setting, pathophysiology, and previous exposure to antibiotics. In
addition to surgical debridement, empiric antimicrobials should include a
broad-spectrum beta-lactam agent, including piperacillin/tazobactam,
carbapenem, or a third- or fourth-generation cephalosporin/metronidazole
combination for coverage directed toward gram-negative, gram-positive, and
anaerobic pathogens. In addition, coverage toward MRSA should be included
with vancomycin typically considered a first-line treatment. Empiric
clindamycin should be considered for NSTI to decrease toxin production
associated with invasive group A streptococcal infections. Those patients
suspected to have a NSTI involving the rhino-orbital-cerebral areas and
paranasal sinuses should receive empiric coverage toward Mucor and
Rhizopus with lipid formulation amphotericin B or posaconazole. Definitive
therapy should target the specific pathogen grown from microbiologic data
and de-escalated to the most narrowed spectrum agent. Specific
recommendations are summarized in Table 19-8. Duration of therapy
ultimately depends on the ability to obtain source control with expert
recommendations suggesting within 72 hours with clinical improvement.

Table 19-8 Summary of NSTI Types

Footnote: 1) Duration of coverage is at least 72 hours after a source control procedure and consider
infectious disease consultation. 2) Broad-spectrum beta-lactam options, including pipercillin/tazobactam
3.375–4.5 g IV every 6 hours, imipenen-cilastatin 1 g IV every 6–8 hours, meropenem 1–2 g IV every
8 hours, ertapenem 1 g IV every 24 hours, and ceftazidime 2 g IV every 8 hours or cefepime 1–2 g IV
every 8 hours given with metronidazole 500 mg IV every 8 hours. 3) 30 mg/kg/day given in 2 divided
doses. 4) 600–900 mg IV every 8 hours. 5) 2–4 million units IV every 4–6 hours. 6) 100 mg IV every
12 hours. 7) 1–2 g IV every 24 hours. 8) 400 mg IV every 12 hours. 9) 3–5 mg/kg/day depending on
formulation. 10) 400 mg PO twice daily with meals. 11) Renal dose adjustments necessary.
Abbreviations: CA-MRSA, Community-acquired methicillin-resistant Staphylococcus aureus; SP.,
species; NSAID, nonsteroidal anti-inflammatory drug; immunosuppression: includes hematologic
malignancies, organ transplant, AIDS, chronic steroid use; AIDS, acquired immunodeficiency
syndrome.
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2011;39(9):2156-62.; Stevens DL, Bisno AL, Chambers HF, et al. Practice guidelines for the diagnosis
and management of skin and soft tissue infections: 2014 Update by the Infectious Disease Society of
America. Clin Infect Dis 2014;59(2):e10-52.

4. Adjunctive Therapies
Patients with NSTI may have electrolyte and acid-base disturbances that
require close monitoring. The most common electrolyte disturbances include
mild hyponatremia and hypocalcemia. The hyponatremia encountered in
NSTI is typically a hypotonic hypovolemic type and thus, responsive to fluid
resuscitation. Hypocalcemia can be treated with calcium gluconate
supplementation. Monitoring with ionized calcium is recommended because of
the low serum albumin that usually occurs in this population. Hyperglycemia
is also a frequent issue in this population. Insulin continuous infusions may be
necessary to allow for better glycemic control, frequent blood glucose
monitoring, and rate adjustments. Subcutaneous administration of insulin may
be hindered by lack of subcutaneous absorption because of fluid resuscitation
and vasopressor therapies. Although not needed for initial management,
nutrition support is necessary for wound healing and should be initiated
within 48 hours if possible. Enteral nutrition is the preferred method for
nutrition and patients should receive an adequate intake of vitamins A, C, and
D along with zinc. Other adjunctive therapies, including hyperbaric oxygen
(HBO) and intravenous immunoglobulin (IVIG) may be considered. However,
these have a controversial and limited role for specific patients and should not
be considered for initial management. Lastly, pain control is essential for
comfort of the patient undergoing multiple surgical procedures. In addition,
preemptive administration of short-acting opioids may be considered prior to
dressing or wound VAC changes.

V. COMPARTMENT SYNDROME
Compartment syndrome in the extremity is an elevation of pressure within a
myofascial compartment resulting in ischemia. It is most commonly seen in
the setting of trauma, particularly fractures and crush injuries. However, it
may also be caused in nontraumatic settings by bleeding (postoperative or
spontaneous in a patient with a bleeding disorder or on anticoagulation,
positioning during surgery or constricting wraps) or by increased
intracompartmental fluid (extravasated intravenous fluid or medication, burn
injury, rhabdomyolysis, ischemiareperfusion). Because of the inelasticity of
the fascial compartment, anything that increases the mass within the
compartment can result in this potentially devastating complication.
Compartment syndrome most commonly occurs in the leg, specifically in the
anterior compartment, followed by the forearm, but may occur in the arm,
thigh, hand, or foot. Of note, compartment syndrome may also occur in the
abdomen or less commonly chest wall, and abdominal compartment
syndrome is covered in Chapter 14.
Unrecognized compartment syndrome can result in loss of limb viability
requiring amputation or an ischemic contracture with loss of limb function. If
not addressed emergently, compartment syndrome can lead to death.
Rhabdomyolysis of the muscle within the compartment may cause
hyperkalemia and acute kidney injury, which may result in the need for
emergent hemodialysis or fatal arrhythmias.
Physiologic compartment pressure is 0–8 mm Hg; elevations above 30 mm
Hg result in venous hypertension and progressive ischemia. Without
treatment, irreversible tissue damage occurs within 6–8 hours. It is a limb-
threatening and ultimately life-threatening emergency; the only cure is
surgical.

A. Diagnosis

The most common early symptom of compartment

syndrome is pain, especially with passive stretch
of the muscles within that compartment. In
contrast, the presence of pulses is not reassuring
in ruling out the diagnosis of compartment
syndrome. Pulselessness is a late symptom, and
irreversible tissue damage frequently occurs
before the patient loses his or her pulse.

The diagnosis of compartment syndrome is primarily a clinical one. A history

of trauma, particularly tibial fractures or crush injuries, should raise suspicion
for ensuing compartment syndrome. Patients with bleeding disorders or on
anticoagulation are also at increased risk. The classic examination findings
include “the 6 P’s”—pain, paresthesia, pallor, poikilothermia, paralysis, and
pulselessness—and a tense or hardened compartment. However, these
findings are rarely all present. Of these, the most common early symptom is
pain, especially with passive stretch of the muscles within that compartment.
However, as compartment syndrome progresses, pain may paradoxically
decrease as nerve function becomes impaired. A high index of suspicion is
critical to recognizing compartment syndrome early and maximizing the
chance of successful intervention. Generally, the diagnosis can be made on
clinical grounds alone. However, if physical examination is equivocal and
compartment syndrome is suspected, compartment pressures may be
measured using either commercial devices or an angiocath connected to a
transducer (eg, arterial line). If the pressure within the compartment exceeds
30 mm Hg, emergent fasciotomy is indicated.
It is crucial to realize that pulselessness is a late finding in compartment
syndrome because the systolic pressure will overcome the increased
compartment pressure until very late in the progression of the disease. As
such, a clinician should not be reassured by the presence of pulses and
mistakenly rule out compartment syndrome because a patient has pulses; this
action can lead to permanent disability or death.

B. Management
Compartment syndrome is a true surgical emergency. The treatment for
compartment syndrome is immediate fasciotomy. Opening the compartment(s)
allows for blood and fluid to be evacuated, soft-tissue expansion, and
restoration of perfusion. The keys to successful management are prompt
diagnosis and early surgical intervention. If compartment syndrome is
suspected, immediate surgical consultation is required.
Uncommonly, compartment syndrome may be caused by external
compression, so removal of any compressive dressings will reduce the
extrinsic elevation of compartment pressure. Elevation of the affected
extremity to the level of the heart may help venous return. Fasciotomy must
be performed emergently to avoid irreversible tissue damage and further
sequelae of compartment syndrome.

Compartment syndrome is a surgical emergency

that requires an immediate operation to avoid
irreversible tissue damage, disability, and
potentially death.
Key Points
Surgical Soft-Tissue Complications and Urgencies
Surgical wound infections are classified as superficial incisional,
deep incisional, and organ/space infections. These infections occur
within 30 days of the surgery.
Physical examination remains the most important and reliable
approach to diagnosis. Local examination findings of pain, swelling,
erythema, purulent drainage, and wound dehiscence all suggest
possible surgical site infection.
Surgeries with more contamination are associated with more
frequent wound complications and increased risk of postoperative
infections.
New serosanguinous drainage from a wound could be nothing more
than a subcutaneous fluid collection or it could also herald a fascial
dehiscence that might progress to evisceration. Prompt surgical
consultation is warranted.
Sternal wound dehiscence requires special attention because it is
almost uniformly caused by infection and requires urgent
debridement and reapproximation to prevent sternal nonunion or
more serious mediastinal infection.
Surgical consultation with early surgical debridement is the
cornerstone for the management of NSTI. Delays in surgical
management are associated with increased mortality and morbidity.
Empiric antimicrobial therapy should be broad-spectrum to include
gram-positive, gram-negative, and anaerobic pathogens with
definitive therapies directed toward specific pathogens identified
from microbiologic data.
Compartment syndrome is a limb-threatening and ultimately life-
threatening true surgical emergency. Irreversible tissue damage
 occurs within 6–8 hours in compartment syndrome without
treatment.
Rhabdomyolysis of the muscle within the compartment may cause
hyperkalemia and acute kidney injury, which may result in the
need for emergent hemodialysis or fatal arrhythmias.
A clinician should not be reassured by the presence of pulses and
mistakenly rule out compartment syndrome because a patient has
pulses; this action can lead to permanent disability or death.
The treatment for compartment syndrome is immediate fasciotomy.

