Anesthesiology Critical Care Board Review, 1st Edition

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 To God who makes all things possible.

To my beautiful wife and best friend, Erin.

To Eden, Emeri, and Gabriel, who bring immeasurable joy to our lives.
 CONTENTS

Preface ix
Contributors xi

1. Central Nervous System 1

Robert Brown
2. Obstetric Critical Care 19
Marc J. Popovich
3. Hematology and Oncology 24
Talia K. Ben-​Jacob, Danielle L. Behrens, and
Christopher P. Potestio
4. Gastroenterology 43
Naveen Kukreja
5. Trauma and Disaster Management 60
Joshua Person and Lillian S. Kao
6. Critical Care Review: Burns 78
James M. Cross, Tonya C. George, and Todd F. Huzar
7. Sedation, Pain Management, and Pharmacology 87
Sophie Samuel and Jennifer Cortes
8. Endocrinology 100
Navneet Kaur Grewal and George W. Williams
9. Immunology and Infectious Diseases 106
Joti Juneja Mucci
10. Statistics, Ethics, and Management 115
George W. Williams
11. Pulmonology 124
Ted Lytle and Marc J. Popovich
12. Cardiovascular I: Physiology and Management 133
Linda W. Young
13. Cardiovascular II: Mechanical Support and Resuscitation 148
John C. Klick
14. Renal Acid–​Base 165
Olakunle Idowu
15. Procedures 179
Navneet Kaur Grewal
16. Nutrition 188
George W. Williams

Index 197

vii
 PR EFACE

The Anesthesiology Critical Care Board Review was forged as the editors have endeavored to make the format and style
a concept rooted in working to prepare critical care fellow of the questions consistent with an examination’s level of
physicians to take and be successful on the American Board difficulty. This book would not have been possible without
of Anesthesiology Critical Care Certification Examination the hard work of my mentor Dr. Popovich and my partner
(ABACCCE). This goal is important because it speaks to our Dr. Grewal; in this effort, we have generated a lasting part-
purpose as clinicians and educators in preparing the next gen- nership focused on education, and they have my thanks.
eration of anesthesiologist intensivists. In my time as a pro- The resulting product is a collective effort of our team, of
gram director (which functionally started in 2011), I found which I am proud to be a member.
there to be a paucity of materials suited for and tailored to Please allow me to express my gratitude to the physicians
physicians preparing for the examination—​in particular, and mentors that made this book possible: Dr. Howard
a perioperative and wide-​ranging examination such as the Nearman, my chairman during my residency who as an
ABACCCE. I experienced this myself when I was a recent anesthesiologist intensivist inspired me to work as hard
fellow graduate. As editors of this book, we sought to do eve- as I could to be emulate his example as a compassionate
rything in our power to prevent others from an anxiety-​laden physician and effective leader; my residency program co-​
experience resulting from minimal opportunities to prac- directors Dr. Matthew Norcia (another intensivist) and
tice for a critical care examination with questions written by Dr. David Wallace, who strongly encouraged me to pursue
authors that shared a background in anesthesiology. a career in critical care; the program director of my fellow-
It is our hope that, after reading this book, our audience ship, Dr. Marc Popovich (co-​editor), who taught me how to
would have learned something new, been able to identify be confident and thorough as an intensivist and provided
their strengths and weaknesses, and gain a perspective of me with the skills to create and lead a new critical care di-
factual content that is important for a successful clinician vision at a new institution; my parents, who always insisted
and leader in the intensive care unit. The editors and authors that I give 100% effort to everything that I do; my patients,
put a great deal of effort toward making the questions chal- who give me the privilege of caring for them in their darkest
lenging yet fair, as well as thorough yet straightforward, for hours and who, to this day, teach me something new in my
the reader. This book was created with the perspective and experience of lifelong learning; and finally, my beautiful
passion of educators from across the country who hope to and incredibly supportive wife and our three children, who
make the process of board preparation less stressful and sacrificed nights and weekends together to allow this book
more productive. to come to fruition.
Each chapter has been written by an author who actively
provides care within the domain of the chapter. Additionally, George W. Williams, MD, FASA, FCCM, FCCP

ix
 CONTR IBUTOR S

Danielle L. Behrens, DO Tonya C. George, PhD, PAC

Assistant Professor of Medicine Physician Assistant
Cooper Medical School of Rowan University Dallas, TX, USA
Attending Physician
Division of Hematology/Oncology Navneet Kaur Grewal, MD
Department of Medicine Assistant Professor of Anesthesiology and Critical Care
MD Anderson/Cooper Cancer Center Medicine
Cooper University Hospital Assistant Program Director, Anesthesiology Critical Care
Camden, NJ, USA Medicine Fellowship Program
Director of Education, Medical/Surgical and Cardiovascular
Talia K. Ben-​Jacob, MD, MSc Intensive Care Units
Division Chief of Critical Care Medicine Memorial Hermann Southwest Hospital
Department of Anesthesiology Houston, TX, USA
Cooper University Hospital
Assistant Professor of Anesthesiology Todd F. Huzar, MD, FACS
Cooper Medical School of Rowan University Associate Professor
Camden, NJ, USA Department of Surgery
McGovern Medical School/UT Health
Robert Brown, MD Houston, TX, USA
Assistant Professor
Department of Neurosurgery Olakunle Idowu, MD
University of Texas Houston Health Science Center Assistant Professor
Houston, TX, USA Department of Anesthesiology and Perioperative Medicine
Department of Critical Care and Respiratory Care
Jennifer Cortes, PharmD, BCPS, BCCCP University of Texas MD Anderson Cancer Center
Medical ICU/​Respiratory ICU Clinical Houston, TX, USA
Pharmacy Specialist
Department of Pharmacy Services Lillian S. Kao, MD, MS
Memorial Hermann-​Texas Medical Center Professor
Houston, TX, USA Department of Surgery
McGovern Medical School at UT Health
James M. Cross, MD, FACS Houston, TX, USA
Professor of Surgery
McGovern Medical School at UT Health John C. Klick, MD
Medical Director Associate Professor
John S. Dunn Burn Center Penn State University College of Medicine
Memorial Hermann-Texas Medical Center Division Chief, Cardiothoracic Anesthesiology
Houston, TX, USA Department of Anesthesiology and Perioperative Medicine
Penn State Milton S. Hershey Medical Center
Hershey, PA, USA

