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OXFORD MEDICAL PUBLICATIONS

Vascular Anaesthesia
Oxford Specialist Handbooks published and forthcoming
General Oxford Specialist Handbooks Oxford Specialist Handbooks
A Resuscitation Room Guide in Oncology
Addiction Medicine Practical Management of Complex
Day Case Surgery Cancer Pain
Perioperative Medicine, 2e Oxford Specialist Handbooks
Pharmaceutical Medicine in Paediatrics
Postoperative Complications, 2e
Renal Transplantation Paediatric Dermatology
Paediatric Endocrinology and
Oxford Specialist Handbooks Diabetes
in Anaesthesia Paediatric Gastroenterology,
Anaesthesia for Medical and Surgical Hepatology, and Nutrition
Emergencies Paediatric Haematology and
Cardiac Anaesthesia Oncology
Neuroanaesthesia Paediatric Intensive Care
Obstetric Anaesthesia Paediatric Nephrology, 2e
Ophthalmic Anaesthesia Paediatric Neurology, 2e
Paediatric Anaesthesia Paediatric Radiology
Regional Anaesthesia, Stimulation and Paediatric Respiratory Medicine
Ultrasound Techniques Paediatric Rheumatology
Thoracic Anaesthesia Oxford Specialist Handbooks
Vascular Anaesthesia in Pain Medicine
Oxford Specialist Handbooks Spinal Interventions in Pain
in Cardiology Management
Adult Congenital Heart Disease Oxford Specialist Handbooks
Cardiac Catheterization and Coronary in Psychiatry
Intervention
Cardiac Electrophysiology and Catheter Child and Adolescent Psychiatry
Ablation Forensic Psychiatry
Cardiovascular Computed Tomography Old Age Psychiatry
Cardiovascular Magnetic Resonance Oxford Specialist Handbooks
Echocardiography, 2e in Radiology
Fetal Cardiology Interventional Radiology
Heart Failure Musculoskeletal Imaging
Hypertension Pulmonary Imaging
Inherited Cardiac Disease Thoracic Imaging
Nuclear Cardiology
Pacemakers and ICDs Oxford Specialist Handbooks
Pulmonary Hypertension in Surgery
Valvular Heart Disease Cardiothoracic Surgery, 2e
Colorectal Surgery
Oxford Specialist Handbooks Gastric and Oesophageal Surgery
in Critical Care Hand Surgery
Advanced Respiratory Critical Care Hepatopancreatobiliary Surgery
Cardiothoracic Critical Care Neurosurgery
Oxford Specialist Handbooks Operative Surgery, 2e
in End of Life Care Oral and Maxillofacial Surgery
End of Life Care in Cardiology Otolaryngology and Head and Neck
End of Life Care in Dementia Surgery
End of Life Care in Nephrology Paediatric Surgery
End of Life Care in Respiratory Disease Plastic and Reconstructive Surgery
End of Life in the Intensive Care Unit Surgical Oncology
Urological Surgery
Oxford Specialist Handbooks Vascular Surgery
in Neurology
Epilepsy
Parkinson’s Disease and Other Movement
Disorders
Stroke Medicine
Oxford Specialist Handbooks
in Anaesthesia
Vascular Anaesthesia
Edited by

Dr Jonathan P. Thompson
Senior Lecturer in Anaesthesia and Critical Care
Department of Cardiovascular Sciences
University of Leicester
and
Honorary Consultant in Anaesthesia and Critical Care
University Hospitals of Leicester NHS Trust
Leicester
UK

Dr Simon J. Howell
Senior Lecturer in Anaesthesia
Biomedical and Clinical Sciences
University of Leeds
Leeds
UK

Dr Richard J. Telford
Consultant Anaesthetist
Royal Devon and Exeter Foundation NHS Trust
Exeter
UK

1
3
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First edition published in 204
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 v

Foreword

Anaesthesia for vascular surgery is possibly one of the most challenging fields
of our clinical practice. By virtue of their primary surgical pathology and its
associated risk factors, patients have a very high incidence of co-morbidities,
particularly hypertension, diabetes, cardiac, cerebrovascular, renal and respira-
tory disease. Advances in anaesthesia must also keep abreast of surgical and
graft developments which have led to a dramatic increase in the use of endo-
vascular stents such that they now constitute the majority of surgery. In turn,
however, this has resulted in the presentation of patients previously regarded
as medically unsuitable for surgery since the perturbations of surgical trauma
are markedly reduced. At the same time, open repair of aneurysmal and sten-
otic disease is still an option for some and may be unavoidable for anatomical
reasons in others. Patients with complex pathology may require hybrid proce-
dures which entail an open surgical component in addition to graft placement.
Further still, correction of graft complications and leaks may necessitate more
complicated open surgery. Hence the traditional skills for handling clamping
and unclamping of the aorta and major haemodynamic disturbance must be
preserved. Perioperative organ protective is pivotal to optimising patient out-
come. There is also a need to protect the kidney from ischaemia and contrast
induced nephropathy, the spinal cord during open or endovascular aortic sur-
gery, the brain in carotid surgery and the heart in all surgery. An understand-
ing of appropriate monitoring of these organs, techniques for protection both
pharmacologic and mechanical, appropriate use of anaesthetic and other drugs
and amelioration of ischaemia-reperfusion injury is essential. Knowledge of
regional anaesthesia, peripheral nerve blocks and sedation techniques is also
important for anaesthesia and analgesia in many of these patients. A successful
outcome is only as “strong as the weakest link” and both preoperative prepara-
tion and postoperative care are integral facets. In negotiating all these aspects
of patient care, vascular anaesthetists can truly be considered model periop-
erative physicians.
Recent developments in both surgery and perioperative care make this
an apposite time to produce this handbook and the editors, all very expe-
rienced and authoritative in this field, have collected an eclectic collection
of clinicians to present a clear and easy to read overview of this challenging
specialty. True to its status as a handbook, chapters are succinct, easy to
read and search with appropriate use of bullet points and avoidance of
verbosity. An excellent companion for the busy clinician both in training and
those seasoned in practice.
Professor Michael G. Irwin MB ChB MD DA FRCA FANZCA FHKAM
Head, Dept of Anaesthesiology
University of Hong Kong
Chief of Service
Queen Mary Hospital / HKU Shenzhen Hospital
K424, Queen Mary Hospital
Pokfulam Road
Hong Kong
 vii

Preface

The management of the patient with vascular disease is evolving rapidly.