Suggested Readings
1. Berrios-Torres SI, Umscheid CA, Bratzler DW, et al. Centers for
Disease Control and Prevention Guideline for the Prevention of
Surgical Site Infection, 2017. JAMA Surg. 2017;152(8):784-
791.
2. Bodansky D, Doorgakant A, Alsousou J, et al. Acute
Compartment Syndrome: Do guidelines for diagnosis and
management make a difference? Injury. 2018;49(9):1699-1702.
3. Fonder MA, Lazarus GS, Cowan DA, Aronson-Cook B, Kohli AR,
Mamelak AJ. Treating the chronic wound: A practical approach to
the care of nonhealing wounds and wound care dressings. J Am
Acad Dermatol. 2008;58(2):185-206.
4. Keung EZ, Liu X, Nuzhad A, et al. Immunocompromised status
in patients with necrotizing soft-tissue infection. JAMA Surg.
2013;148(5):419-426.
5. Psoinos CM, Flahive JM, Shaw JJ, et al. Contemporary trends in
necrotizing soft-tissue infections in the United States. Surgery.
2013;153(6):819-827.
 6. Sarani B, Strong M, Pascual J, Schwab CW. Necrotizing fasciitis:
current concepts and review of the literature. J Am Coll Surg.
2009;208(2):279-288.
7. Sartelli M, Malangoni MA, May AK, et al. World Society of
Emergency Surgery (WSES) guidelines for management of skin
and soft tissue infections. World J Emerg Surg. 2014;9(1):57.
8. Schmidt A. Acute Compartment Syndrome. Injury.
2017;48(Suppl 1):S22-S25.
9. Stevens DL, Bisno AL, Chambers HF, et al. Practice guidelines
for the diagnosis and management of skin and soft tissue
infections: 2014 Update by the Infectious Diseases Society of
America. Clin Infect Dis. 2014;59(2):147-159.
10. Stevens DL, Bryant AE. Necrotizing Soft-Tissue Infections. N
Engl J Med. 2017;377:2253.
11. Ustin JS, Malangoni MA. Necrotizing soft-tissue infections. Crit
Care Med. 2011;39(9):2156-2162.
12. Wong CH, Khin LW, Heng KS, Tan KC, Low CO. The LRINEC
(Laboratory Risk Indicator for Necrotizing Fasciitis) score: a tool
for distinguishing necrotizing fasciitis from other soft tissue
infections. Crit Care Med. 2004;32(7):1535-1541.

Suggested Websites
1. CDC; https://www.cdc.gov/features/necrotizingfasciitis/index.html
2. CDC; Trends in US Hospital Admissions for Skin and Soft Tissue
Infections https://wwwnc.cdc.gov/eid/article/15/9/08-1228_article
3. British Orthopaedic Association, BAoPRaAS, Royal College of
Nursing. BOAST: Diagnosis and Management of Compartment
Syndrome of the Limbs. Br Orthopaedic Assoc Stand Trauma,
2014. https://www.boa.ac.uk/resources/boast-10-pdf.html
 Appendix 1
RAPID RESPONSE SYSTEM

I. INTRODUCTION
Rapid response systems (RRS) have emerged as important resources that
focus on the hospitalized patient with unexpected, sudden deterioration in a
condition from any cause. Historically, crisis teams were activated only after a
significant event, such as cardiac arrest; there was no organized approach to
preventing an untoward event in an at-risk hospitalized patient. Most patients
who experience a cardiac arrest while in the hospital demonstrate identifiable
signs of deterioration in the previous 8 hours. Early recognition of
deterioration and timely intervention can reduce the incidence of in-hospital
cardiac arrest or the need for intensive care. RRSs have been shown to
reduce in-hospital mortality and cardiopulmonary arrest, although the
presence of a physician is not significantly associated with a mortality
reduction.
Unfortunately, the early indicators of clinical deterioration can be difficult to
identify. Assessing the physiologic reserve of a patient is challenging. RRSs
bring additional experienced providers with advanced monitoring tools to the
patient’s bedside. If needed, more advanced monitoring and therapy can be
initiated immediately, and a decision can be made about the most appropriate
care level. The most important action in the process is the call for help.

The RRS model can be divided into four components, each of which plays an
integral role in the success of the system (Figure A1-1). The administrative
arm oversees appropriate staffing, provides resources, drafts protocols and
guidelines, and ensures staff education regarding the presence and utility of
the service. The afferent arm is concerned with detecting impending
deterioration, while the efferent arm is focused on rendering therapy and
mobilizing additional resources quickly. Lastly, the performance improvement
arm seeks to identify recurrent patterns of deterioration and assess
improvement in quality measures following system-wide interventions.

Figure A1-1. Rapid Response System Structure

Abbreviations: AMI, acute myocardial infarction; LOS, length of stay; MET, medical
emergency team; RRT, rapid response team; VIPPS, ventilation infusion of volume,
pressors/pump, pharmacy, and specific interventions Adapted from Sebat F, ed.
Designing, Implementing, and Enhancing a Rapid Response System. Mount Prospect,
IL: Society of Critical Care Medicine; 2009:41.
II. BUILDING A MEDICAL EMERGENCY OR RAPID
RESPONSE TEAM
Rapid response teams (RRTs) represent an intuitively simple concept: When a
patient demonstrates signs of imminent clinical deterioration, a team of
providers is summoned to the bedside to immediately assess and treat the
patient with the goal of preventing transfer to the ICU, cardiac arrest, or
death. An RRT is the intervention limb of the RRS. By consensus, a medical
emergency team (MET) is led by a prescribing clinician (physician or
advanced practice provider), whereas an RRT is led by a nurse and/or
respiratory therapist (nonprescribing clinician). However, most recently, these
two terms have been used interchangeably.

A. Response Team Composition

Although there is no single perfect team composition, the most successful
METs and RRTs have been developed by leveraging existing hospital
resources and targeting particular at-risk patient populations.
Multidisciplinary, physician-led teams (METs) are prevalent in academic
centers with training programs. Nurse-led or nurse–respiratory therapist
teams (RRTs) with physician backup (or medical control similar to the
emergency medical services model) are more often found in community
hospitals without training programs. Regardless of the team composition,
effective teamwork skills are essential to the success of the program. The
implementation of standardized protocols or standing orders allows the team
to use evidence-based best practices to address commonly identified clinical
issues. The RRS administrative leadership should develop these protocols and
standing orders in accordance with institutional policies and procedures.
Possible members of an MET or RRT are identified in Table A1-1.

Table A1-1 Possible Members of Medical Emergency or Rapid Response Team

At an academic hospital, the composition of the responding team may include
the following combinations of caregivers:
ICU attending and/or fellow, ICU nurse, respiratory therapist,
pharmacist
Hospitalist, medicine resident or advanced practice provider, ICU
nurse, respiratory therapist
ICU nurse, respiratory therapist, physician (backup)

At a non-teaching hospital, the team may consist of one of the following

combinations:
Emergency department physician or advanced practice provider,
hospitalist, ICU nurse, respiratory therapist
Emergency department nurse, ICU nurse, respiratory therapist
Postanesthesia care unit nurse, respiratory therapist, physician
(backup)

Typically, physician members are trained (or are training) in critical care,
emergency medicine, anesthesia, or internal medicine. They bring their
knowledge of critical illness and their skills in the management of life-
threatening problems to the patient’s bedside. Nurse members usually have
many years of bedside experience and most often have extensive critical care
training. Team members from other disciplines add value to the MET or RRT
with their knowledge of such factors as airway and respiratory management,
drug therapies, traumatic injury management, and critical care transport.
Team members usually are expected to maintain current provider status in
basic and advanced cardiac life support, pediatric advanced life support
(where applicable), and fundamental critical care. Periodic teamwork
exercises in mock events or medical simulation centers can hone members’
evaluation and management skills. Treatment protocols and standing orders
should be reviewed and amended based on feedback from MET or RRT calls
and quality improvement data.

B. Response Team Equipment

The use of advanced physiologic monitors and equipment by appropriately
trained MET members can provide crucial support to the at-risk patient. This
can greatly enhance the team’s ability to evaluate and manage signs and
symptoms of clinical deterioration. Clearly, the earlier clinical abnormalities
are identified and addressed, the greater the potential for a positive outcome
and, often, the simpler the needed intervention. The MET or RRT should first
evaluate the resources that are readily available in the areas it will support
and then create a list of additional needed equipment (Table A1-2). The
response team must have access to cardiac, respiratory, and simple
hemodynamic monitors. Other equipment and medications should be selected
based on the patient populations served, the team composition, and local
regulations and policies. Because the MET or RRT is expected to respond
quickly, any additional necessary equipment and supplies should be
organized in appropriate bags or carts that can be readily transported to the
patient.

Table A1-2 Response Team Equipment Lista

aNecessary equipment and supplies should be available on the patient unit or carried by the team.

III. ACTIVATING THE MEDICAL EMERGENCY OR RAPID

RESPONSE TEAM
A. Activation Criteria and Triggers
The most important activation criterion is the concern of the bedside
physician, nursing staff, or family that something is wrong, even if other
indicators are within acceptable limits. This intuition is often quite sensitive
and warrants additional assessment. The fact that an intuition or a gut feeling
is not very specific should not discourage activation of the MET or RRT.
The distribution of a predefined set of MET or RRT activation criteria may
help to focus attention on important early indicators and empower the bedside
staff to call for help early. These criteria may be based on the detection of
acute changes in physiology, organ system–specific signs and symptoms, and
event triggers (Table A1-3). Acute changes in physiology may include
changes in vital signs that exceed predefined limits, such as tachycardia,
tachypnea, hypotension, and oliguria.

Table A1-3 Models of Activation Criteria

Abbreviations: SpO2, oxygen saturation on pulse oximetry; FIO2, fraction of inspired oxygen.

The detection of one or more indicators of organ system dysfunction may

trigger activation of the response team. Such pattern recognition may be more
effective in detecting clinical deterioration when there is a gradual change in
physiologic variables.