xi
Naveen Kukreja, MD Marc J. Popovich, MD, FCCM
Assistant Professor Helmut F Cascorbi Professor and Chair
Department of Anesthesiology Department of Anesthesiology and Perioperative Medicine
University of Colorado Case Western Reserve University School of Medicine
Denver, CO, USA University Hospitals Cleveland Medical Center
Cleveland, OH, USA
Ted Lytle, MD
Medical Director Christopher P. Potestio, MD
Cardiothoracic Intensive Care University Hospitals Assistant Professor of Anesthesiology
Cleveland Medical Center Cooper Medical School of Rowan University
Section Chief Critical Care Attending Physician
Harrington Heart and Vascular Institute University Division of Critical Care
Hospitals Cleveland Medical Center Department of Anesthesiology
Associate Chief Medical Officer Cooper University Hospital
University Hospitals Cleveland Medical Center Camden, NJ, USA
Assistant Professor
Department of Anesthesiology Sophie Samuel, PharmD, BCPS, BCCCP
Case Western Reserve University Critical Care Clinical Specialist, Neurosciences
Cleveland, OH, USA Department of Pharmacy Services
Memorial Hermann-​Texas Medical Center
Joti Juneja Mucci, MD Houston, TX, USA
Assistant Professor
Case Western Reserve University School of Medicine George W. Williams, MD, FASA, FCCM, FCCP
Medical Director Associate Professor of Anesthesiology and Critical
Surgical Intensive Care Unit Care Medicine
Program Director Vice Chair for Critical Care Medicine
Anesthesiology Critical Care Fellowship Program Director, Anesthesiology Critical Care
Department of Anesthesiology and Perioperative Medicine Medicine Fellowship
University Hospitals Cleveland Medical Center Medical Co-Director, Surgical Intensive Care Unit
Cleveland, OH, USA Lyndon B. Johnson General Hospital
Houston, TX, USA
Joshua Person, MD
Assistant Professor of Surgery Linda W. Young, MD, MS
Division of Acute Care Surgery Critical Care Intensivist
Department of Surgery Anesthesiologist
University of Texas McGovern Medical School at Houston Critical Care Medicine
Houston, TX, USA Halifax Health
Daytona Beach, FL, USA

x ii • con t r i bu tor s
A N E S T H E S IOL O G Y CR I T IC A L
C A R E B OA R D R E V I E W
 1.
CENTR A L NERVOUS SYSTEM

Robert Brown

QU E STIONS 3. A 67-​year-​old man is admitted to the intensive care

unit (ICU) following a pulseless electrical activity
1. A 71-​year-​old man with a history of heart failure, (PEA) arrest with restoration of spontaneous circula-
poorly controlled diabetes, and chronic kidney disease tion (ROSC) after 17 minutes of cardiopulmonary re-
is brought to the emergency department (ED) by his suscitation (CPR). Initial examination reveals 3-​mm
family with altered mental status. He is found to have pupils with absent pupillary light reflex bilaterally, ab-
a serum creatinine of 5.3 mg/​dL, blood urea nitrogen sent corneal reflex, and no motor response to pain. He
(BUN) of 81 mg/​dL, glucose of 313 mg/​dL, and pH of is breathing over the ventilator. He undergoes targeted
7.17. On arrival to the ED, he does not open his eyes but temperature management with a temperature target of
swats your hand away with both arms when you squeeze 33° C and is rewarmed slowly after 24 hours. During
his trapezius muscles. He moans but does not speak or rewarming, he has diffuse jerking involving sponta-
follow commands. The cranial nerves are intact; how- neous eye opening and twitching of all four limbs,
ever, you notice an irregular breathing pattern of al- which are not suppressed with levetiracetam and val-
ternating periods of hyperventilation and apnea in a proic acid. Which of the following would MOST sup-
crescendo-​decrescendo repeating pattern. Which of port a poor prognosis in this patient?
the following MOST likely describes this respiratory
pattern? A. Absent pupillary light reflex before cooling
B. Bilateral absence of N2O response with
A. Brainstem injury somatosensory evoked potentials (SSEPs)
B. Metabolic derangement C. Early status myoclonus
C. Stroke
D. Seizure 4. During morning rounds, a 37-​ year-​old patient
admitted with severe traumatic brain injury (TBI)
2. An 88-​year-​old man with a history of heart failure now has absent cranial nerve reflexes. On examination,
and mild dementia is intubated with a diagnosis of pupils are 5 mm and nonreactive; corneal nerve reflexes,
community-​acquired pneumonia. He takes donepezil oculocephalic reflex, gag, cough, and motor response to
daily. His daughter informs you that he was hospitalized painful stimulation are all absent. The patient’s respi-
several years ago following a hip fracture and required ratory rate is the same as the prescribed rate on the ven-
four-​point restraints due to hallucinations, agitation, tilator. You have reviewed your hospital’s brain death
and injuring a staff member. Which of the following policy and confirm that all prerequisites have been met.
would MOST reduce the risk for a similar issue during Which of the following statements is NOT required to
this hospitalization? declare brain death?