Population screening for vascular disease has been introduced and its effects
on practice are being evaluated. The management of associated medical
conditions is also changing. New guidelines have been published for the
management of acute coronary syndromes, stable coronary heart disease,
diabetes, implantable pacemakers, and defibrillators. Decisions regarding
surgical intervention and anaesthetic management remain complicated due
to the co-existence of vascular disease at other sites or other co-morbid
conditions, but have been aided by improved approaches to preopera-
tive risk assessment, perioperative monitoring and postoperative care.
Radiological expertise and procedures are increasingly used to treat condi-
tions previously treated by open surgery, such as aortic aneurysms, occlu-
sive lower limb arterial disease, or carotid disease. Priorities have evolved
so that carotid endarterectomy is now performed as an urgent procedure
after TIA or minor stroke. In addition, the pace of change over the last two
decades has made it difficult for those involved in the care of the vascular
surgical patient to remain updated with recent progress in perioperative
management. The literature describes an increasing array of techniques for
preoperative investigation and monitoring during anaesthesia, with dispa-
rate evidence and recommendations. When faced in clinical practice with
a patient with vascular disease, the anaesthetist needs to know what to do
and when to do it, as well as what not to do and why.
In this new addition to the Oxford Specialist Handbooks series we have
tried to produce a concise volume that will enable the vascular practi-
tioner (in its broadest sense) to adopt a practical, current, evidence-based
approach to all aspects of perioperative care for the patient with vascular
disease, particularly those undergoing interventional radiological, diagnos-
tic, and surgical procedures. Although primarily aimed at anaesthetists, we
hope the book will be relevant to vascular nurses, theatre practitioners,
trainees in Intensive Care Medicine and possibly even vascular surgeons.
Our approach has been to combine essential background knowledge with
useful, clinically relevant sections on management, so the book can be used
to enhance awareness of potential problems, as an aid to revision, but also
as a practical ‘How to do it’ guide for patient management.
The book is divided into sections and starts with what we consider
essential details on the epidemiology of vascular disease, followed by rel-
evant anatomy and pathophysiology. Good preoperative evaluation is vital
to a successful outcome, but the vascular anaesthetist must also be aware
of the processes involved in complex surgical decision-making; these are
detailed together. Current approaches to risk assessment and risk reduction
are emphasized, including advice on how to set up and run a preoperative
assessment clinic. In the sections on medical management of common co-
existing diseases, monitoring, practical procedures and common regional
anaesthetic techniques, we have tried to summarize what the practitioner
needs to know for everyday practice, based on the most recent data.
viii PREFACE

Radiologists are taking an ever greater role in the care of the vascular
patient; this can be a difficult and complex area of practice and we have
deliberately included a section dedicated to radiological management. The
final three sections are intended to be a convenient guide to the manage-
ment of different vascular procedures and complications during and after
surgery. They are intended to be used as an ‘aide-memoire’ for periopera-
tive care and include guidance on the management of common postopera-
tive problems.
The contributors are all experienced clinicians actively caring for patients
with vascular diseases. They are predominantly consultant anaesthetists
with a special interest in vascular anaesthesia, but include vascular surgeons,
radiologists, cardiologists and other physicians. We hope this book will fulfil
its aims and be useful, relevant and helpful in the day-to-day management
of the vascular surgical patient.
Jonathan P. Thompson
Simon J. Howell
Richard J. Telford
March 203
 ix

Contents

Symbols and Abbreviations╇ x

Contributors╇ xx

 Epidemiology of vascular disease ╇╇

2 Anatomy physiology and responses to
vascular surgery ╇25
3 Evaluation of the vascular surgical patient ╇85
4 Management of specific medical conditions
and medications 59
5 Principles of perioperative care 22
6 Practical procedures, regional anaesthesia,
and pain management in vascular surgery 25
7 Monitoring of the vascular patient 3
8 Anaesthesia for vascular radiology 333
9 Management of patients undergoing specific
elective vascular procedures 349
0 Emergencies in vascular surgery 447
 Post-operative management 467

Index╇ 525
x

Symbols and
Abbreviations
° primary
2° secondary
< less than
> more than
+ve positive
–ve negative
AAA abdominal aortic aneurysms
AbCS abdominal compartment syndrome
ABG arterial blood gases
ABPI ankle brachial pressure index
ACC American College of Cardiology
ACE angiotensin-converting enzyme
AcLI acute limb ischaemia
ACS acute coronary syndrome
ACST Asymptomatic Carotid Surgery Trial
ACT activated clotting times
ADH anti-diuretic hormone
ADP adenosine di-phosphate
AF atrial fibrillation
AHA American Heart Association
AKA above knee amputations
AKI acute kidney injury
ALI acute lung injury
ANH acute normovolaemic haemodilution
ANP atrial natriuretic peptide
AP anteroposterior
APC abnormalities of protein C
APL adjustable pressure limiting
APTT activated partial thromboplastin time
APTTR activated partial thromboplastin time ratio
ARB angiotensin II receptor blocker
ARDS adult respiratory distress syndrome
ARR absolute risk reduction
AT angiotensin
 SYMBOLS AND ABBREVIATIONS xi

ATD adult therapeutic dose

ATh anaerobic threshold
AU aggregation units
AUC area under the concentration curve
AUI aorto-uniiliac
AV atrioventricular
AVM arteriovenous malformations
AXC aortic cross-clamp
BAE bronchial artery embolization
BAEP brainstem auditory-evoked responses
bd twice daily
BioMS biomedical scientist
BIS bispectral index
Biv-CRT biventricular cardiac resynchronization therapy
BKA below knee amputations
BMI body mass index
BMS bare metal stents
BNP brain natriuretic peptide
BP blood pressure
BPEG British Pacing and Electrophysiology Group
CABG coronary artery bypass grafting
CAD coronary artery disease
CAS carotid angioplasty with stenting
CBF cerebral blood flow
CCB calcium channel blocker
CCU critical care unit
CEA carotid endarterectomy
CePB cervical plexus block
CFAM cerebral function analysing monitor
CGRP calcitonin gene-related peptide
CH cerebral hyperperfusion
CHS cerebral hyperperfusion syndrome
CIN contrast-induced nephropathy
CKD chronic kidney disease
CLI critical limb ischaemia
CMI chronic mesenteric ischaemia
CMV cytomegalovirus
CNS central nervous system
xii SYMBOLS AND ABBREVIATIONS