Event triggers help emphasize that some patient incidents or interventions

warrant further evaluation. The event may be a sign or a result of a larger
issue that could be an ongoing threat to the patient’s safety. For example, any
administration of naloxone is an indicator that one or more undesirable
adverse effects of opiates may be present. Although naloxone may temporarily
reverse these adverse effects, they can recur as the antagonist effects wane. A
focused evaluation by the MET or RRT may avoid the undesirable
consequences of these events.

B. Response Team Scoring Systems

The use of a scoring system in evaluating the at-risk patient can provide a
graded assessment of clinical status and help to determine the level of
response needed. An overall score is calculated based on the aggregate of
points assigned to various symptoms, vital signs, and laboratory studies.
Additional points are assigned to results that vary greatly from normal.
Several patented early warning scoring systems are available, although not all
are validated. The Modified Early Warning Score, which evaluates a patient’s
vital signs and mental status, has been validated in hospitalized medical
patients. A score of 5 or greater has been associated with an increased
mortality rate and increased incidence of ICU admission.

Individual MET or RRT programs may choose to define absolute value or

trend thresholds that trigger a move to a higher level of care or mobilization of
additional clinical resources. Collection and analysis of aggregate scores in
patients receiving MET or RRT services can be used for quality improvement
efforts, such as evaluation of standing orders, event cluster identification, and
resource utilization.
IV. TEAM RESPONSE
A. Response Team Interventions
Interventions should be aimed at rapidly stabilizing the patient and preventing
further deterioration or full arrest. Studies have shown that the three most
common reasons for activating an MET or RRT are hypoxemia,
hypotension, and altered mental status. Teams should identify the
primary activating events in their institutions and build protocols to address
each rapidly.

Respiratory distress is the leading physiologic cause of MET or RRT

activation. The reasons for acute changes can be related to fluid status,
medications (eg, narcotics), progression of underlying disease, or patient
noncompliance with physician-ordered oxygen therapies. Initial treatment is
stabilization of the airway and application of high-flow oxygen to relieve the
patient’s distress and improve oxygen saturation. Following improvement in
patient status, the team can evaluate for potential reversible causes.

Hypotension can be related to volume status (both overall volume and blood
volume); medications, including narcotics and antihypertensives; and the
potential for sepsis. Initial treatment is administration of fluids to raise systolic
pressure and/or the immediate reversal of a known cause, such as narcotics.
Consideration should be given to empiric antibiotic therapy in cases of
suspected severe sepsis or septic shock.
Altered mental status is most often associated with hypoxemia, hypotension,
or hypoglycemia. These should be evaluated and treated first. Altered mental
status unrelated to those issues should be evaluated for either neurologic or
medication causes. Treatment, including evaluation with computed
tomography scanning, should be guided accordingly.

The responding team should make every effort to involve the patient’s
primary physician and rounding team in decisions regarding disposition and
care. The role of a MET or RRT is not to take the place of the primary team
but to act for – and with – them at the bedside in an emergency.
B. Response Team Communications
In the complex hospital environment, the use of a structured communication
tool and a common critical language fosters the open communication among
caregivers that is essential to the prompt evaluation and management of the
at-risk patient. Incorporating the Situation, Background, Assessment, and
Recommendation (SBAR) Tool into MET or RRT documentation can facilitate
effective communication by gathering all pertinent data in one place for any
discussions to follow. This tool has proven to be most valuable in the effective
communication of critical information (Table A1-4).

Table A1-4 SBAR Communication Tool

C. Response Team Utilizing Attending Physician Expertise via

Telemedicine
With telemedicine being widely used in institutions, providing early attending
physician expertise via telemedicine can improve RRT evaluations. In a quasi-
experimental study done in a single center, RRTs used a smart phone-based
telemedicine platform to facilitate early co-assessment and disposition at the
patient’s bedside with the ICU attending. Results showed that the RRT
providers spent less time outside the ICU, and among patients transferred to
the ICU there was a significant decrease in the likelihood of patients requiring
vasopressors or intubation within the first 60 minutes of transfer. Utilizing
early ICU attending involvement can improve efficiency of the RRT
evaluations.

D. Response Team Education

One of the primary goals of METs and RRTs is education. The detection limb
of the RRS model relies heavily on the early recognition of signs and
symptoms of clinical deterioration. Regularly scheduled staff in-services and
mock-event drills are effective in maintaining competencies in identifying the
at-risk patient. Public posting and discussion of activation criteria can further
enhance the use of MET or RRT services and reduce patient clinical crises.
Review of aggregate quality improvement data from response team activity
also can reinforce education. Post hoc review of a patient event with the entire
unit staff after an MET or RRT call serves to raise the collective knowledge
and skill of the entire group. This may reduce the likelihood of subsequent
problems and increase the likelihood that signs and symptoms of clinical
deterioration will be detected at the earliest indication in future patients.
Topic-of-the-week presentations, MET or RRT case reviews, and SBAR
practice sessions are examples of targeted educational activities.

V. STRATEGIES FOR SUCCESS

Hospitals that use an RRS report various factors that lead to successful team
implementation. Some common themes in their success include:
1. Training/Education – The MET or RRT members and the bedside
nursing staff must understand when and how to activate the team and
the scope of team capabilities. The response team members will need
ongoing training in management of common indicators in at-risk
patients and effective intervention and communication strategies. The
mentoring of the bedside nursing staff in critical assessment skills
and effective communication skills is a primary team education
objective. High-fidelity simulation in a simulation center is helpful,
but low-fidelity simulations with mock medical emergency scenarios
or table-top exercises are effective as well. Scenario-based case
presentations using a chalkboard or paper can be offered in any
clinical setting.
2. Equipment/Supplies – The equipment and supplies carried by the
response team should be tailored to the needs of the patient
population served, but then standardized to ensure that the
 appropriate resources reach the bedside with each call. If multiple
RRT bags are used, the items should be organized within each bag to
facilitate rapid access at the bedside. It is impractical to carry every
item available in the ICU. Equipment use should be reviewed as part
of the quality improvement program. Seldom-used items should be
removed unless they serve an important role in the management of
infrequent, but high-risk events. The response team should strive to
carry only the necessary equipment and supplies.
3. Culture of Empowerment – Staff nurses should be trained to
recognize signs of clinical deterioration before a crisis and to trust
their experience and skills. They should be empowered, and
supported by leadership, to activate the MET or RRT according to
established criteria. There should be no penalty for activating the
MET or RRT, especially if the findings do not point to an impending
clinical crisis. Such events can identify areas for targeted education
in the detection of signs of clinical deterioration or focused review of
the risks inherent to that patient population.
4. Evaluation – Data collection should be embedded into the clinical
workflow to facilitate monitoring of clinical and service outcomes.
Regular reporting, monitoring, and evaluation of response team
activities and outcomes guide rapid cycle improvement of team
processes. Patient and family satisfaction data help prioritize program
development and resource allocation. Constant dialogue among the
stakeholders to identify improvement opportunities is essential.

VI. SUMMARY
Hospitalized patients can be at risk for clinical deterioration in part because of
the complex nature of healthcare delivery systems. The goal of the RRS
model is to identify and manage signs and symptoms of clinical deterioration
in at-risk patients through detection strategies at the bedside and mobilization
of appropriate resources. Important factors in the successful implementation
of an RRS include: (1) appropriate team composition; (2) activation criteria
based on bedside staff concern, acute changes in physiology, or the use of
scoring systems to identify at-risk patients; (3) interventions aimed at rapidly
stabilizing the patient; (4) effective communication strategies like SBAR; (5)
ongoing education to enhance detection and management of potential clinical
crises; (6) availability of appropriate advanced clinical monitors, equipment,
and medications to conduct MET or RRT activities; and (7) evaluation and
correction of processes and causes of patient risk.

Suggested Readings
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and-after trial of a medical emergency team. Med J Aust.
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emergency team on reduction of incidence of and mortality from
unexpected cardiac arrests in hospital: preliminary study. BMJ.
2002;324:387-390.
3. Chen Q, Hawker F. Modifications to predefined rapid response
team calling criteria: prevalence, characteristics and associated
outcomes. Critical Care Resus. 2020;22(1):86.
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consensus conference on medical emergency teams. Crit Care
Med. 2006;9:2463-2478.
5. DeVita MA, Hillman K, Bellomo R, eds. Medical Emergency
Teams: Implementation and Outcome Measurement. New York,
NY: Springer Science + Business Media Inc; 2006.
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attending physician expertise via telemedicine to improve rapid
response team evaluations. Pediatr Crit Care Med.
2020;21(5):e221-e227.
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Maunder R. Building a rapid response team. AACN Adv Crit
Care. 2007;18:129-140.
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critical importance of effective teamwork and communication in
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factors influencing success. Crit Care Nurse Clin North Am.
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11. Sebat F, ed. Designing, Implementing, and Enhancing a Rapid
Response System. Mount Prospect, IL: Society of Critical Care
Medicine; 2009.
12. Sebat F, Musthafa AA, Johnson D, et al. Effect of a rapid
response system for patients in shock on time to treatment and
mortality during 5 years. Crit Care Med. 2007;35:2568-2575.
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modified Early Warning Score in medical admissions. QJM.
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 Appendix 2
ARTERIAL BLOOD GAS ANALYSIS
AND TREATMENT
These acid-base problems are provided for practice in analyzing arterial
blood gas and electrolyte information and determining appropriate
interventions.
For complicated acid-base disorders, it may be helpful to understand the
utility of the delta gap (Δgap). In an uncomplicated anion gap (AG) metabolic
acidosis, every AG increase of 1 mmol/L beyond the normal value should
result in a concomitant decrease of approximately 1 mmol/L in [HCO3].
Deviation from this relationship suggests a mixed acid-base disorder. The
difference between the change in the AG and the change in [HCO3] from the
normal values is the Δgap, which can be expressed as:

Δgap = (deviation of AG from normal) – (deviation of [HCO3] from normal)

The normal value for Δgap should be 0. However, variance in measurements

can result in a Δgap of 0 ± 6. If the Δgap is positive, then a simultaneous
metabolic alkalosis exists. If the decrease in [HCO3] is greater than the
increase in AG, which results in a negative Δgap, then a concomitant normal
AG acidosis (hyperchloremic) may exist. Small deviations of the Δgap may not
indicate mixed acid-base disorders, and clinical information must always be
considered.