A. Avoidance of central alpha agonists A. Cerebral blood flow study

B. Scheduled haloperidol B. Oculovestibular reflex testing (cold calorics)
C. Utilization of the ABCDEF bundle C. Normothermia
D. Increased sedation D. Lack of vasopressors

1
5. A 24-​ year-​
old female with past medical history 7. A 42-​year-​old male is admitted for sudden onset of
significant for polysubstance abuse presents after a severe headache associated with nausea, vomiting, and
witnessed seizure. En route to the hospital, the patient neck pain. He is otherwise neurologically intact. A CT
has another seizure and is given 10 mg intramuscular scan of the brain is completed and shows the following
(IM) midazolam. In the ED, she has two more seizures image. What is the next best step in management?
and is given 2 mg intravenous (IV) lorazepam each time,
ultimately resulting in intubation with etomidate and
rocuronium. What is the next MOST appropriate drug
to administer?

A. Propofol
B. Levetiracetam
C. Lacosamide
D. Phenytoin

6. A patient presents with status epilepticus re-

fractory to lorazepam and is intubated in the ED.
Convulsive activity stops after treatment with a
loading dose of phenytoin and a midazolam infu-
sion. An electroencephalogram (EEG) is obtained
and shows frequent epileptiform discharges without
seizures. The patient is noted to have a tempera-
ture of 38.7° C, and lab results reveal a white blood
cell (WBC) count of 18 (80% polymorphonuclear
A. Administer levetiracetam
neutrophils [PMNs]). A computed tomography (CT)
B. Administer nimodipine
scan of the head is shown here. What is the next
C. Ventriculostomy placement
MOST appropriate step?
D. CT angiogram of the brain

8. A 62-​year-​old patient with past medical history of

hypertension, hyperlipidemia, type 2 diabetes, and
coronary artery disease presents at 5 a.m. with acute
onset of confusion. On exam, he has a left gaze pref-
erence, has dense right hemiplegia, and is globally
aphasic. He was found by his family this morning and
was last seen normal at 10 p.m. the previous night. A CT
scan of the brain is completed and is remarkable for a
dense left middle cerebral artery (MCA) sign with an
Alberta Stroke Program Early Computed Tomography
(ASPECT) score of 8. What is your next MOST imme-
diate step in management?

A. IV thrombolytics
B. Diffusion-​weighted MRI of the brain
C. CT angiogram of the brain with perfusion
D. Aspirin

A. Obtain a lumbar puncture 9. Which of the following is FALSE regarding trau-

B. Titrate midazolam to obtain a suppression-​burst matic intracranial epidural hemorrhage?
pattern
C. Magnetic resonance imaging (MRI) of the brain A. Good prognosis with early evacuation
with or without contrast B. Biconvex shape
D. Administer vancomycin, ceftriaxone, C. Always due to arterial bleeds
or acyclovir D. Most commonly in the temporoparietal region

2 • A n e s t h e s i o l o g y C r i t i c a l Ca r e B oa r d  Re v i e w
10. A 53-​year-​old 70-​kg female with a history of my- 13. A 45-​year-​old male presents to the ED with pro-
asthenia gravis presents to the ED with dyspnea and gressive lower extremity weakness. The symptoms
worsening dysphagia over the past week. She takes pyr- started 4 days ago with vague tingling in his toes. He
idostigmine 90 mg four times daily. On examination, denies respiratory symptoms. On exam, his lower ex-
there is weakness of the neck flexors and proximal mus- tremity strength is 1/​5 bilaterally, while his upper
cles of the upper extremity, significant dysarthria, and extremities are 2/​5 distally and 4/​5 proximally. Deep
use of accessory muscles of respiration. Forced vital tendon reflexes are absent, sensory exam shows partial
capacity (FVC) is 1 L and negative inspiratory force numbness over all distal extremities without a spinal
(NIF) is –​17 cm H2O. Arterial blood gas (ABG) analysis level, and cranial nerve function is intact. He reports
reveals: having an upper respiratory illness 1 month ago.
He is admitted to the Neurology ICU, where a nerve
pH: 7.42 conduction study/​ electromyography (NCS/​ EMG) is
PaCO2: 37 mm Hg performed. What is one of the earliest and MOST sen-
PaO2: 90 mm Hg sitive electrophysiological findings in patients with
Hemoglobin saturation: 97% on room air this diagnosis?

Which of the following options is the MOST appro- A. Absent tibial nerve H reflex
priate next step? B. Reduced F-​wave latency
C. Abnormal sural sensory nerve action
A. Close clinical monitoring potential (SNAP)
B. Endotracheal intubation D. Absent temporal dispersion of proximal compound
C. Prednisone muscle action potential (CMAP) responses
D. Pyridostigmine
14. Which among these are NOT included in the dif-
11. A patient with myasthenia gravis on pyridostigmine ferential diagnosis for a patient presenting with acute
is admitted with shortness of breath. She is started on flaccid paralysis?
biphasic positive airway pressure (BiPAP) with an in-
spiratory pressure of 12 cm H2O and expiratory pres- A. Acute poliomyelitis
sure of 5 cm H2O, with stabilization in her symptoms. B. West Nile virus (WNV) meningoencephalitis
She is afebrile and demonstrates no clinical signs of C. Critical illness myopathy
infection. Which of the following is the MOST appro- D. Charcot-​Marie-​Tooth syndrome
priate next step in this patient’s management?
15. A 37-​year-​old male suffers a severe asthma at-
A. High-​dose IV methylprednisolone tack that results in cardiac arrest. ROSC is achieved
B. Increased pyridostigmine in the field, and hypothermia is initiated in the ED.
C. IV immunoglobulin The patient undergoes controlled rewarming on day
D. Levofloxacin 2; however, overnight he becomes hypotensive, and
norepinephrine is started to maintain mean arterial
12. A 65-​year-​old male presents with a 5-​day history pressure (MAP) above 60 mm Hg. Over the course
of progressively worsening mental status and fever. of the night, the patient’s vasopressor requirement
A lumbar puncture is performed, followed by IV van- increases significantly, and loss of cranial nerve
comycin and ceftriaxone administration. A 20-​minute ref lexes is noted. Serum sodium increased from
EEG shows periodic lateralized epileptiform discharges 142 mEq/​L the day before to 159 mEq/​L currently.
(PLEDs). Which diagnostic test would be MOST ap- Urine output has been 300 to 500mL/​hour for the
propriate to evaluate this patient’s condition? past several hours. Which of the following is the next
BEST step?
A. CT of the brain with contrast
B. MRI of the brain with contrast A. D5W infusion
C. Cerebrospinal fluid (CSF) polymerase chain reaction B. Isotonic fluid bolus
(PCR) testing C. Urine osmolality
D. Continuous EEG D. Brain death testing