CO cardiac output
CoNS coagulase –ve staphylococci
COPD chronic obstructive pulmonary disease
CPAP continuous positive airways pressure
CPB cardiopulmonary bypass
CPD continuous peritoneal dialysis
CPET cardiopulmonary exercise testing
CPI Customized Probability Index
CPP cerebral perfusion pressure
CPX cardiopulmonary exercise testing
CSA cross-sectional area
CSE combined-spinal epidural
CSF cerebrospinal fluid
CSpA continuous spinal anaesthesia
CsT closure time
CT computed tomogram
CTA CT angiography
cTN cardiac troponin
CVA central venous access
CVC central venous catheter
CVD cerebrovascular disease
CVI chronic venous insufficiency
CVP central venous pressure
CVR cerebral vascular resistance
CVVH continuous veno-venous haemofiltration
CXR chest X-ray
DBP diastolic blood pressure
DCT distal convoluted tubule
DES drug-eluting stents
DHCA deep hypothermic cardiac arrest
DLT double lumen tube
DM diabetes mellitus
DNIC diffuse noxious inhibitory control
DPG diphosphoglycerate
DRG dorsal root ganglia
DSE dobutamine stress echocardiography
DVT deep vein thrombosis
ECG electrocardiogram
EEG electroencephalogram
 SYMBOLS AND ABBREVIATIONS xiii

EET eicosatrienoic acids

EF ejection fraction
eGFR estimated glomerular filtration rate
EMG electromyogram
eNOS endothelial NO synthase
EPO erythropoietin
ESRD end-stage renal disease
ESRF end stage renal failure
ETS endoscopic thoracic sympathectomy
EVAR endovascular aneurysm repair
EVLA endovenous laser ablation
EVLT endovenous laser treatment
EWS Early Warning Score
FAST focused assessment with sonography in trauma
FBC full blood count
FDP fibrin degradation products
FEV forced expiratory volume
FFP fresh frozen plasma
FMR functional mitral regurgitation
FPG fasting plasma glucose
FRC functional residual capacity
FTc flow time corrected for heart rate
G&S group & save
GA general anaesthesia/anaesthetic
GCS Glasgow Coma Score
GDT goal-directed therapy
GFR glomerular filtration rate
GI gastrointestinal
GIB gastrointestinal bleeding
GP general practitioner
GRACE Global Registry of Acute Coronary Events
GTN glyceryl trinitrate
Hct haematocrit
Hcy homocysteine
HDU high dependency unit
HF heart failure
HHcy hyperhomocysteinaemia
HIT heparin-induced thrombocytopenia
HITT heparin-induced thrombocytopenia and thrombosis
xiv SYMBOLS AND ABBREVIATIONS

HME heat and moisture exchanger

hsCRP high sensitivity C-reactive protein
IABP invasive arterial blood pressure
IAH intra- abdominal hypertension
IAP intra-abdominal pressure
IBP intra-arterial blood pressure
IC intermittent claudication
ICD implantable cardiac defibrillators
ICP intracranial pressure
ICS intracoronary stents
ICU intensive care unit
IFG impaired fasting glycaemia
IGT impaired glucose tolerance
IHD ischaemic heart disease
IIA internal iliac artery
IJV internal jugular vein
iNOS inducible nitric oxide synthase
INR international normalized ratio
IOCS intraoperative cell salvage
IPPV intermittent positive pressure ventilation
IR interventional radiology
ISWT incremental shuttle walking test
ITU intensive therapy unit
IV intravenous
IVC inferior vena cava
JVP jugular venous pressure
KATP adenosine triphosphate (ATP)-sensitive potassium
(K+) channel
KDIGO Kidney Disease: Improving Global Outcomes
LA local anaesthesia/anaesthetic
LBBB left bundle branch block
LCA left coronary artery
LDL low density lipoprotein
LFT liver function test
LiDCO lithium indicator dilution
LIJ left internal jugular
LLA lower limb amputation
LLL left lower lobe
LMA laryngeal mask airway
 SYMBOLS AND ABBREVIATIONS xv

LMWH low molecular weight heparin

LUL left upper lobe
LV left ventricle/ventricular
LVEDP left ventricular end-diastolic pressure
LVEF left ventricular ejection fraction
LVF left ventricular failure
MA mean acceleration
MAC minimum alveolar concentration
MAP mean arterial pressure
MASS Multicentre Aneurysm Screening Study
MCA middle cerebral artery
MCF maximum clot firmness
MDRD modification of diet in renal disease
MDT multidisciplinary team
MEP motor-evoked potential
MET metabolic equivalent
MEWS Modified Early Warning Score
MI myocardial infarction
MR modified release
MRA magnetic resonance angiography
MRI magnetic resonance imaging
MRSA meticillin-resistant Staphylococcus aureus
MTPP mitochondrial transition permeability pore
NANC non-adrenergic non-cholinergic
NASSE North American Society of Pacing and Electrophysiology
NGAL Neutrophil gelatinase-associated lipocalin
NGT nasogastric tube
NHANES National Health and Nutrition Examination Survey
NIBP non-invasive blood pressure
NICE National Institute of Health and Care Excellence
NIRS near infrared spectroscopy
NMB neuromuscular blockers
NMDA N-methyl-d-aspartate
nNOS neural nitric oxide synthase
NNT numbers needed to treat
NO nitric oxide
NPV negative predictive value
NSAID non-steroidal anti-inflammatory drug
NSTEMI non-ST segment elevation myocardial infarction
xvi SYMBOLS AND ABBREVIATIONS

NT-proBNP N-terminal pro-BNP

NVD national vascular database
NYHA New York Heart Association
ODM oesophageal Doppler monitoring
ODP operating department practitioner
OGTT oral glucose tolerance test
OIH opioid-induced hyperalgesia
OLV one-lung ventilation
PA pulmonary artery
PAC pulmonary artery catheter
PACU post-anaesthesia care unit
PAD peripheral arterial disease
PAOP pulmonary artery occlusion pressure
PbrO2 brain tissue O2 partial pressure
PCA patient-controlled analgesia
PCC prothrombin complex concentrate
PCEA patient-controlled epidural analgesia
PCI percutaneous coronary intervention
PCR polymerase chain reaction
PCT proximal convoluted tubule
PCV packed cell volume
PCWP pulmonary capillary wedge pressure
PE pulmonary embolism
PEEP positive end expiratory pressure
PES post-embolization syndrome
PICC peripherally-inserted central catheters
PIP peak inspiratory pressure
PKCε proteinkinase C espsilon
PLP phantom limb pain
po by mouth
POC point of care
POCD post-operative cognitive dysfunction
POISE perioperative ischaemia evaluation
PONV post-operative nausea and vomiting
PPC post-operative pulmonary complication
PPV positive predictive value
PreAD preoperative autologous donation
PSIS posterior superior iliac spine
PT prothrombin time
 SYMBOLS AND ABBREVIATIONS xvii