For purposes of analyzing the following cases, assume that a normal HCO3 is
24 mmol/L and a normal AG is 12 mmol/L using the formula:

[Na] – ([Cl] + [HCO3])

Case 1
A 78-year-old woman with hypertension and hyperlipidemia is admitted to the
intermediate care unit for ongoing evaluation and management of a
community-acquired pneumonia. She was admitted 12 hours ago from the
emergency department. She remains tachypneic with increased work of
breathing. Vital signs are: heart rate 105 beats/min, blood pressure 110/68
mm Hg, respiratory rate 22 breaths/min, and temperature 38.4°C
(101.2°F). Physical examination reveals bilateral rhonchi and normal mental
status. She is receiving supplemental oxygen at 3 L/min via nasal cannula,
and oxygen saturation on pulse oximetry is 88%. An arterial blood gas
measurement is made as part of her ongoing workup, with the following
results:
pH 7.47
PaCO2 31 mm Hg (4.13 k Pa)
PaO2 55 mm Hg (7.33 k Pa)
HCO3 (calculated) 22 mmol/L

1a. Which one of the following best describes the acid-base disorder?
A. Metabolic acidosis
B. Respiratory alkalosis
C. Respiratory alkalosis and metabolic acidosis
D. Respiratory alkalosis and metabolic alkalosis

1b. Which one of the following is the most appropriate intervention?

A. Intubation and mechanical ventilation
B. Noninvasive ventilation
C. Increase in supplemental oxygen concentration
D. No new intervention
Case 2
A 26-year-old man arrives at the emergency department with multisystem
trauma following a motorcycle collision. He is somnolent with a Glasgow
Coma Scale score of 13. The primary survey reveals an open airway with
equal breath sounds bilaterally. Vital signs are: temperature 36.2°C
(97.2°F), heart rate 116 beats/min, respiratory rate 20 breaths/min, blood
pressure 100/50 mm Hg, and oxygen saturation on pulse oximetry 99% with
a non-rebreather mask in place. The patient undergoes diagnostic radiological
evaluations that reveal left rib fractures without hemothorax or pneumothorax.
As part of his initial workup, he has blood sent for laboratory analysis. The
results are as follows:

pH 7.31
PaCO2 32 mm Hg (4.27 k Pa)
PaO2 163 mm Hg (21.73 k Pa)
Na 140 mmol/L
Cl 105 mmol/L
HCO3 15 mmol/L

2a. Which acid-base disorder is present?

A. Non-anion gap metabolic acidosis
B. Respiratory acidosis
C. Anion gap metabolic acidosis
D. Metabolic acidosis with respiratory alkalosis

2b. What is the suspected cause of the acid-base disorder?

A. Diabetic ketoacidosis
B. Lactic acidosis
C. Uremia
D. Hyperventilation
2c. Which of the following is the most appropriate intervention?
A. Administration of intravenous bicarbonate
B. Fluid and blood product administration
C. No intervention required at this time
D. Intubation

Case 3
A 21-year-old female college student did not wake up the morning after
attending a fraternity party where alcohol and drugs were available.
Emergency services was called, the patient was placed on supplemental
oxygen via non-rebreather mask, peripheral intravenous access was obtained,
and fluids were started. Initial vital signs in the emergency department are:
heart rate 102 beats/min, respiratory rate 10 breaths/min, blood pressure
92/60 mm Hg, and oxygen saturation on pulse oximetry 94%. The patient
only moans when exposed to noxious stimuli but does localize. Blood is drawn
for laboratory evaluation, including an arterial blood gas. The result are as
follows:

pH 7.23
PaCO2 60 mm Hg (8.0 k Pa)
Na 141 mmol/L
K 4.0 mmol/L
Cl 110 mmol/L
HCO3 26 mmol/L

3a. Which acid-base disorder is present?

A. Non-anion gap metabolic acidosis
B. Respiratory acidosis
C. Respiratory acidosis and non-anion gap metabolic acidosis
D. Respiratory acidosis and metabolic alkalosis
3b. Which of the following should be the initial intervention?
A. Intubation and intravenous administration of naloxone
B. Administration of activated charcoal
C. Noninvasive positive pressure ventilation
D. No additional intervention

Case 4
A 55-year-old man is admitted to the surgical ICU after elective laparoscopic
cholecystectomy. An iatrogenic injury to the hepatic artery required
conversion to an open cholecystectomy and fluid resuscitation with normal
saline and blood products. Vital signs are: heart rate 115 beats/min,
respiratory rate 12 breaths/min (ventilator rate), blood pressure 105/68 mm
Hg, and oxygen saturation on pulse oximetry 99% at fraction of inspired
oxygen of 50%. Laboratory values are as follows:
pH 7.32
PaCO2 36 mm Hg (4.8 k Pa)
Na 146 mmol/L
K 3.8 mmol/L
Cl 117 mmol/L
HCO3 18 mmol/L

4a. Which acid-base disorder is present?

A. Anion gap metabolic acidosis
B. Anion gap metabolic acidosis and respiratory acidosis
C. Anion gap metabolic acidosis and non-anion gap metabolic acidosis
D. Non-anion gap metabolic acidosis

4b. Which of the following is the most likely cause of the acid-base disorder
in this patient?
 A. Cardiogenic shock
B. Hemorrhagic shock
C. Normal saline administration
D. Hypoventilation

Case 5
An 81-year-old man was admitted to the medical floor for an exacerbation of
congestive heart failure. He received high-dose intravenous furosemide over
the last 48 hours, which allowed him to be weaned off noninvasive positive
pressure ventilation. He is currently on supplemental oxygen via nasal
cannula. Vital signs are: heart rate 88 beats/min, respiratory rate 18
breaths/min, blood pressure 120/72 mm Hg, and oxygen saturation on pulse
oximetry 97% on supplemental oxygen at 6 L/min. Laboratory values are as
follows:
pH 7.50
PaCO2 45 mm Hg (5.87 k Pa)
Na 136 mmol/L
Cl 96 mmol/L
HCO3 33 mmol/L

5a. Which acid-base disorder is present?

A. Metabolic alkalosis and respiratory acidosis
B. Metabolic alkalosis
C. Metabolic alkalosis and non-anion gap acidosis
D. Respiratory acidosis

5b. Which of the following is the most likely cause of the acid-base disorder?
A. Hypercapnic respiratory failure
B. Volume overload related to congestive heart failure
 C. Hypercortisolism
D. Diuretic administration

5c. Which of the following is an appropriate treatment option?

A. Restart noninvasive positive pressure ventilation
B. Administer acetazolamide
C. Continue diuresis with furosemide
D. Decrease administration of furosemide and consider administration of
fluids

Case 6
A 58-year-old woman with hypertension and chronic kidney disease is
admitted to the hospital with alcohol intoxication. She is somnolent and
arouses to painful stimuli. Vital signs are: heart rate 110 beats/min, blood
pressure 142/88 mm Hg, respiratory rate 10 breaths/min, temperature 37°C
(98.6°F), and oxygen saturation on pulse oximetry 94%. Laboratory results
are as follows:

pH 7.23 Na 134 mmol/L

PaCO2 38 mm Hg (5.06 k K 6.1 mmol/L
Pa) Cl 100 mmol/L
PaO2 78 mm Hg (10.4 k Pa) HCO3 15 mmol/L
Blood urea nitrogen 62
mg/dL
Creatinine 3.7 mg/dL
Glucose 125 mg/dL

6. Which one of the following best describes the acid-base disorder?

A. Anion gap metabolic acidosis
B. Anion gap metabolic acidosis and metabolic alkalosis
 C. Anion gap metabolic acidosis and respiratory acidosis
D. Anion gap metabolic acidosis and non-anion gap metabolic acidosis

Case 7
An 80-year-old man with hypertension, diabetes, and malnutrition is admitted
to the hospital with cough, fever, and hypotension. Chest radiograph shows a
right lower lobe pneumonia. Vital signs are: heart rate 115 beats/min, blood
pressure 90/52 mm Hg, respiratory rate 20 breaths/min, temperature 38.3°C
(101°F), and oxygen saturation on pulse oximetry 95% on oxygen
supplemented at 8 L/min via nasal cannula. Laboratory results are as follows:

pH 7.35 Na 132 mmol/L

PaCO2 32 mm Hg (4.27 k K 4.0 mmol/L
Pa) Cl 103 mmol/L
PaO2 78 mm Hg (10.4 k Pa) HCO3 17 mmol/L
Blood urea nitrogen 20
mg/dL
Creatinine 1.4 mg/dL
Albumin 1.5 g/dL

7. Which one of the following best describes the acid-base disorder?

A. Anion gap metabolic acidosis
B. Non-anion gap metabolic acidosis
C. Non-anion gap metabolic acidosis and respiratory alkalosis
D. Anion gap metabolic acidosis and non-anion gap metabolic acidosis

Case 8
A 60-year-old man with arterial vascular disease and hypertension presented
to the emergency department with complaints of shortness of breath and
abdominal pain. Vital signs are: heart rate 90 beats/min, blood pressure
168/96 mm Hg, respiratory rate 25 breaths/min, temperature 37.2°C
(99°F), and oxygen saturation on pulse oximetry 98% while receiving oxygen
at 2 L/min via nasal cannula. Laboratory results are as follows:

pH 7.55 Na 135 mmol/L

PaCO2 15 mm Hg (2.0 k Pa) K 3.8 mmol/L
PaO2 98 mm Hg (13.07 k Pa) Cl 101 mmol/L
HCO3 13 mmol/L