1. Ce n t r a l Ne rvo u s  S y s t e m • 3
16. A 42-​year-​old female with a history of IV drug abuse
presents to the ED complaining of severe back pain. She
is reluctant to participate in the neurological examina-
tion because of shooting pain with movement; however,
she does not seem to have weakness or sensory loss. She
denies bowel or bladder dysfunction and is afebrile.
Laboratory findings include:

WBC count: 11.2 × 103

Hemoglobin: 12.6 g/​dL
Hematocrit: 37%
Platelets: 214 × 109/​L

Which of the following is the MOST appropriate next

step in management?

A. Urgent MRI of the cervical, thoracic, and

lumbar spine
B. No further workup because she is likely drug-​seeking
C. Cervical radiograph A. Decreasing sedation
D. Lumbar puncture B. Reducing the patient’s minute ventilation
C. Cerebral perfusion pressure (CPP) augmentation
17. A 57-​year-​old is involved in a high-​speed motor ve- with norepinephrine
hicle collision. In the ED, the patient is quadriplegic, D. Red blood cell (RBC) transfusion
breath sounds are shallow, and O2 saturation is 88% on
a non-​rebreather mask. The patient undergoes endotra- 19. In a patient with severe TBI undergoing
cheal intubation, and a CT scan of the spine shows bi- multimodality monitoring, which of the following
lateral facet dislocations at C5–​6. The patient is taken MOST suggests an increased risk for further neuronal
emergently to the operating room for spinal stabiliza- injury?
tion and is now admitted to the ICU for further man-
agement. On arrival, the patient is awake and alert A. EEG reactivity to painful stimuli
but has no movement or sensation below the deltoids. B. Decreased jugular venous bulb O2 saturation
Which of the following is FALSE? C. Decreased cerebral lactate-​to-​pyruvate ratio
D. ICP of 25 mm Hg
A. MAP should be maintained above 85 mm Hg
B. The patient can be safely extubated 20. A 62-​year-​old female with a history of hypertension,
C. IV glucocorticoids are not recommended dyslipidemia, and type 2 diabetes mellitus is undergoing
D. The long-​term prognosis for ambulation is poor a diagnostic cardiac catheterization. She receives 2 mg
of IV midazolam before the procedure. Twenty minutes
18. A 32-​year-​old male is admitted with severe TBI. into the procedure, the patient is noted to be unrespon-
Admission Glasgow Coma Scale (GCS) score is 6T; ad- sive, although she is breathing well. A closer examina-
mission CT scan is shown here. A ventriculostomy is in tion shows that the patient does not open her eyes to
place for intracranial pressure (ICP) monitoring. He is stimulation, her pupils are 1.5 mm and reactive, and
sedated with propofol and fentanyl with an ICP of 15 mm the left eye is lower than the right eye. The left upper ex-
Hg and MAP of 66 mm Hg. He is intubated and me- tremity weakly withdraws to noxious stimulation, and
chanically ventilated on assist control mode with a respi- there is no motor response on the right. What is the
ratory rate of 20 breaths/​minute and tidal volume of 500 MOST likely cause of the patient’s clinical symptoms?
mL. The patient’s ABG reveals a pH of 7.49, PaCO2 of
29 mm Hg, and PaO2 of 113 mm Hg. The patient’s brain A. Left frontal lobe intracerebral hemorrhage (ICH)
tissue oxygen monitor reads 13 mm Hg; hemoglobin is B. Brainstem infarction
7.2 g/​dL. Which of the following is LEAST likely to im- C. Left lacunar infarction
prove the patient’s brain tissue oxygenation? D. Oversedation

4 • A n e s t h e s i o l o g y C r i t i c a l Ca r e B oa r d  Re v i e w
21. A 50-​year-​old female admitted with moderate TBI 24. A 34-​ year-​
old woman with a history of a
and small bifrontal contusions is found acutely unre- prolactinoma presents to the ED with thunderclap
sponsive by a nurse. Her vital signs are as follows: headache. The CT scan of the brain is read as normal.
She is drowsy but follows commands and has no focal
Heart rate: 93 bpm neurological deficits. Shortly after admission to the
Blood pressure: 162/​82 mm Hg ICU, she complains of lightheadedness and is noted to
Respiratory rate: 18 breaths/​minute (on mechanical have a blood pressure of 77/​40 mm Hg. Serum sodium
ventilation) is 132 mEq/​L , and urine output is 80 to 100 mL/​hour
Temperature: 99.1° F since admission. Which of the following is the BEST
initial treatment?
The patient localizes bilaterally, opens eyes to sternal
rub, has equal and reactive pupils, and has intact gag/​ A. Vasopressin
cough and corneal reflexes. The patient then has a B. Hydrocortisone
sudden clinical deterioration manifested by extension C. Hypertonic saline 3%
in all extremities with a 5-​mm nonreactive left pupil. D. Norepinephrine infusion
After emergent intubation, what is the next MOST ap-
propriate management? 25. A 67-​year-​old man with a history of hypertension is
“found down” by his neighbors. A CT scan of the brain
A. Mannitol shows ICH in the left basal ganglia (see the following
B. Levetiracetam image). His blood pressure is 210/​120 mm Hg. On
C. Dexamethasone neurological examination, the patient is alert, follows
D. Hypertonic saline 23.4% simple commands, and answers simple questions. He
extends his right arm and strongly follows with the left
22. A 27-​year-​old female, G1P1001 at 34 weeks’ ges- arm. The patient’s home medications include aspirin
tational age, is brought to the ED after she had a and lisinopril. Which of the following is the next BEST
witnessed generalized tonic-​clonic convulsion at home. step in management?
She has no prior medical history. Her blood pressure is
163/​102 mm Hg. She slowly regains consciousness but
has no focal neurological deficits. What would be the
MOST appropriate next step in management of this
patient?