PTFE polytetrafluoroethylene
PTH parathyroid hormone
PTT partial thromboplastin time
PuPV pulse pressure variation
PV peak velocity
PVC premature ventricular contractions
PVD peripheral vascular disease
PVGI prosthetic vascular graft infection
PVR peripheral vascular reconstruction
RA regional anaesthesia/anaesthetic
RAAA ruptured open abdominal aortic aneurysm repair
RAAS renin-angiotensin-aldosterone system
RBC red blood cells
RBF renal blood flow
RCA right coronary artery
RCRI revised cardiac risk index
RCT randomized controlled trial
RFA radiofrequency ablation
RIJ right internal jugular
RLL right lower lobe
RMB right main bronchus
RML right middle lobe
RMP resting membrane potential
ROC receiver operating characteristic
RPF renal plasma flow
RR respiratory rate
RRR relative risk reduction
RRT renal replacement therapy
r-TEG rapid-TEG
rtPA recombinant tissue plasminogen activator
RUL right upper lobe
RV right ventricle
SA sino-atrial
SACU surgical acute care unit
SAG-M saline, adenine, glucose, and mannitol
SAM S-adenosylmethionine
SBP systolic blood pressure
sc subcutaneous
SCM sternocleidomastoid
xviii SYMBOLS AND ABBREVIATIONS

ScO2 calculated O2 saturation

SCPP spinal cord perfusion pressure
SCV subclavian vein
SFA superficial femoral artery
SHO senior house officer
SIRS systemic inflammatory response
SPECT single photon emission computed tomographic
SpO2 oxygen saturation
SpR specialist registrar
SPV systolic pressure variation
SR sarcoplasmic reticulum
SSEP somatosensory-evoked potentials
STEMI ST elevation myocardial infarction
SV stroke volume
SVC superior vena cava
SVR systemic vascular resistance
SVT supraventricular tachycardia
SVV stroke volume variation
SWMA systolic wall motion abnormalities
TAA thoracic aortic aneurysm
TAAA thoraco-abdominal aortic aneurysm
TAI thoracic aorta injury
TAP transversus abdominis plane
TASC TransAtlantic Inter-society Consensus
TAVI transcatheter aortic valve implantation
TCD transcranial Doppler
TCI target-controlled infusion
TEA thoracic epidural analgesia
TEDS thrombo-embolic stockings
TEVAR thoracic endovascular aneurysm repair
TIA transient ischaemic attacks
TIPPS trans-hepatic porto-systemic shunt
TIPS trans-jugular porto-systemic shunts
TIVA total intravenous anaesthesia
TIVAD totally in-dwelling venous access devices
TOE transoesophageal echocardiography
TOS thoracic outlet syndrome
TP threshold potential
TPN total parenteral nutrition
 SYMBOLS AND ABBREVIATIONS xix

TRP transient receptor potential

TT thrombin time
TTE transthoracic echocardiography
TV tidal volume
U&E urea & electrolytes
UFH unfractionated heparin
UGRA ultrasound-guided regional anaesthesia
UKSAT UK Small Aneurysm Trial
UO urine output
VASGBI Vascular Anaesthesia Society of Great Britain and Ireland
vCJD variant Creutzfeldt–Jacob disease
VF ventricular fibrillation
VIB vertical infraclavicular block
VRIII variable rate intravenous insulin infusion
VT ventricular tachycardia
VTI velocity time index
VV varicose veins
vWF von Willebrand factor
WCC white cell count
WMSI wall motion score index
XM cross-match
xx

Contributors

Andrew R. Bodenham Pierre Foex

Consultant in Anaesthesia and Emeritus Nuffield Professor of
Intensive Care Medicine Anaesthetics
Department of Anaesthesia, Nuffield Division of Anaesthetics,
Leeds General Infirmary The John Radcliffe Hospital
Leeds, UK Oxford, UK
Matthew J. Bown Fiona Gamlin
Senior Lecturer in Vascular Surgery Consultant Anaesthetist
Department of Cardiovascular Department of Anaesthesia,
Sciences, Leicester Royal St James’s University Hospital
Infirmary Leicester, UK Leeds, UK
Edward Choke William Harrop-Griffiths
Clinical Lecturer in Vascular Consultant Anaesthetist
Surgery Department of Anaesthesia,
Department of Cardiovascular Imperial College Healthcare NHS
Sciences, University of Leicester Trust, St Mary’s Hospital
Leicester, UK London, UK
Michael Cross Simon J. Howell
Consultant Anaesthetist Senior Lecturer in Anaesthesia
Department of Anaesthesia, Leeds Institute of Biomedical and
Leeds General Infirmary Clinical Sciences, University of Leeds
Leeds, UK Leeds, UK
Gerard Danjoux Phil Jackson
Consultant in Anaesthesia and Consultant in Anaesthesia and
Sleep Medicine, Intensive Care Medicine
Department of Anaesthesia, Department of Anaesthesia, Leeds
South Tees NHS Foundation General Infirmary
Trust Leeds, UK
Middlesbrough, UK
Jeremy A. Langton
Visiting Professor Consultant Anaesthetist
Teesside University Department of Anaesthesia,
Middlesbrough, UK Plymouth Hospitals NHS Trust
Neil Flint Plymouth, UK
Consultant in Critical Care & Simon Logan
Anaesthesia Consultant Neuro-vascular
Department of Anaesthesia, Anaesthetist
Critical Care and Pain Department of Anaesthesia, Pain
Management, Leicester Royal Medicine and Intensive Care,
Infirmary Leicester, UK University Hospital of Wales
Cardiff, UK
 CONTRIBUTORS xxi