8a. Which one of the following best describes the acid-base disorder?
A. Acute respiratory alkalosis
B. Chronic respiratory alkalosis
C. Acute respiratory alkalosis and metabolic alkalosis
D. Acute respiratory alkalosis and metabolic acidosis

8b. Which one of the following is a potential etiology of the acid-base

disorder?
A. Pulmonary embolism
B. Sepsis
C. Diuretics
D. Chronic obstructive lung disease and renal failure

Case 9
A 70-year-old woman is admitted to the ICU with syncope after several days
of vomiting. Vital signs are: heart rate 140 beats/min, blood pressure 80/50
mm Hg, respiratory rate 24 breaths/min, and temperature 37.0°C (98.6°F).
Laboratory results are as follows:

pH 7.30 Na 138 mmol/L

PaCO2 36 mm Hg (4.8 k Pa) K 3.0 mmol/L
Cl 93 mmol/L
PaO2 88 mm Hg (11.73 k Pa) HCO3 20 mmol/L
Glucose 90 mg/dL

9. Which one of the following best describes the acid-base disorder?

A. Anion gap metabolic acidosis
B. Anion gap metabolic acidosis and metabolic alkalosis
C. Anion gap metabolic acidosis and respiratory acidosis
D. Anion gap metabolic acidosis and non-anion gap metabolic acidosis

Case 10
A 55-year-old diabetic, hypertensive man presents with nausea, vomiting, and
abdominal pain. Vital signs are: heart rate 124 beats/min, blood pressure
102/50 mm Hg, respiratory rate 22 breaths/min, and temperature 36.4°C
(97.6°F). Laboratory results are as follows:

pH 7.45 Na 134 mmol/L

PaCO2 34 mm Hg (4.53 k Pa) K 3.2 mmol/L
PaO2 85 mm Hg (11.33 k Pa) Cl 85 mmol/L
HCO3 23 mmol/L
Glucose 420 mg/dL

10. Which one of the following best describes the acid-base disorder?
A. Respiratory acidosis and metabolic acidosis
B. Respiratory acidosis, metabolic acidosis, and metabolic alkalosis
C. Respiratory alkalosis, metabolic acidosis, and metabolic alkalosis
D. Respiratory alkalosis and metabolic acidosis

CASE STUDY ANSWERS AND RATIONALES

Case 1
1a. The correct answer is B, Respiratory alkalosis.
The pH is alkalemic. The low PaCO2 suggests a respiratory process rather
than a metabolic process. The formula to determine if the respiratory process
is acute is:

Using the information from the case, the expected increase in pH would be
0.072, resulting in an expected pH 7.47. This finding suggests a pure
respiratory process. You can further analyze it by considering whether there
is appropriate buffering of HCO3 using the following formula:

Data from the blood gas measurements suggest a decrease of [HCO3] of 1.8
mmol/L, which is close to the decrease of 2 mmol/L of the calculated
[HCO3].

Although the patient is at risk for a metabolic acidosis, the appropriate

decrease of [HCO3] in relation to the respiratory alkalosis makes that a less
likely condition. Clinically, you would always review the electrolytes along
with the arterial blood gas and calculate the anion gap. There is no suggestion
of a metabolic alkalosis with the near normal [HCO3].

1b. The correct answer is C, Increase in supplemental oxygen concentration.

The patient is significantly hypoxic but based solely on the information

presented, she may not need any more support than an increase in oxygen
concentration and continued monitoring. Any worsening of her respiratory
rate or mental status may necessitate positive pressure support.

Case 2
2a. The correct answer is C, Anion gap metabolic acidosis.

The pH is acidemic. The low bicarbonate concentration is consistent with a

metabolic process. The next step is to determine if appropriate respiratory
compensation is present.

Appropriate PaCO2 compensation = 1.5 x [HCO3] + 8 ± 2

In this case, the appropriate compensation would yield PaCO2 30.5 ± 2 mm

Hg. Thus, respiratory compensation is appropriate. The next step is to
calculate the anion gap.

AG = [Na] – ([Cl] + [HCO3])

AG for this case = [140] – [(105+15)] = 20 mmol/L

This patient has an elevated anion gap metabolic acidosis. With an anion gap
acidosis, the Δgap should be calculated to determine if additional metabolic
processes are present.
Δgap = (deviation of AG from normal) – (deviation of [HCO3] from normal)
= (20-12) – (24-15)
= -1 mmol/L
This is within the normal range of 0 + 6, indicating that no additional
metabolic process is present.

2b. The correct answer is B, Lactic acidosis.

The causes of elevated anion gap metabolic acidosis can be remembered with
the following mnemonic MUDPILES, which stands for methanol, uremia,
diabetic ketoacidosis, paracetamol/acetaminophen, isoniazid, lactic acidosis,
ethylene glycol or methanol, and salicylates.

This case depicts a trauma patient in shock with hypoperfusion, resulting in

lactic acidosis.

2c. The correct answer is B, Fluid and blood product administration.

The goal is restore perfusion to the tissues. This patient is experiencing
hypovolemic hemorrhagic shock. The treatment is fluid and blood product
administration and control of the hemorrhage.

Case 3
3a. The correct answer is B, Respiratory acidosis.

The pH is acidemic. The increase in PaCO2 indicates a respiratory process.

Next, determine if this is an acute or chronic respiratory process.

Thus, the decrease in pH = 0.08 x 20/10 = 0.16, which is close to the

observed value of 60 mm Hg (8.0 k Pa). This is an acute respiratory process.
If metabolic compensation is present, the bicarbonate concentration will
increase 1 mmol/L for every 10 mm Hg (1.33 k Pa) increase in PaCO2. For
this case, there is a 20 mm Hg change in PaCO2 that should translate into a
2 mmol/L increase in bicarbonate. The HCO3 concentration is 26 mmol/L,
which is 2 mmol/L above the normal value of 24 mmol/L and consistent with
appropriate metabolic compensation.

3b. The correct answer is A, Intubation and intravenous administration of

naloxone

This patient has hypoventilation related to drug and alcohol intoxication.

Activated charcoal will not reverse the respiratory depression. The patient
also was not found until the following morning, making it too late for use of
activated charcoal. The severely depressed mental status prohibits the use of
noninvasive positive pressure ventilation; a patient must be conscious with the
ability to protect the airway for noninvasive positive pressure ventilation to be
used. This patient should be intubated to control her respiratory failure, and
naloxone can be administered simultaneously.
Case 4
4a. The correct answer is D, Non-anion gap metabolic acidosis.
The correct answer is D, Non-anion gap metabolic acidosis.
The pH is academic and the change in HCO3 concentration would indicate a
metabolic process. The next step is to evaluate whether the respiratory
compensation is appropriate.
Respiratory compensation: 1.5 x [HCO3] + 8 ± 2

Respiratory compensation: 1.5 x [18] + 8 ± 2 = 35 ± 2

In this case the patient has appropriate respiratory compensation. The next
step is to determine if the anion gap is elevated.
AG = [Na] – ([Cl] + [HCO3])
146 – (117 + 18) = 11 mmol/L

There is no elevation in the anion gap, so this patient has a non-anion gap
metabolic acidosis.

4b. The correct answer is C, Normal saline administration.

Metabolic acidosis with a normal anion gap, which is a hyperchloremic
acidosis, may result from gastrointestinal or renal loss of HCO3 or volume
resuscitation with normal saline. In this case, the patient received excess fluid
resuscitation due to hemorrhage in surgery. This patient has metabolic
acidosis as a result of hyperchloremia from normal saline resuscitation.
Cardiogenic shock and hemorrhagic shock would result in metabolic acidosis
with an elevated anion gap. Hypoventilation would be associated with a
respiratory acidosis. The appropriate intervention is to change to an
intravenous fluid with lower chloride content, such as Ringer lactate.

Case 5
5a. The correct answer is B, Metabolic alkalosis.
The pH is alkalemic. The increase in [HCO3] indicates a metabolic process.
Respiratory compensation in metabolic alkalosis is determined by the
following formula:
Increase in PaCO2 = 0.6-0.7 x Δ[HCO3] = 0.6-0.7 x 9 = 5.4-6.3 mm Hg
(0.72-0.84 k Pa)
Thus, the increase in PaCO2 is appropriate respiratory compensation.
Calculation of the anion gap yields a normal result of 7 mmol/L.

5b. The correct answer is D, Diuretic administration.

Metabolic alkaloses are usually characterized as chloride-depleted
(hypovolemic) or chloride-expanded (hypervolemic). In this patient, diuretic
use is the most likely cause of the alkalosis.

5c. The correct answer is D, Decrease administration of furosemide and

consider administration of fluids.

Chloride-depleted metabolic alkalosis is corrected by administration of an

intravenous normal saline infusion. Discontinuation of the furosemide should
occur to prevent further depletion of chloride and further exacerbation of
metabolic alkalosis. Careful monitoring of the fluid status is indicated in a
patient with history of heart failure, and expert consultation is required.

Case 6
6. The correct answer is C, Anion gap metabolic acidosis and respiratory
acidosis.
The pH is acidemic and the low [HCO3] indicates a metabolic process. The
formula for determining the expected respiratory compensation is:

PaCO2 = 1.5 x [HCO3] + 8 ± 2

The expected PaCO2 would be approximately 30 mm Hg (4.0 k Pa). Thus,
the finding of a higher PaCO2 than expected indicates another acid-base
process of respiratory acidosis. The respiratory acidosis is most likely
secondary to depressed respiratory drive from intoxication. This patient has
ventilatory insufficiency and must be monitored closely for worsening and the
potential need for more aggressive ventilatory support. The anion gap is
calculated as an increased value of 19 mmol/L, which is likely secondary to
chronic kidney disease, but other unmeasured anions (such as lactate) may be
contributing.
The Δgap can be calculated for this case. The deviation of the anion gap from
normal is 7 mmol/L, and the deviation of the [HCO33] from normal is 9
mmol/L. The difference of -2 mmol/L is not likely to represent a third acid-
base process.