A. Diazepam
B. Fosphenytoin
C. Magnesium sulfate
D. Levetiracetam

23. A 57-​year-​old female with no known medical history

presents after being found in a confused state by family
members. On examination, she is afebrile and appears
cachectic and with poor dentition. Neurological exam-
ination demonstrates aphasia and a right facial droop.
Cardiac examination reveals normal S1 and S2 without
murmurs. A CT scan shows an ovoid lesion with sur-
rounding vasogenic edema in the left parietal lobe,
which is concerning for cerebral metastasis versus ab- A. Emergent craniotomy and hematoma evacuation
scess. Which of the following features MOST favor ce- B. Nicardipine infusion
rebral abscess over metastasis? C. Factor VIIa
D. Emergent cerebral angiogram
A. Rim enhancement
B. Multiple lesions 26. On your rounds, you visit a 49-​year-​old male who is
C. Restricted diffusion on diffusion-​weighted post-​bleed day 6 from an aneurysmal subarachnoid hem-
imaging (DWI) orrhage. The patient had an external ventricular drain
D. Vasogenic edema that spares the cortex (EVD) placed on admission for hydrocephalus and then

1. Ce n t r a l Ne rvo u s  S y s t e m • 5
underwent coiling of an anterior communicating ar- 27. A 57-​year-​old female with a history of smoking and
tery aneurysm. The clinical course has been unremark- hypertension presents with thunderclap headache. On
able; however, your resident tells you that the patient’s arrival, she does not open her eyes to pain, moans, and
transcranial Doppler ultrasound exams from this localizes bilaterally. A CT scan shows diffuse cisternal
morning were abnormal. The results include: subarachnoid hemorrhage with mild hydrocephalus.
She is intubated for airway protection, and an external
Left MCA velocity: 156 cm/​second ventriculostomy drain is placed. A CT angiogram is
Right MCA velocity: 207 cm/​second performed that shows a left posterior communicating
artery aneurysm. She arrives to the ICU in the eve-
On examination, you now note a right-​sided facial ning and is scheduled for a cerebral angiogram in the
droop and new pronator drift. Which of the following morning. Which of the following treatments is MOST
is the MOST appropriate management at this time? indicated?

A. Maintenance fluids A. Vasopressors

B. Vasopressors B. Avoidance of antifibrinolytics
C. MRI C. Phenytoin
D. Brain CT with angiography D. EVD drainage

6 • A n e s t h e s i o l o g y C r i t i c a l Ca r e B oa r d  Re v i e w
 A NSW E RS and mechanical ventilation in patients with these brain
injuries. This patient’s active heart failure with signs of end-​
1. ANSWER: B organ dysfunction is more likely the cause of this patient’s
presentation.
An often overlooked component of the neurological exam-
Keywords: Central nervous system (CNS) diagnosis;
ination is the patient’s respiratory pattern. This is largely
Altered mental status (coma)
because the patient’s natural respiratory pattern can be
obscured by mechanical ventilation. However, two patterns
are commonly seen in the ICU but are often misunderstood.
R E F E R E NC E
These patterns are post-​ hyperventilation apnea and
Cheyne-​ Stokes respirations. Cheyne-​ Stokes respirations Posner JB, Saper, CB, Schiff ND, Plum F. Plum and Posner’s diagnosis of
can be quite dramatic when observed, and if not familiar stupor and coma, 4th ed. New York: Oxford University Press; 2007,
with the pattern, healthcare providers usually impute this pp. 46–​52.
to a severe structural brain abnormality. However, this is
almost never the case. To understand Cheyne-​Stokes respi-
ration requires an understanding of post-​hyperventilation
apnea. While the medullary respiratory center is respon- 2. ANSWER: C
sible for controlling the respiratory drive, the frontal lobes
have hegemony over the process (this is why one can hold Delirium is associated with increased mortality, pro-
one’s breath under water but may hyperventilate when longed ICU and hospital length of stay, and post-​ICU
nervous). When a patient is hypocapnic, rather than an ap- cognitive impairment. A multifaceted approach should be
neic period until CO2 is normalized, the respiratory rate implemented for its prevention, detection, and treatment.
is simple slowed, and tidal volumes are decreased to allow One method is the ABCDEF bundle. This is an acronym
CO2 to return to normal more gradually. If the frontal lobes for pain assessment and utilization of analgesics, daily
are damaged or malfunctioning owing to a systemic process awakening and spontaneous breathing trials, choosing an
causing encephalopathy (much more common), apnea is appropriate sedation strategy, employing a delirium detec-
commonly seen following periods of hypocapnia. This can tion method, early mobilization, and family engagement.
be observed by asking an encephalopathic patient to take Daily awakening periods with interruption of sedatives
several deep breaths and observing for apnea; however, in and spontaneous breathing trials (SBTs) have been shown
day-​to-​day practice, apnea is typically encountered in anx- to decrease delirium incidence and ventilator and ICU
ious or agitated patients who are causing apnea alarms on lengths of stay. Indeed, a randomized controlled trial
a ventilator during spontaneous breathing trials. Instead of daily sedation interruptions (frequently called “holi-
of returning to an assisted mode of ventilation and de- days”) with SBTs demonstrated reductions in ICU and
laying extubation, the amount of pressure support can be hospital lengths of stay of 3.8 and 4.3 days, respectively.
reduced to avoid large tidal volumes, and the patient can Benzodiazepines may lead to delirium and prolonged
be directed to relax, or other measures to control agitation ventilator and ICU lengths of stay, while sedation with
can be employed. The apnea alarm on the ventilator can also dexmedetomidine may have the opposite effect. Depth of
be extended. However, the best way to solve this issue is to sedation should be monitored with an appropriate sedation
extubate the patient. Cheyne-​Stokes is a more extreme ver- scale (e.g., Richmond Agitation and Sedation Scale), and
sion of post-​hyperventilation apnea and results from a delay sedatives should be regularly titrated to achieve a lighter
between alveolar CO2 and the partial pressure of CO2 in level of sedation. Additionally, CAM-​ICU is a simple as-
the medullary interstitium such that the brain is always sessment tool used to detect delirium and has been shown
trying to “catch up” to the alveolar CO2 . Low-​output states to have a high sensitivity and specificity. Once delirium has
can exacerbate this condition because changes in alveolar been detected, one can then review potential causes and ad-
CO2 take much longer to reach the medullary respiratory dress them accordingly. Results of trials investigating anti-
centers. Many clinicians, after observing a patient with this psychotic medication have not been conclusive, although
respiratory pattern, assume a severe structural or brainstem the recent REDUCE trial demonstrated that prophylactic
injury when in fact the pattern demonstrates intact brain- haloperidol (1 or 2 mg) is not effective in preventing de-
stem reflexes, as is the case with this patient. Respiratory lirium. Typical antipsychotics such as haloperidol are not
patterns that are reflective of brainstem pathology in- recommended, while atypical antipsychotics should be
clude apneustic breathing (inspiratory pauses, seen with used only when other measured have failed. Early mobi-
pontine injuries), ataxic breathing (irregular pattern, lization has been shown to reduce delirium as well as im-
seen with rostral medullary lesions), and apnea (seen with prove functional status at discharge, likely by reducing
caudal medullary lesions). These are typically not observed the incidence of ICU-​acquired weakness. Mobilization
(with the exception of apnea) owing to early intubation and exercise with physical and occupational therapy can