Andy Lumb Adam Pichel

Consultant Anaesthetist Consultant in Anaesthesia
Department of Anaesthesia, Department of Anaesthesia
St James’s University Hospital Manchester Royal Infirmary
Leeds, UK Manchester, UK
Sue Mallett Mark Salmon
Consultant Anaesthetist Specialty Registrar in Anaesthesia
Department of Anaesthesia, Department of Anaesthesia,
Royal Free London St George’s Healthcare
London, UK NHS Trust
London, UK
Graeme A. McLeod
Consultant and Honorary Clinical Robert J. Sapsford
Reader Consultant Cardiologist
Institute of Academic Anaesthesia Department of Cardiology, Leeds
Dundee, UK General Infirmary
Leeds, UK
Directorate of Neuroscience
University of Dundee Robert Sayers
Dundee, UK Professor of Vascular Surgery
Simon McPherson Department of Cardiovascular
Sciences, University of Leicester
Consultant Vascular and Leicester, UK
Interventional Radiologist
Department of Radiology, Leeds Christopher Snowden
Teaching Hospitals NHS Trust Consultant Anaesthetist and Senior
Leeds, UK Lecturer
Peter McQuillan Department of Perioperative
and Critical Care Medicine,
Consultant in Critical Care & Freeman Hospital, Newcastle
Anaesthesia Hospitals NHS Trust & Institute
Departments of Critical Care and of Cellular Medicine, Newcastle
Anaesthesia, Queen Alexandra University
Hospital Newcastle, UK
Portsmouth, UK
Michael Swart
Iain Moppett
Consultant in Anaesthesia and
Clinical Associate Professor Critical Care
Faculty of Medicine & Health Department of Anaesthesia and
Sciences, Division of Anaesthesia Perioperative Medicine, Torbay
& Intensive Care, University of Hospital
Nottingham Torquay, UK
Nottingham, UK
Richard J. Telford
Marina S. Morgan
Consultant Anaesthetist
Consultant Medical Microbiologist Department of Anaesthesia
Medical Microbiology, Royal Devon Royal Devon & Exeter Hospital
& Exeter Hospital NHS Foundation NHS Foundation Trust
Trust Exeter, UK
Exeter, UK
xxii CONTRIBUTORS

Dafydd Thomas Max Troxler

Consultant in Anaesthesia and Consultant Vascular Surgeon
Intensive Care Medicine Leeds Vascular Institute, Leeds
General and Cardiac Intensive Teaching Hospitals NHS Trust
Care Unit, Morriston Hospital Leeds, UK
Swansea, UK
J-P van Besouw
Jonathan P. Thompson Consultant Anaesthetist
Senior Lecturer and Honorary Department of Anaesthesia, St
Consultant in Anaesthesia & George’s Healthcare NHS Trust
Critical Care London, UK
Department of Cardiovascular
Sciences, University of Leicester, President
Leicester Royal Infirmary Leicester, Royal College of Anaesthetists
UK London, UK

Edward Todman Morné Wolmarans

Specialty Registrar in Anaesthesia Consultant Anaesthetist
Department of Anaesthesia, Department of Anaesthesia,
Imperial College Healthcare NHS Norfolk & Norwich University
Trust, St Mary’s Hospital NHS Foundation Trust
London, UK Norwich, UK
 Chapter  1

Epidemiology of
vascular disease

Incidence, prevalence, and risk factors of vascular disease 2

Screening for vascular disease 
Primary and secondary prevention of vascular disease 4
Vascular databases 20
2 CHAPTER  Epidemiology of vascular disease

Incidence, prevalence, and risk factors

of vascular disease
Occlusive disease
Occlusive disease of the lower limbs and carotid artery disease are aspects
of the atherosclerotic disease that is widespread in the populations of
developed countries. The true incidence of atherosclerosis itself is diffi-
cult to determine because it is an asymptomatic disease in the majority of
patients. Post-mortem studies in humans who died from non-cardiac disease
revealed early morphological signs of aortic and coronary atherosclerosis
that ranged widely from 50 to 00% of young people aged below 35yrs.
Risk factors for occlusive atherosclerotic disease include:
• Smoking.
• Increasing age.
• Hypertension.
• Diabetes.
• Previous cardiovascular disease.
• Hypercholesterolaemia.
• Hypertriglyceridaemia.
• Physical inactivity.
Diabetes is a particularly important risk factor for atherosclerosis. Post-
mortem studies reveal that nearly 75% of diabetic individuals who did
not have clinical coronary artery disease (CAD) had high grade coronary
atherosclerosis.
It should be noted that atherosclerosis is a global disease of the circulation.
• In patients (without previously recognized extracranial cerebrovascular
disease) who undergo elective peripheral vascular reconstruction,
approximately 3% will have incidental asymptomatic carotid stenosis of
more than 50%.
• Severe, potentially surgically-correctable CAD will be present in 24–29%
of patients who undergo elective peripheral vascular reconstruction.
• Patients with asymptomatic peripheral arterial disease (PAD) have a
much higher risk of systemic cardiovascular events than the general
population.
• The Edinburgh Artery Study revealed that the incidence and mortality
from acute myocardial infarction was increased in the presence of PAD,
and was the same whether PAD patients were symptomatic or not.
This highlights the high incidence of significant atherosclerotic disease in ter-
ritories other than that for which surgery is required in vascular surgery
patients. These synchronous atherosclerotic diseases may need prior opti-
mization to achieve best possible perioperative outcomes.
 INCIDENCE, PREVALENCE, AND RISK FACTORS 3

Peripheral arterial disease

PAD (atherosclerotic disease affecting the lower legs) is very common.
• It is asymptomatic in the majority of patients.
• If symptomatic, the first presentation is usually with intermittent
claudication (pain in the leg on walking).
• In claudicants, over a 5-yr period:
• 50% will remain relatively stable.
• 25% will get worse, 5% will undergo revascularization (angioplasty or
surgery), and % will undergo amputation.
• Therefore, a minority will progress to critical limb ischaemia (CLI) when
the blood supply to the legs becomes further reduced with progression
of atherosclerosis or failure of collateralization of new blood vessels.
• A European Consensus document published in 990 defined CLI as rest
pain for >2 weeks, or ulceration/gangrene, and an ankle pressure of
<50mmHg, or toe pressure of <30mmHg.
Survey-based assessment of PAD epidemiology
Accurate assessment of the epidemiology of PAD is not straightforward
and is dependent on the sample group. Previous epidemiological studies,
which have focused on referrals to hospitals or workplace settings, are not
truly representative of the wider population.
• The Edinburgh Artery Study, which was a random cross-sectional
survey conducted on an age-stratified sample of men and women aged
55–74yrs selected from age–sex registers in ten general practices in
the city, is one of the largest and most reliable source of information
on the prevalence of PAD. In this study the prevalence of intermittent
claudication was 4.5%.
• The Scottish Heart Study reported a prevalence of intermittent
claudication of .% in subjects aged 40–59yrs.
• In the Limburg Study, the reported prevalence in their subjects aged
40–79yrs was between .4 and 6.%.
• In these population-based questionnaire studies, the prevalence of
intermittent claudication increased with age.
Ankle brachial pressure index or ultrasound based assessment of
PAD epidemiology
The technique used to establish the presence or absence of PAD is also an
important consideration when assessing the epidemiology of PAD.
• The prevalence of asymptomatic PAD as defined by ankle brachial
pressure index (ABPI) measurements less than 0.9 in the middle aged to
elderly population is about 7–5%.
• The PERART study of a Spanish primary care population that defined
peripheral vascular disease as ABPI <0.9 reported a PAD prevalence
of 7.6% (6.7–8.4%). The prevalence in males was 0.2% that in females
5.3%. In this study, regular walking or a BMI >25kg/m2 were protective.
• The National Health and Nutrition Examination Survey (NHANES,
999–2000) from the USA analysed data from 274 participants and
reported that the prevalence of PAD (defined as ABPI <0.9 in either
leg) was 4.3% in adults aged over 40yrs old. In those over 70yrs old, the
prevalence was 4.5%.
4 CHAPTER  Epidemiology of vascular disease