Case 7
7. The correct answer is A, Anion gap metabolic acidosis.
The pH is acidemic and the low [HCO3] indicates a metabolic process. The
formula for determining the expected respiratory compensation is:
PaCO2 = 1.5 x [HCO3] + 8 ± 2

Thus, the expected PaCO2 would be approximately 33 mm Hg (4.4 k Pa).

The anion gap is calculated as 12 mmol/L, which appears normal. However,
the albumin concentration must be taken into account. A limitation of the
traditional approach to acid-base analysis is the effect of hypoalbuminemia on
the anion gap. The expected anion gap decreases by 2.5 to 3 mmol/L for
every 1 g/dL. In this patient, an albumin of 1.5 g/dL (assuming a normal
albumin of 4 g/dL) would decrease the expected anion gap to 5 to 6 mmol/L.
Thus, the calculated anion gap of 12 mmol/L is increased by 6 mmol/L. It is
important to recognize the presence of the anion gap metabolic acidosis in
assessing the severity of illness of this patient. The clinical scenario is
consistent with severe sepsis, and a lactic measurement is indicated.
Case 8
8a. The correct answer is D, Acute respiratory alkalosis and metabolic
acidosis.

The pH is alkalemic and the low PaCO2 indicates a respiratory process. The
next step is to determine if this is an acute or chronic respiratory alkalosis.
The formula for acute respiratory alkalosis is:

Increase in pH = 0.08 × (40 – PaCO2)/10

Using the data from this case, the expected increase in pH would be 0.2 or
pH 7.6, which is higher than 7.55. The formula for chronic respiratory
alkalosis is:
Increase in pH = 0.03 × (40 – PaCO2)/10,

Applying it yields a pH increase of 0.075 or pH 7.475. These calculations

suggest that there is likely to be a second acid-base disorder present.
Calculation of the anion gap as 21 mmol/L identifies the second process of
anion gap metabolic acidosis. The Δgap can be also be calculated for this
case. The deviation of the anion gap from normal is 9 mmol/L, and the
deviation of the [HCO3] from normal is 11 mmol/L. The difference of -2 is
not likely to represent a third acid-base process.

8b. The correct answer is B, Sepsis.

The acid-base pattern can be helpful in suggesting an etiology of a patient’s
condition. In this case, respiratory alkalosis with anion gap metabolic acidosis
is the typical acid-base disorder of sepsis. Salicylate intoxication would also be
associated with this acid-base pattern. Pulmonary embolism would typically
result in a respiratory alkalosis, with acidosis being unlikely in a
hemodynamically stable patient. Diuretic use would primarily result in
metabolic alkalosis rather than acidosis.

Chronic obstructive lung disease and renal failure would most likely result in
a respiratory acidosis and metabolic acidosis.
Case 9
9. The correct answer is B, Anion gap metabolic acidosis and metabolic
alkalosis.
The pH is acidemic and the lower HCO3 indicates a metabolic process. The
formula for determining the expected respiratory compensation is:
PaCO2 = 1.5 x [HCO3] + 8 ± 2

Using this, the expected PaCO2 would be approximately 38 mm Hg (5.07 k

Pa), which is close to the PaCO2 of 36 mm Hg (4.8 k Pa). The anion gap is
calculated as 25 mmol/L, which identifies the presence of an anion gap
metabolic acidosis. The Δgap should also be calculated for this case. The
deviation of the anion gap from normal is 13 mmol/L, and the deviation of the
[HCO3] from normal is 4 mmol/L. The difference of 9 mmol/L suggests the
presence of a metabolic alkalosis. The [HCO3] did not decrease as much as
expected for the degree of acidosis. The clinical scenario is also suggestive of
volume depletion from vomiting, resulting in the metabolic alkalosis. An anion
gap metabolic acidosis (lactic acidosis) was the result of hypotension.

Case 10
10. The correct answer is C, Respiratory alkalosis, metabolic acidosis, and
metabolic alkalosis.
The pH in this very ill patient is nearly normal, which should immediately
raise the suspicion for complex acid-base disorders. The history is suggestive
of possible diabetic ketoacidosis, so the first calculation could be the anion
gap, which is increased at 26 mmol/L. Using the formula for determining the
expected respiratory compensation for a metabolic acidosis—PaCO2 = 1.5 x
[HCO3] + 8 ± 2—the expected PaCO2 would be approximately 42 mm Hg
(5.60 k Pa). Since the patient’s PaCO2 is lower at 34 mm Hg (4.53 k Pa), a
respiratory alkalosis is present. The Δgap should definitely be calculated for
this case. The deviation of the anion gap from normal is 14 mmol/L, and the
deviation of the [HCO3] from normal is 1 mmol/L. The difference of 13
mmol/L suggests the presence of a metabolic alkalosis. The [HCO3] did not
decrease as much as expected for the degree of acidosis. The clinical scenario
is consistent with diabetic ketoacidosis with volume depletion from vomiting
and a respiratory alkalosis, possibly secondary to pain.
You could also approach the problem by identifying the pH as alkalemic. The
lower PaCO2 would prompt assessment of whether it is an acute or chronic
respiratory process. Acute is more likely, so the formula for acute respiratory
alkalosis would be used: Increase in pH = 0.08 × (40 – PaCO2)/10. Based
on the data from this case, the expected increase in pH would be 0.048 or
pH 7.45, which is similar to the patient’s value. The other acid-base
processes would still be identified because the anion gap is always calculated.
 Appendix 3
BRAIN DEATH

BRAIN DEATH (DEATH BY NEUROLOGIC CRITERIA)

In 1981, the Uniform Determination of Death Act (UDDA) was developed by the
President’s Commission for the Study of Ethical Problems in Medicine and
Biomedical and Behavioral Research working in conjunction with the American
Bar Association, the American Medical Association (AMA), and the National
Conference of Commissioners on Uniform State Laws.

Important Milestones in the History of Defining

Brain Death
1968 Harvard Ad Hoc Committee
First attempt to define death by
neurologic criteria
1981 Uniform Determination of Death
Act
Established physiologic standards
defining death as irreversible
cessation of circulatory and
respiratory functions
(cardiopulmonary criteria) AND/OR
irreversible cessation of all functions
of the brain, including the brain stem
(neurologic criteria)
2008 President’s Council on Bioethics
Affirmed the concept of brain death
2019 American Academy of Neurology
Position Statement
 Called for the uniformity of brain
death determination criteria, citing
variation in law and policy regarding
testing procedures
The UDDA defined death as occurring in the
presence of one or both of the following:
irreversible cessation of circulatory and
respiratory functions (cardiopulmonary
criteria)
irreversible cessation of all brain functions,
including those of the brain stem (neurologic
criteria)

The American Academy of Neurology (AAN) endorses the UDDA definition that
brain death has occurred when the irreversible loss of all functions of the entire
brain, including the brain stem, has occurred and has been determined by the
demonstration of complete loss of consciousness (coma), brain stem reflexes, and
ventilatory drive (apnea), in the absence of any reversible factors. It also
recognizes that neuroendocrine function may persist in patients with irreversible
injury to the brain and brain stem. This is presumed to occur because of the
possible protective anatomic location of the pituitary gland and its vasculature.
At present, brain death is diagnosed clinically at the bedside when there is
evidence of the complete loss of brain stem function as noted by lack of response
to prescribed noxious stimuli and hypercapnia; the “apnea test.” A patient in a
comatose state may exhibit some of the clinical findings of a patient that has
progressed to brain death. It is therefore imperative to rule out other causes of
comatose state (toxic, metabolic, etc.) prior to concluding that brain death has
occurred.
Because there can be some ambiguity with the clinical examination, especially if
there are not skilled individuals to perform the examination, as well as anatomic
and physiologic limitations that prevent completion of the examination
components, eg, if the patient is hemodynamically unstable to tolerate the testing
or has sustained significant facial trauma, there may be a need to perform
confirmatory testing. Confirmatory tests include cerebral blood flow
examinations, such as four-vessel digital subtraction angiography, technetium
radionuclide angiography or scintigraphy, magnetic resonance angiography, CT
angiography, and transcranial Doppler studies. Ancillary testing includes EEG
and evoked potentials (somatosensory, auditory, or visual). Confirmatory and
ancillary testing are performed to complement the clinical examination and, in
some jurisdictions, may eliminate the requirement for a second examiner or a
second examination after a prescribed delay to reexamination.
Some limitations to confirmatory and ancillary testing include its availability at
the facility, its accuracy across multiple operators and interpreters, its ability to
be performed at the bedside, and whether it has any potentially deleterious
adverse effects to the patient or organs (especially when considering organ
donation).

Diagnosis of brain death can be further challenged by medical, cultural, and

societal barriers that must be overcome before such consensus becomes possible.
Barriers to the diagnosis of brain death can include the acceptance of brain
death as death, religious beliefs about death, legal standards of death
determination, cultural norms about death, requirements for organ donation,
knowledge deficits of professionals, examination technical requirements, and
availability and quality of ancillary tests.
The determination of brain death is further complicated by practice variation
between hospitals and jurisdictions as well as individual physicians. In the United
States, despite having accepted diagnostic criteria proposed by the AAN and
allied specialty societies, it has been challenging to standardize practices of brain
death determination. In other countries, practice disparities arise more because
of legal, cultural, or religious differences.