1. Ce n t r a l Ne rvo u s  S y s t e m • 7
be paired with the patient’s daily sedation holiday and thresholds that predict poor prognosis with high specificity,
breathing trial. Restraints, while often necessary to avoid which has limited their clinical utility.
self-​extubation or removal of other life-​sustaining medical
Keywords: CNS diagnosis; AMS; Other (hypoxic/​met-
devices (e.g., ventriculostomies), can agitate patients and
abolic encephalopathy); CNS; Diagnostic modalities;
exacerbate delirium and their use should be minimized.
Evoked potential; CNS; Diagnostic modalities; EEG
Keywords: CNS diagnoses; Altered mental status (de-
lirium, hallucinations)
R E F E R E NC E S

Oddo M, Rossetti AO. Early multimodal outcome prediction after

R E F E R E NC E S cardiac arrest in patients treated with hypothermia. Crit Care Med
2014;42:1340–​1347.
Barr J, Fraser GL, Puntillo K et al. Clinical practice guidelines for the Sandroni C, Cariou A, Cavallaro F et al. Prognostication in comatose
management of pain, agitation, and delirium in adult patients in the survivors of cardiac arrest: an advisory statement from the European
intensive care unit. Crit Care Med 2013;41:263–​306. Resuscitation Council and the European Society of Intensive Care
Girard TD, Kress JP, Fuchs, BD et al. Efficacy and safety of a paired se- Medicine. Resuscitation 2014;85:1779–​1789.
dation and ventilator weaning protocol for mechanically ventilated Solari D, Rossetti AO, Carteron L et al. Early prediction of coma re-
patients in intensive care (Awakening and Breathing Controlled covery after cardiac arrest with blinded pupillometry. Ann Neurol
trial): a randomized controlled trial. Lancet 2008;12:126–​134. 2017;81(6):804–​810.
Morandi A, Brummel NE, Ely EW. Sedation, delirium and mechan-
ical ventilation: the “ABCDE” approach. Curr Opin Crit Care
2011;17:43–​49.
van den Boogaard M, Slooter AJC, Brüggemann RJM et al. Effect of
haloperidol on survival among critically ill adults with a high risk 4. ANSWER: D
of delirium: The REDUCE Randomized Clinical Trial. JAMA
2018;319(7):680– ​690. While guidelines have been published for brain death
declaration, some details are left to the discretion of in-
dividual hospitals. In general, however, the first step in
declaring brain death is confirming that all prerequisites
3. ANSWER: B have been met and that there are no confounding factors.
This involves knowing the cause of injury and having that
Prognostication following cardiac arrest is complex and is be compatible with causing brain death. For example, se-
most accurate when utilizing a multimodal approach. Some vere Guillain-​Barré syndrome (GBS) has mimicked brain
features have been consistently associated with a poor prog- death, including absent cranial nerve reflexes, absent
nosis and can thus be used with a high degree of confidence. motor response, and failed apnea testing. A brain death
These include absent pupillary light reflexes at 72 hours and examination would incorrectly diagnose brain death,
bilateral absence of N2O response during SSEP testing; loss yet cerebral function might be normal. A patient who is
of N2O is defined as no negative deflection 20 seconds after “found down” with an unknown cause of injury should
stimulation on both sides. Of note, automated methods be approached cautiously. Severe metabolic derangements
of assessing pupillary light reflex have been developed and should be excluded because these may confound the ex-
tested and may be expected to be seen more often in the amination, although what defines a severe derangement
coming years. Other features may be strongly associated is mostly left to the provider. The patient should be ad-
but have lower specificity and should therefore not be used equately resuscitated, normothermic, and normotensive
as the sole indictor of poor prognosis. These include early (although vasopressors to achieve normotension do not
(within the first 48 hours) status myoclonus, neuroimaging preclude the ability to declare brain death). Brain im-
features (other than frank herniation), and malignant EEG aging compatible with brain death is not mandatory but
findings. Neuroimaging features associated with poor prog- is performed almost universally. For example, in a patient
nosis include loss of gray-​white differentiation and sulcal ef- with anoxic brain injury, imaging demonstrating hernia-
facement on CT imaging, and restricted diffusion on MRI. tion and diffuse loss of gray-​white differentiation is not
Of note, patchy or regional abnormalities, including iso- required and often not present because CT imaging may
lated basal ganglia abnormalities, do not preclude neurolog- be performed before the development of cerebral edema;
ical recovery. Malignant EEG findings that augur poor however, a CT scan obtained on day 4 without evidence
prognosis include suppression or a suppression-​burst pat- of anoxic injury would not be consistent with brain
tern, absent reactivity, and low voltage. Hypothermia and death. Medications that may confound the examination,
sedatives can confound the EEG; thus, the patient should including benzodiazepines, barbiturates, and opiates,
be normothermic and off sedation. Serum biomarkers have should be held, and testing should be delayed until these
also been used, with neuron-​specific enolase being the most medications have been fully metabolized. The brain death
studied. However, studies have demonstrated a range of examination should demonstrate lack of response to