• However, if direct assessment of the femoral artery using ultrasound

was used, as in the British Regional Heart Study, 64% of subjects aged
56–77yrs had significant femoral atherosclerosis. Of these, only 0% of
these were symptomatic.
Approximately 70% of patients with PAD diagnosed on ABPI are asympto-
matic. The anaesthetist must remember that the patients who present for
surgical or radiological intervention are those with most severe disease—
they are a subset of a larger population whose condition could be man-
aged medically or which goes undetected. Many patients are managed in
the vascular clinic or in general practice with measures including blood pres-
sure (BP) control, glycaemic control, smoking cessation, and lipid lowering
therapy (in particular the use of statins).
The Vascular Society of Great Britain and Ireland carried out a prospec-
tive national survey of patients with critical lower limb ischaemia to estimate
the prevalence of critical lower limb ischaemia. The report revealed that the
extrapolated incidence of critical lower limb ischaemia in Great Britain and
Ireland was a total of 2,450 limbs in 20,000 patients in the population as a
whole, equating to a prevalence of  in 2500 of the population annually. Of
these 25% will undergo major amputations
Amputation
Amputation of lower limbs in patients with severe lower limb ischaemia
is indicated to achieve relief of pain or removal of gangrenous or necrotic
or severely ischaemic tissue. It can restore function and quality of life.
• About 5,000 lower limb amputations are carried out in the UK
every year, of which 48% are for amputation of toes and 7% for foot
amputations.
• Vascular causes account for >80% of all amputations in the UK.
• Diabetes is involved for 20–30% of these cases.
• Insulin-dependent diabetics are at a higher risk (6-fold) than non-insulin-
dependent diabetics.
• In patients referred to prosthetic centres in the UK, 52% were transtibial
(i.e. below knee) amputations and 38% were transfemoral (i.e. above
knee) amputations.
• 30% of vascular amputees will undergo amputation of the other leg
within 2yrs.
• The mortality of amputee patients is about 50% in 5yrs.
• The survival of amputees is lower in diabetics than non-diabetics.
• The incidence of amputation fell by about 27% from 980 to 990 due
to aggressive reconstruction policy and increased use of infra-inguinal
bypass operations.
Carotid artery disease
Stroke is a loss of cerebral function from a vascular cause lasting more
than 24h. About 80% of strokes are ischaemic and about 80% of ischaemic
strokes originate from the carotid territory.
• Annually about 20,000 people in the United Kingdom develop a stroke.
• 20–30% of these patients will die within a month.
 INCIDENCE, PREVALENCE, AND RISK FACTORS 5

• The incidence of a first ever stroke is 2.4/000, increasing with age.

• Stroke is responsible for 2% of UK deaths, and is the third commonest
cause of mortality after heart disease and cancer.
• It is also the single largest cause of severe disability in adults. There
are nearly  million people living with the consequences of stroke, and
a third of these patients have long-term disabilities. As a result, the
economic costs of stroke are enormous (7£7 billion/yr).
Transient ischaemic attacks (TIA) cause symptoms and signs lasting
less than 24h
• The annual incidence of TIA is 0.5/000.
• Each year approximately 2,000 patients in England and Wales (about
half of whom are greater than 70yrs old) consult a doctor for the first
time with a TIA.
• The incidence of TIAs increases sharply with age, from 0.9/000 in
those aged 55–64yrs to 2.6/000 for those aged 75–84yrs.
Carotid endarterectomy
In the UK, around 4500 carotid endarterectomies (CEA) are performed
each year to reduce the risk of stroke.
• CEA is indicated in symptomatic >50% carotid stenosis.
• CEA does not confer any benefit if the carotid artery is occluded or
nearly occluded (string sign).
• For asymptomatic stenosis, the Asymptomatic Carotid Surgery Trial
(ACST) reported that CEA for patients younger than 75yrs of age with
>60% stenosis reduced 0-yr stroke risks.
• Numbers needed to treat (NNT) to prevent any stroke at 5yrs are:
• Six for symptomatic 70–99% stenosis.
• Thirteen for symptomatic 50–69% stenosis.
• Nineteen for asymptomatic >60% stenosis.
• Asymptomatic carotid disease is a common condition that is usually
detected from incidental finding of a carotid bruit or as an investigation
of the contralateral side.
• About 4% of people over 45yrs old will have a carotid bruit and this
increases to 2% in people over 60yrs old.
• However, the presence or absence of a bruit or the quality of bruit
correlates poorly with the degree of carotid stenosis.
• In the population over 65yrs, the prevalence of 50–99% stenosis is
about 5–0%. This prevalence is increased in the presence of PAD
(2%) and hypertension (25%).
Chronic mesenteric ischaemia
• Chronic mesenteric ischaemia (CMI) is much more uncommon than
acute mesenteric ischaemia.
• CMI constitutes only 5% of all mesenteric ischaemia.
• The incidence of atherosclerotic lesions affecting the mesenteric arteries
in people more than 65yrs old is approximately 8%
6 CHAPTER  Epidemiology of vascular disease