Examination of the patient with concern for brain death can be challenging for
many reasons. The clinical examination is the foundation of determining brain
death and may be complemented by ancillary confirmatory testing as needed
(Table A3-1). It is recommended that a protocol be developed at your facility
that is supported by the guidance of the AAN, the Neurocritical Care Society
(NCS), and policies set forth by your state, jurisdiction, and hospital. To facilitate
training and uniformity, the NCS has developed a Brain Death Determination
credentialing program which can be found at
https://www.neurocriticalcare.org/education/braindeath
Brain death diagnosis by means of transcranial Doppler (TCD) ultrasound is a
good example of the point-of-care ultrasound (POCUS) concept applied to critical
care. It could be easily performed bedside and results are clear and
reproducible. There are two options to perform the examination: spectral or
“blind” devices (TCD) and transcranial coded color Doppler (TCCD), which is
included in most of ultrasound machines available at the ICU.
Using both transtemporal and occipital windows, middle cerebral arteries and the
basilar artery should be insonated for at least 30 seconds. If no ultrasound
images are found in these windows, the proximal arteries (ipsilateral internal
carotid siphon or both vertebral, respectively) are acceptable for the diagnosis of
cerebral circulatory arrest. The examination must be repeated after 30 minutes.
Arterial blood pressure must be greater than 90/50 mm Hg or mean arterial
pressure greater than 60 mm Hg at the beginning of the study and sustained
among the different diagnostic stages.

Figure A3-1 shows a summary of cerebral circulatory arrest (CCA) patterns.

A false negative result could occur in cases of loss of tightness of the skull (large
craniectomies, ventricular drainage, multiple skull fractures). In that situation,
changes in intracranial pressure (ICP) or cerebral perfusion pressure (CPP) may
be not so important to produce the CCA patterns. However, a large percentage of
these patients evolve to CCA, so the study is not only not contraindicated, but on
the contrary, its repetition over time becomes peremptory for its diagnosis.
A false positive result could occur when ancillary circulatory devices are present
(aortic balloon pump, extracorporeal membrane oxygenation) in which biphasic
flow may be identified in the absence of cerebral circulation.
In summary, TCD or TCCD are useful and available tools as ancillary tests for
brain death diagnosis in cases in which clinical examinations are not possible or
conclusive as a result of large cranial or facial destruction or depressant drugs.
Physician training is simple and results are not operator-dependent.

Table A3-1 Accepted Medical Standards for Brain Death

Abbreviations: CNS, central nervous system; SBP, systolic blood pressure
This research was originally published in JNM. Zuckier L. Radionuclide Evaluation of Brain Death in the
Post-McMath Era. J Nucl Med. 2016;57(10):1560-1568. © SNMMI.
Figure A3-1. Brain Death Patterns

As ICP increases and CPP decreases, Doppler spectral waveforms become extinct. Complete
cerebral circulatory arrest is suggested by equalization of forward and reverse flow
components. Absence of flow should be considered as cerebral circulatory arrest only when
the same operator had found it in a previous examination.
Reprinted from J Neurol Sci., 159(2), Ducrocq X, et al., Consensus opinion on diagnosis of
cerebral circulatory arrest using Doppler-sonography: Task Force Group on cerebral death of
the Neurosonology Research Group of the World Federation of Neurology, 145-150,
Copyright (1998), with permission from Elsevier.

Suggested Readings
1. Consensus Group on Transcranial Doppler in Diagnosis of Brain
Death. Latin American consensus on the use of transcranial Doppler
in the diagnosis of brain death. Rev Bras Ter Intensiva.
2014;26:240-252.
2. Ducrocq X, Hassler W, Moritake K, et al. Consensus opinion on
diagnosis of cerebral circulatory arrest using Doppler-sonography:
Task Force Group on cerebral death of the Neurosonology Research
Group of the World Federation of Neurology. J Neurol Sci.
1998;59:145-150.
3. Milliken A and Uveges M. CE: Brain Death: History, Updates, and
Implications for Nurses. Am J Nurs. 2020;120(3):32-38.
4. Russell JA, Epstein LG, Greer DM, Kirschen M, Rubin MA, Lewis
A. Brain death, the determination of brain death, and member
guidance for brain death accommodation requests: AAN position
statement. Neurology. 2019 January 2.
5. Schiff ND, Fins JJ. Brain death and disorders of consciousness. Curr
Biol. 2016:26(13):R572-R576.
6. Shemie SD, Hornby L, Baker A, et al. The International Guidelines
for Determination of Death phase 1 participants, in collaboration with
the World Health Organization. International guideline development
for the determination of death. Intensive Care Med. 2014;40:788-
797.
7. Wahlster S, Wijdicks EFM, Patel PV, et al. Brain death declaration:
practices and perceptions worldwide. Neurology. 2015;84:1870-
1879.
8. Zuckier LS. Radionuclide Evaluation of Brain Death in the Post-
McMath Era. J Nucl Med. 2016;57(10):1560-1568.
 Appendix 4
ORGAN DONATION
Organ donation is a process consisting of giving an organ or a part of an organ
to be transplanted into another person. Over the past 10 years, transplant
surgery has advanced in the organ recovery and preservation process in the
hopes of meeting the increasing community need for organ transplantation.
Transplant surgery has evolved to meet the public needs for function and
quality of life with the expansion of organ donation to include tissue graft
transplantation, such as extremity and face, as well as infertility with uterine
transplant. Organ donation can occur with a deceased donor or a living
donor.

I. HISTORY
The first successful human organ transplant occurred in 1954. In 1968, the
Uniform Anatomical Gift Act (UAGA) provided the legal foundation upon
which human organs and tissues could be donated for transplantation. Since
1972, all states in the United States and the District of Columbia have
adopted this Act, or amended forms of this Act. Worldwide over 100,000
transplants occur yearly. In the United States, almost 40,000 transplants were
coordinated in 2019. Unfortunately, the waiting list for men, women, and
children for organ transplantation still is in excess of 100,000 in the United
States with more being added to the list daily. On average, only 3 in 1000
deaths allow for organ donation.

The dead-donor rule was developed by Robertson in 1999 to refer to a norm

that organ donation policies have implicitly held since the beginning of
multiorgan procurement in the late 1960s. Although it is not a law, the rule
established the relationship between the two most relevant laws governing
organ donation from deceased donors: The Uniform Anatomical Gift Act and
state homicide law. The key point is that organ donation must not kill the
donor; the person must first be declared dead. It applies only to organ
donation from deceased donors.

As organ transplantation evolved, the regulation and oversight of the process

evolved as well. In 1984, The National Organ Transplant Act (NOTA) called
for the creation of an Organ Procurement and Transplantation Network
(OPTN). The OPTN is overseen by the Health Resources & Service
Administration (HRSA), an agency of the U.S. Department of Health and
Human Services (HHS). The United Network for Organ Sharing (UNOS), an
independent nonprofit company incorporated in 1984, is charged with
operationalizing the goals of the OPTN. Examples of critical requirements the
OPTN must support include the establishment and maintenance of an organ
transplant waitlist, the process and procedures to match organ donors to
recipients, securing an allocation process that is equitable, ethical, and
medically sound in manner, the ability to collect and process data into
meaningful information to improve the transplant process, the presence of a
24-hour availability, and the establishment of a forum for public comment on
policy and process. The United States is divided into different regions to
facilitate transplantation. These regions help determine how the 200+
transplant hospitals, 50+ organ procurement organizations, and 150+
histocompatibility laboratories interact with one another.

A. Organ Procurement Organization (OPO)

An organization designated by the Centers for Medicare and Medicaid
Services (CMS) is responsible for the procurement of organs for
transplantation and the promotion of organ donation. OPOs and their
transplant coordinators (TCs) serve as the vital link between the donor and
recipient and are responsible for the identification of donors and the retrieval,
preservation, and transportation of organs for transplantation.

There are several similar organizations around the world, but the one that has
had more impact in organ donation is the Spanish National Transplant
Organization (ONT). Since its creation in 1989, the so-called “Spanish
model” allowed the increase from 14 donors per million population to 48 in
2018, making Spain the world leader in organ donation. This model has been
recreated in Latin-America and Europe with different rates of success. The
model is based on “transplant coordinators” who are physicians and/or nurses
from intensive care units that take care of the complete organ donation
process, from donor identification and management to the family interview.

In the United States, the administration of organ allocation and geographic

representation requires the territorial division into 11 different regions.
Members of each region share policy structure and are linked primarily to the
other members of the region. Historically, when an organ is available, the
priority is given to the members of the region. As transplant surgery evolves,
so has the process for organ allocation. In March 2021, OPTN launched a
new policy for kidney and pancreas to increase equity in transplant access
nationwide. This new policy consists of replacing distribution based on
donation service area and OPTN region with a more consistent measure of
distance between the donor hospital and the transplant hospital. For more
information regarding these regions and about the OPTN, you can visit
https://optn.transplant.hrsa.gov.

II. DONOR CLASSIFICATION

A. Donationafter Declaration of Brain Death (Controlled)
The recovery of organs or tissue after irreversible damage of cerebral and
brain stem function; characterized by absence of electrical activity in the
brain, blood flow to the brain, and brain function as determined by clinical
assessment of responses. A brain-dead person is dead, although his or her
cardiopulmonary functioning may be artificially maintained for some time.

Ongoing communication by the healthcare team with the family is encouraged

when a patient is expected to progress to brain death. Prior to pronouncement
of brain death, the regional OPO should be contacted by the healthcare team
for patient evaluation for possible organ donation. Once the pronouncement of
brain death is made, further conversations with the family must occur to
discuss the pronouncement and perhaps explain what brain death means.
Family is informed of the brain death declaration prior to the discussion of
organ donation. The TC of the OPO is introduced to the family and then
communicates with the family about the opportunity for organ donation and
obtains consent. The donor patient must be supported until the recovery
process occurs in the operating room after coordination with family and
recovery surgeons.

B. Donation After Circulatory Death (DCD)

Recovery of organs and or tissues from a donor whose heart has irreversible
cessation of circulatory and respiratory function, previously referred to as
donation after cardiac death, non-heart-beating or asystolic donation. This
process can be controlled or uncontrolled depending on the organ donor’s
clinical status.