8 • A n e s t h e s i o l o g y C r i t i c a l Ca r e B oa r d  Re v i e w
simulation, absent pupillary light reflex, corneal reflex, hydrolyzed to phenytoin by serum phosphatases with a con-
oculocephalic reflex, oculovestibular reflex, gag reflex, version half-​time of 15 minutes; the loading dose is 20 mg/​
cough reflex, and motor response. Finally, a formal apnea kg (considered phenytoin equivalents) and is infused at a
test should be performed to demonstrate no respiratory ef- rate of 100 to 150 mg/​minute. It should be noted that while
fort despite an arterial PaCO2 higher than 60 mm Hg (or hypotension is less likely to be seen with phosphenytoin, it
20 mm Hg above baseline in patients with chronic CO2 may still be occur, and hemodynamic monitoring remains
retention). This is typically performed by disconnecting indicated.
the patient from the ventilator and providing continuous Levetiracetam can be considered in this case, but ev-
oxygen through a catheter inserted into the endotracheal idence for its efficacy in aborting status epilepticus is
tube (passive oxygenation). Patients may become hypo- unclear. An appropriate dose per guidelines is 20 to 60
tensive during apnea testing as acidosis develops; however, mg/​kg, up to a maximum of 4500 mg. The mechanism
this can be managed with vasopressor titration and does of action for levetiracetam is not known, although it is
not usually prevent one from completing the test. Because hypothesized to modulate GABA receptors indirectly
brain death is a clinical diagnosis, ancillary tests are not and bind to protein SV2A (which has been linked to
required unless part of the clinical examination cannot be seizures in animal models). Since levetiracetam does not
performed. It is also for this reason that one should use induce CYP, it has minimal interactions with other drugs
the term “ancillary test” rather than “confirmatory test” to such as immunosuppressants, and IV to oral dosing and
avoid the misconception that the brain death examination bioequivalence are identical.
requires confirmation. Acceptable ancillary tests include Lacosamide works by helping inactivate sodium
EEG, transcranial Doppler ultrasound, catheter angiog- channels, thereby preventing repetitive firing of neurons,
raphy, and cerebral blood flow testing using single photon and it can be used to treat focal-​onset seizures; unfortu-
emission computed tomography (SPECT). The latter is nately, lacosamide has no role in treating generalized status
typically the most commonly used test because of its avail- epilepticus. If the patient does not respond to phenytoin,
ability and ease of performance. Importantly, while brain while second-​line alternatives or third-​line agents such as
death is considered “whole brain death,” certain features valproic acid and phenobarbital are acceptable, an infu-
such as absence of diabetes insipidus and blood pressure sion of midazolam or propofol has a higher likelihood of
variability do not preclude the diagnosis. aborting the status epilepticus.
Keywords: CNS; Diagnoses; Brain death; Basic physi- Keywords: CNS; Diagnoses; Seizures and status epilep-
ology; CNS; Brain death; CNS; Diagnostic modalities; ticus; CNS; Management strategies; Anticonvulsants
Nuclear medicine studies

R E F E R E NC E S
R E F E R E NC E S
Chokshi R, Openshaw J, Mehta N, Mohler E. Purple glove syn-
Bonetti MG, Ciritella P, Valle G, Perrone E. 99mTc HM-​PAO brain drome following intravenous phenytoin administration. Vasc Med
perfusion SPECT in brain death. Neuroradiology 1995;37(5):365. 2007;12:29–​31.
Wijdicks EF, Varelas PN, Gronseth GS et al. Evidence-​based guideline Glauser T, Shinnar S, Gloss D et al. Evidence-​based guideline: treat-
update: determining brain death in adults. A report of the Quality ment of convulsive status epilepticus in children and adults: a re-
Standards Subcommittee of the American Academy of Neurology. port of the guideline committee of the American epilepsy society.
Neurology 2010;74:1911–​1918. Epilepsy Currents 2016;16:48–​61.