Aneurysmal disease
Aneurysm is defined as an abnormal focal dilatation of a vessel, of greater
than 50% in diameter. Aneurysms that are considered within the remit of
vascular surgery are either aortic aneurysms or peripheral aneurysms (iliac,
popliteal, and femoral aneurysms). Aneurysms can be fusiform (cylindrical
dilatation of the whole vessel) or saccular (focal bulge arising from the side
of the vessel).
Abdominal aortic aneurysm
The normal diameter of the abdominal aorta is up to 2cm and dilatation
above 3cm is, therefore, generally considered to be aneurysmal.
Classification and risk factors
• 90% of abdominal aortic aneurysms (AAA) are infrarenal with the
remaining 0% being juxtarenal or suprarenal.
• Inflammatory AAAs, defined as thickened aneurysm wall with marked
peri-aneurysmal or retroperitoneal fibrosis and dense adhesions to
adjacent organs, represent 3–0% of all AAAs.
• AAAs are four times more common in men than women.
• The mean age for presentation is 65–70yrs.
• Risk factors for AAAs include smoking, male sex, increasing age,
hypertension, and presence of chronic obstructive pulmonary disease
(independent of smoking).
• AAAs are less common in diabetics. The reason for this is unclear.
Incidence and mortality
• Historically, the prevalence in men over the age of 60 is approximately
2–6% and its incidence was considered to be rising in the
developed world.
• However, recent evidence suggests that the AAA epidemic has stopped,
and its incidence and mortality is on the decline. This is attributed to
the decline in smoking and perhaps better control of BP and uptake in
statin therapy.
• Ruptured AAA accounts for .4% of deaths in men and 0.5% of deaths
in women over the age of 65yrs in England and Wales.
• In men, a peak in mortality rate due to ruptured AAA occurs between
65 and 85yrs of age
• In England, AAA accounts for over ,000 hospital admissions and 5000
deaths a year.
• In USA, abdominal aortic aneurysm (AAA) ranks as the 3th leading
cause of death and is responsible for 0.8% of all deaths.
• Currently, there is no pharmacological treatment available to effectively
inhibit aneurysm expansion or rupture; and the only treatment option
remains surgical repair by conventional or endovascular means.
• A mortality rate of less than 5% is expected for a high quality service
undertaking elective surgical repair (open or endovascular) of the
asymptomatic lesion.
• In contrast, the reported in-hospital mortality rate of ruptured AAA
varies between 47 and 83%. When including the patients with rupture
who do not reach hospital alive, the overall mortality rate of rupture is
much higher (between 78 and 94%).
 INCIDENCE, PREVALENCE, AND RISK FACTORS 7

Natural history (expansion and rupture)

The natural history of AAAs is continued expansion and eventual rupture.
• The annual expansion is approximately about 0% of the sac diameter
but there is a wide variation in growth rates.
• There is equivocal evidence for the role of statins in retarding AAA
expansion.
• Current clinical trials are investigating the effects of angiotensin-
converting enzyme (ACE) inhibitors and mast cell inhibitors on
AAA growth.
• The classic triad of rupture is abdominal pain (frequently radiating to
the back), shock and pulsatile mass. Any two of these three symptoms
should alert the attending physician to the possibility of a ruptured AAA.
• Free intra-peritoneal rupture of an AAA is rapidly fatal.
• The risk of AAA rupture increases exponentially with the maximum
diameter of the aneurysm (Table .).
• The UK Small Aneurysm Trial (UK SAT) determined that it is
appropriate to observe small AAAs until they reach a size of 5.5cm. At
this threshold diameter, surgically intervention is recommended because
the risk of death from rupture outweighs the risk of death from surgery.
• Other risk factors for aneurysm rupture include higher than expected
rate of aneurysm expansion, female sex, hypertension, smoking, and
chronic obstructive pulmonary disease.
AAA screening
Most AAAs are asymptomatic until rupture, when the mortality exceeds
80%. These asymptomatic AAAs are detected either during routine
physical examination or during imaging investigation for other non-related
conditions.
• Population screening for AAAs using ultrasound scan for 65-yr-old
men is expected to be fully implemented in England by 203 to detect
asymptomatic AAAs.

Table . Annual rupture rates of abdominal aortic aneurysms according

to size (based on pooled available data)
Initial aneurysm diameter (cm) Annual risk of rupture
3.0 0.2–0.4%
4.0 0.8–.%
4.0–5.5 0.6–.0%
5.5–5.9 5.0–9.4%
6.0–6.9 0.2%
>7.0 30.5–32.5%
8 CHAPTER  Epidemiology of vascular disease

• The Multicentre Aneurysm Screening Study (MASS) trial showed that

aneurysm-related mortality was significantly reduced in screened male
population between 65 and 74yrs old, with about 53% reduction in
those who attended for screening.
• Over 4yrs, the MASS trial showed that the incremental cost effective ratio
for screening was £28,400 per life-year gained (£36,000 per quality-adjusted
life year. This falls to approximately £8000 per life year gained at 8yrs.
• This compares favourably with other existing screening programmes,
such as breast and cervical cancer.
Thoracic aortic aneurysm
The most common location for thoracic aortic aneurysms (TAAs) is the
descending thoracic aorta.
• The majority are degenerative and a minority are caused by Marfan’s
syndrome, Ehler–Danlos syndrome, syphilis, and connective tissue
disorders.
• 25% are related to chronic dissections.
• Other causes include mycotic aneurysms, trauma-related (false
aneurysms) and previous coarctation repair.
• They are classified according to their location in relation to the 6th
intercostal space; above (type A), below (type B), and the entire
descending aorta (type C).
• Risk factors include increasing age and male sex (3: ratio). Interestingly,
the gender difference is less than that for infrarenal AAAs, where the
ratio is 7:, suggesting a difference in aetiology.
• The incidence is approximately 0/00,000 patient years.
• At 5yrs, only 3–39% of untreated TAAs survive.
• The risk of rupture increases with size. The rupture risk for a 6cm TAA
is about 3.6% per year.
• Most clinicians would repair TAAs 6cm in size or more.
Thoraco-abdominal aortic aneurysm
Thoraco-abdominal aortic aneurysm (TAAA) formation affects various seg-
ments of the thoracic and abdominal aorta beginning from the left subcla-
vian artery to variable components of the abdominal aorta. By definition,
TAAA involves one or more of the origins of the coeliac, superior mesen-
teric and renal arteries.
• Crawford’s classification (with Safi’s modification), described five types
of TAAAs:
• Type I—from the level of the left subclavian artery extending into the
proximal abdominal aorta just above the level of the renal arteries.
• Type II—from the level of the left subclavian artery extending all the
way down to the aortic bifurcation.
• Type III—begins in the lower part of the descending thoracic aorta,
classically at the sixth intercostal space to below the level of the renal
arteries.
• Type IV—begins at the diaphragm to the aortic bifurcation.
• Type V—from the level of the 6th intercostal space of the descending
thoracic aorta to just above the renal arteries.
Reprinted from Cardiovascular Surgery, 7, 6, HJ Safi, ‘How I do it: thoracoabdominal aortic aneurysm
graft replacement’, pp. 607–63, Copyright 999, with permission from Elsevier.
 INCIDENCE, PREVALENCE, AND RISK FACTORS 9