Controlled
Potential donors are limited to patients who have died, whose death is
imminent, or whose medical treatment no longer offers a medical benefit to
the patient as determined by the patient, the patient’s authorized surrogate, or
the patient’s advanced directive in constitution with the healthcare team. Prior
to the OPO initiating discussion regarding potential DCD organ donation, the
OPO must confirm the decision to withdraw life-sustaining medical
interventions. Prior to withdrawal of life-sustaining measures, the healthcare
team and OPO coordinate donation discussion with the patient’s family or
legally appointed representative.
Once organ donation consent has been obtained by the TC, a time is
coordinated with the family and recovery surgeons for the patient to be
separated from all life-supporting interventions and comfort care is initiated.
This usually occurs in the operating room but may occur in the ICU and the
family may or may not chose to be at the patient bedside. The patient is
pronounced dead by circulatory/cardiac death. Pronouncement of death is
made by the donor hospital healthcare team member who is authorized to
declare death and must not be part of the organ recovery team. This must
occur within 60 to 90 minutes of separation of life support for the donation to
proceed. If transition to comfort measures occurs in the ICU, the patient is
transported to the operating room; if comfort care is initiated in the OR, the
family is escorted out of the OR. A period of 2 to 10 minutes of asystole
(pulselessness, apnea, unresponsiveness) is observed prior to organ recovery
in the operating room. Up to 10% of potential donors maintain cardiac
activity for more than 90 minutes after discontinuation of life support. These
individuals are not candidates for organ donation and will receive ongoing
end-of-life care.

Uncontrolled
Rapid organ recovery donation after circulatory death (uncontrolled DCD)
involves recovery of organs following death from an unexpected circulatory
arrest and can be an out-of-hospital, refractory cardiac arrest or an
unexpected cardiac arrest in hospital. Optimally an OPO TC will be present
or available during the arrest event; if a representative is not present, the
OPO should be contacted by healthcare staff not participating in the
resuscitation. After resuscitation attempts are judged futile by the healthcare
team, the OPO assesses the patient as eligible to proceed with rapid organ
recovery. The family/legal representative must have made the decision to
withdraw life support and stop resuscitative efforts prior to the discussion of
donation. Resuscitation is continued as the TC has a conversation with family
regarding possible donation. If consent is obtained and the plan is to move
forward with rapid organ recovery, all interventions are terminated and the
patient is pronounced dead. The diagnosis of death may occur after
resuscitation is terminated on scene or after arrival to the hospital. There is a
“no touch” period after which death is determined, usually 2 to 5 minutes.
After this time, organ preservation may be restarted with cardiac
compressions and mechanical ventilation initiated to preserve the organs for
donation only. Compressions are maintained by healthcare staff or using a
compression/CPR device until a recovery surgeon and OR are available.

C. Living Donation
A living individual from whom at least one organ is recovered for use in a
transplant. A kidney, or a portion of a liver, lung, pancreas, or intestine are
examples.

III. DONATION PROCESS

A. Potential Organ Donor Recognition
Consider patient as a potential organ donor and communicate with OPO:

At the first indication the patient has sustained a non-survivable

neurologic or anoxic injury/illness
Prior to the first formal brain death examination
Prior to family discussion of do-not-resuscitate (DNR) or withdrawal
of support
Patient has sustained: anoxia, cerebrovascular accident, head
trauma

B. Communication
Consider phases of communication with the family: Provide up-to-date
information in small amounts. Set aside time to answer questions. Use visual
aids to describe the brain injury. When possible, bring the family to the
bedside to observe clinical tests. Choose words carefully when discussing the
patient’s condition. Do not mention donation until a systematic, timed,
collaborative approach can be orchestrated with the OPO transplant
coordinator and a member of the care team.

Phase 1 (Serious Injury) YOUR RELATIVE has sustained severe

damage to his/her brain. We are doing everything we can but
he/she may not recover.
– Critical care team continues to support the potential organ donor
patient through all phases.
 Phase II (Grave Prognosis) Despite everything we have done,
things are getting worse. There is nothing more we can do to save
your loved one’s life. Ensure that OPO has been notified.
Phase III (First Examination for brain death) YOUR LOVED ONE
appears to be dead because there is no brain function. We have
begun a series of tests to confirm this. We want to be extremely
thorough and careful to ensure that we are absolutely correct.
(Provide the family with information about additional testing and
timeframes.)
Phase IV (Pronouncement) We have finished the testing and found
that YOUR RELATIVE______ has died @ (INFORM family of the
time of death). (Where appropriate, repeat clinical examination
with the family present.)
Phase V (Team Huddle and Care Team Introduces the OPO TC)
This is ______, a member of our team and a specialist who works
with families such as yours.

The communication process for controlled and uncontrolled DCD would not
include a brain death examination or pronouncement prior to discussion of
donation with the family. For the DCD communication process, a family
discussion with the appropriate hospital recommended support staff present
(palliative care, Chaplain service, case management) should be conducted to
discuss goals of care. The OPO TC should be available and present in the
hospital at the time of the meeting. If the family wishes to transition to comfort
measures/withdraw/hospice, this would be the time to introduce the OPO TC
to discuss DCD organ donation.

C. Management Goals for Potential Organ Donors

In 2015, the Society of Critical Care Medicine, the American College of
Physicians, and the Organ Procurement Organization Donor Management
Task Force published a Consensus Statement in organ donation. More
recently (2020), the Spanish Society of Intensive Care Medicine (SEMICYUC)
updated their guidelines on regards to the goals for the management of
potential organ donors.

Some of the points highlighted in those position papers are summarized

below.

Fluid Management Recommendations

Crystalloids (isotonic saline) is the preferred fluid therapy

Colloid infusions can be used as a bolus to treat hypotension
Hypotonic saline can be used to treat hypernatremia
Bicarbonate might be needed to treat metabolic acidosis
Replacement of fluids should be directed by hemodynamic
monitoring

Monitoring Goals and Recommendations

Continuous cardiac monitoring and SpO2

Hourly vital signs and Input/Output documentation

Left ventricular ejection fraction > 45%
Maintain urine output > 1mL/kg/h and < 4mL/kg/h
Goal temperature 36-38°C (96.8-100.4°F) (warming/cooling
blanket, as needed)
Donor management focuses on improving and maintaining appropriate organ
perfusion. Critical care management is still required during this phase of care.
Interventions, such as mechanical ventilation, renal replacement therapy, and
titration of vasopressors, are necessary to achieve the goal of organ
transplantation. OPOs work in coordination with hospitals and healthcare
providers on management recommendations and goals. Institution and OPO
collaborative projects, such as the creation of donor management order sets
and protocols, have improved donor management and successful organ
recovery for transplantation.
IV. ORGAN PLACEMENT PROCESS
When organs are donated, the regional OPO accesses the national transplant
computer system. Information about the donor is entered into the system and
a donor/recipient match is run for each donated organ. The resulting match
list of potential recipients is ranked according to criteria defined in that
organ’s allocation policy. Each organ has its own specific criteria.

Using the match list of potential recipients, the regional OPO’s TC contacts
the transplant center of the highest ranked patient. If the organ is not
accepted, the next potential recipient’s transplant center on the match list is
contacted until the organ is placed. Once the organ is accepted for a patient,
transportation arrangements are made and transplant surgery is scheduled.
This narrative is a summary of organ donation. It does not encompass all
involved with the process. The intention of this section is to introduce organ
donation and provide an overview of the history, the types of organ donation,
and to state the importance of ongoing critical care management of the donor
patient. For more information on the process, please refer to the suggested
readings and consider contacting your regional OPO.

Suggested Readings
1. Chamorro-Jambrina C, Muñoz-Ramírez MR, Martínez-Melgar JL,
Pérez-Cornejo MS. Organ donor management: Eight common
recommendations and actions that deserve reflection. Med
Intensiva. 2017;41(9):559-568.
2. Institute of Medicine, Committee on Non-Heart- Beating
Transplantation II, “Non-Heart-Beating Organ Transplantation-
Practice and Protocols”, report from conference convened on
May 24, 25, 1999. https://pubmed.ncbi.nlm.nih.gov/25077239/
3. Korte C, Garber JL, Descourouez JL, Richards KR, Hardinger K.
Pharmacists’ guide to the management of organ donors after brain
 death. Am J Health Syst Pharm. 2016;73(22):1829-1839.
4. Kotloff RM, Blosser S, Fulda GJ, et al. Management of the
Potential Organ Donor in the ICU. Crit Care Med.
2015;43(6):1291-1325.
5. Organ Procurement and Transplant Network. US Department of
Health and Human Services website.
https://optn.transplant.hrsa.gov. Accessed May 2, 2020
6. Organ Transplant Data. US Department of Health and Human
Services website. https://data.hrsa.gov/topics/health-
systems/organ-donation. Updated February 21, 2019. Accessed
May 2, 2020.
7. Ortega-Deballon I, Hornby L, Shemie SD. Protocols for
uncontrolled donation after circulatory death: a systematic review
of international guidelines, practices and transplant outcomes.
Crit Care. 2015;19(1):268.
8. “Report of a National Conference on Donation after Cardiac
Death”, conference held April 7,8, 2005, Philadelphia.
https://www.onelegacy.org/docs/NationalConferenceOnDCD_2006
.pdf
9. Thoracic and Critical Care Community. American Society of
Transplantation. https://www.myast.org/about-ast/about-ast.
Accessed May 2, 2020.
10. United Network for Organ Sharing. https://unos.org/about/history-
of-unos/ Accessed May 2, 2020.
11. US Department of Health and Human Services Advisory
Committee on Organ Transplantation Recommendations,
November 6,7, 2003. https://www.organdonor.gov/about-
dot/acot/acotrecs2935.html

Suggested Websites
1. Protocolo Nacional de Mantenimiento del Potencial Donante de
Organos (SEMICYUC-ONT)
https://semicyuc.org/2020/05/protocolo-nacional-
demantenimiento-del-potencial-donante-de-organos-semicyuc-ont/
2. United Network for Organ Sharing (UNOS). https://unos.org/
3. OPTN: Organ Procurement and Transplantation.
https://optn.transplant.hrsa.gov/