5. ANSWER: D 6. ANSWER: D

Status epilepticus is defined as a seizure duration of greater Antibiotics to cover both bacterial meningitis and herpes
than 5 minutes or recurrent seizures without return to base- encephalitis are indicated. Ceftriaxone would cover the
line. Benzodiazepines, including midazolam (IV or IM) most likely bacterial agents (Streptococcus pneumoniae,
and lorazepam (IV), have the highest efficacy and are thus Haemophilus influenzae, and Neisseria meningitidis),
first-​line agents to arrest a seizure. Phenytoin is an appro- while vancomycin would cover beta-​ lactam-​
resistant
priate second-​line agent. Phenytoin can cause hypotension pneumococcus. Acyclovir would cover herpes encepha-
if infused too quickly and also has the risk for skin necrosis litis. Ampicillin would be added in immunocompromised
if the infusion infiltrates, a condition known as purple-​ or elderly patients or to cover Listeria monocytogenes.
glove syndrome. For these reasons, a recent guideline has Additionally, it is appropriate to include dexamethasone
recommended fosphenytoin, a prodrug of phenytoin, if until pneumococcal meningitis is ruled out because this
available because it can be infused rapidly. Fosphenytoin is may improve mortality and reduce neurological sequalae.

1. Ce n t r a l Ne rvo u s  S y s t e m • 9
Glucocorticoids should be administered shortly before anticonvulsants may lead to worse cognitive outcomes,
(or at the same time as) antibiotics because this approach although these studies were performed with phenytoin.
has been shown to reduce unfavorable outcomes. It is It should be noted that generalized status epilepticus
hypothesized that glucocorticoid administration (usu- has an incidence of 0.2%, but nonconvulsive status epi-
ally dexamethasone) reduces cerebral edema as well as lepticus occurs 31% of the time when SAH patients have
cytokine levels in the CSF. A lumbar puncture should stupor or coma; such seizures are associated with poor
be performed ideally within 6 hours of starting treat- neurological outcome. Nimodipine may improve neu-
ment in order to improve yield from cultures. A diag- rological outcomes and reduce the incidence of cerebral
nosis on the basis of the CSF profile can still be made infarctions in patients with aneurysmal SAH but does
if the lumbar puncture is delayed more than 6 hours but not reduce the actual rate of vasospasm. Nimodipine is
may yield less useful information, especially in cases of normally administered in doses of 60 mg every 4 hours
meningococcal meningitis. While a CT scan was appro- and can be given less frequently in smaller doses when
priate in this patient, it is not necessary in most patients hypotension is seen after administration. The most im-
and if performed often leads to an unnecessary delay in portant first step in a patient with SAH is to prevent an-
treatment, as would waiting for results of the lumbar eurysmal rebleeding. This is done by surgical clipping or
puncture. Continuous EEG monitoring should be ap- endovascular coiling. There is no clear evidence that dex-
plied because the patient could be having subclinical amethasone is beneficial.
events; however, starting treatment for the likely infec-
Keywords: CNS; Diagnoses; Stroke; Hemorrhagic (SAH);
tion is of utmost importance. The advantage of titrating
Diagnostic modalities; Other imaging (e.g., CTA)
sedation to a suppression-​burst pattern if the patient is
no longer seizing is unclear and thus would not be the
most appropriate next step in this patient. The head CT
R E F E R E NC E S
shown is normal, and while an MRI would likely assist
with diagnosis and prognosis, it would be the last step in Diringer MN, Bleck TP, Claude Hemphill J 3rd et al. Critical care
the management of this patient. management of patients following aneurysmal subarachnoid
hemorrhage: recommendations from the Neurocritical Care
Keywords: CNS; Diagnoses; Infectious; Encephalitis/​ Society’s Multidisciplinary Consensus Conference. Neurocrit Care
meningitis; CNS; Diagnostic modalities; EEG; CNS; 2011;15:211–​240.
Diagnostic modalities; Lumbar puncture; CNS; Dorhout Mees S, Rinkel GJE, Feigin VL et al. Calcium antagonists for
aneurysmal subarachnoid haemorrhage. Cochrane Database Syst Rev
Management strategies; Antimicrobials 2007;(3):CD000277.
Feigin VL, Anderson N, Rinkel GJE et al. Corticosteroids for an-
eurysmal subarachnoid haemorrhage and primary intracerebral
R E F E R E NC E haemorrhage. Cochrane Database Syst Rev 2005;(3):CD004583.
Kelliny M, Maeder P, Binaghi S et al. Cerebral aneurysm exclusion by
CT angiography based on subarachnoid hemorrhage pattern: a ret-
Hasbun R, Abrahams J, Jekel J, Quagliarelllo VJ. Computed tomog-
rospective study. BMC Neurol 2018;11: 8.
raphy of the head before lumbar puncture in adults with suspected
meningitis. N Engl J Med 2001;345:1727.

8. ANSWER: C
7. ANSWER: B
The ASPECTS score was used to predict outcome with
The patient has spontaneous subarachnoid hemorrhage thrombolytic use and demonstrated improved outcomes in
(SAH), which is most commonly caused by a ruptured patients with scores of 8 or higher. Patients with “wake-​up
aneurysm. SAH affects nearly 30,000 patients in the stroke” such as this one often present outside of the accept-
United States each year and has a mortality rate of able window for administration of IV thrombolytics (up to
around 45%. CT angiography of the brain will assist 4.5 hours from last seen normal). This does not, however,
both in accurate diagnosis and surgical planning if an an- exclude them from receiving treatment for their stroke by
eurysm is found. The yield of CT angiography in aneu- endovascular modalities, and the ASPECT score is one
rysmal detection is approximately 95% when compared modality that has been used in selecting patients who may
with digital subtraction angiography. This makes it a have favorable outcome with mechanical thrombectomy.
quick and important step in the workup before surgical A recent study known as the DAWN trial demonstrated
interventions. Although seizure prophylaxis is com- that mechanical thrombectomy improves outcome in
monly used for patients with SAH, there are no studies patients presenting 6 to 24 hours from when they were
suggesting that it improves outcomes. Furthermore, there last seen normal who still have a mismatch between clin-
is evidence demonstrating that long-​term treatment with ical deficits and infarct volume. In this case, the patient’s

10 • A n e s t h e s i o l o g y C r i t i c a l Ca r e B oa r d  Re v i e w