• The aetiology of TAAAs are degenerative (80%), dissection (5%), or

connective tissue disorders, arteritis, or trauma (5%).
• Prospective follow-up studies have demonstrated that TAAA rupture
was more likely to occur in aneurysms with larger diameters and higher
rates of expansion.
• The median size for TAAA rupture was estimated at 7.2cm.
• In aneurysms exceeding 6.0cm in size, the annual rate of rupture or
dissection was at least 6.9% and the death rate was .8%. The rate of
rupture rises exponentially, such that aneurysms equal to or >8cm have
an 80% risk of rupture within a year of diagnosis.
Peripheral aneurysm
Popliteal artery aneurysm is the most common peripheral aneurysm,
accounting for more than 80%:
• 40% are associated with AAAs.
• 50% are bilateral.
• Unlike AAAs, the majority (70%) are symptomatic.
• The ratio of popliteal aneurysm to AAA is about :5.
• 5–0% of patients with AAAs also have popliteal aneurysm.
• The prevalence is about % for people in their 8th decade.
• 50% will present as peripheral limb-threatening ischaemia.
• Laminated thrombus within the popliteal aneurysm is an indication for
elective surgical intervention to prevent limb loss from embolization as a
result of flexion and extension of the knee.
• In the absence of thrombus, 2cm is generally regarded as the threshold
diameter for surgical repair.
Femoral arterial aneurysms are the second commonest peripheral
aneurysms:
• They occur in 2–3% of patients with AAAs.
• They are also more common with increasing age and show a 30:
preponderance for men.
• Surgical treatment is usually indicated for size of more than 3 cm.
Isolated iliac aneurysm is unusual and they are usually present in association
with aortic aneurysms.
• They involve either common or internal iliac arteries, with involvement
of the external iliac artery being an extremely rare event.
• Surgical intervention is generally recommended for asymptomatic iliac
aneurysms greater than 3–4cm.
Aortic dissection
Aortic dissection is considered acute if less than 2 weeks since symptoms
and chronic if more than 2 weeks.
• The incidence is approximately 3/00,000 per year, but accurate data
are difficult to obtain as there is a high out-of-hospital mortality and
autopsy rates are low.
• Ratio of men to women is 2:.
• The risk increases with age.
• Using the Stanford classification, Type A dissection involves the
ascending aorta and Type B dissection does not.
10 CHAPTER  Epidemiology of vascular disease

• Type A dissection has a % mortality per hour and needs emergency

surgical repair.
• Type B dissection is mainly treated medically with pharmacological
control of BP, but surgical intervention may be needed if
complications arise
• Overall mortality for uncomplicated medically treated type B dissection
is only .2%, but this rises to 8% in complicated dissections (rupture,
malperfusion, persistent pain, refractory hypertension, and false
aneurysm formation).
Venous disease
Varicose veins have a slightly higher prevalence in males compared with
females (4:3.2):
• Age-adjusted prevalence of truncal varices (dilation of veins of the
superficial venous system) from the Edinburgh Vein Study was 40% in
men and 32% in women.
• The prevalence of smaller thread-like non-truncal varices (reticular or
hyphenweb varices) is about 80%.
• 35% of the population between 8 and 64yrs is estimated to have
significant venous reflux ≥0.5s.
• The prevalence of varicose veins increases with age.
• Risk factors for primary varicose veins include age, parity (female sex
hormones), obesity, standing occupation, diet, and genetics.
• 2° varicosities are caused by previous deep vein thrombosis, pelvic
obstruction, or deep venous reflux.
Chronic venous insufficiency (CVI) is the result of impaired venous return
and leads to increased ambulatory venous pressure within the lower limbs.
This, in turn, leads to skin changes, such as eczema, pigmentation, lipoder-
matosclerosis, and ulceration. Causes of CVI include venous reflux, venous
obstruction, or failure of calf muscle pump.
• The prevalence of CVI is slightly greater in men than women (9% versus
7% in population aged 8–64yrs).
• The prevalence increases with age.
Further reading
Aneurysm Detection and Management Veterans Affairs Cooperative Study Group. Immediate
repair compared with surveillance of small abdominal aortic aneurysms. N Engl J Med 2002;
346(9): 437–44.
Choke E, Vijaynagar B, Thompson J, et al. Changing epidemiology of abdominal aortic aneurysms in
England and wales: older and more benign? Circulation 202; 25: 67–25.
Coady MA, Rizzo JA, Hammond GL, Kopf GS, Elefteriades JA. Surgical intervention criteria for
thoracic aortic aneurysms: a study of growth rates and complications. Annl Thorac.Surg 999;
67:922–6.
Davies RR, Goldstein LJ, Coady MA, Tittle SL, Rizzo JA, Kopf GS, et al. Yearly rupture or dissec-
tion rates for thoracic aortic aneurysms: simple prediction based on size. Annl Thorac.Surg 2002;
73: 7–27.
Dennis MS, Bamford JM, Sandercock PA, et al. Incidence of transient ischemic attacks in Oxfordshire,
England. Stroke 989; 20: 333–9.
Evans CJ, Fowkes FG, Ruckley CV, et al. Prevalence of varicose veins and chronic venous insufficiency
in men and women in the general population: Edinburgh Vein Study. J Epidemiol Commun Hlth
999; 53: 49–53.
 Screening for vascular disease 11

Fowkes FG, Housley E, Cawood EH, et al. Edinburgh Artery Study: prevalence of asymptomatic and
symptomatic peripheral arterial disease in the general population. Int J Epidemiol 99; 20: 384–92.
Rothwell PM, Eliasziw M, Gutnikov SA, et al. Analysis of pooled data from the randomised controlled
trials of endarterectomy for symptomatic carotid stenosis. Lancet 2003; 36: 07–6.
Selvin E, Erlinger TP. Prevalence of and risk factors for peripheral arterial disease in the United States:
results from the National Health and Nutrition Examination Survey, 999–2000. Circulation 2004;
0: 738–43.
UK Small Aneurysm Trial Participants. Mortality results for randomised controlled trial of early elec-
tive surgery or ultrasonographic surveillance for small abdominal aortic aneurysms. Lancet 998;
352: 649–55.
Vascular Surgical Society of Great Britain and Ireland. Critical limb ischaemia: management and out-
come. Report of a national survey. Eur J Vasc Endovasc Surg 995; 0: 08–3.

Screening for vascular disease

Screening programme criteria
Screening is a method to detect disease in a population, in individuals with
no signs or symptoms of the disease. The aim of screening is the early
identification of disease in an at-risk population, in order to reduce the mor-
bidity and mortality associated with the condition. In order for a screening
programme to be of clinical use several criteria must be met:
• The condition should be an important health problem.
• There should be an accepted treatment for patients with the disease.
• There should be adequate facilities for screening.
• There should a recognizable latent phase of the condition.
• There should be a suitable test or examination for the disease.
• The test should be acceptable to the population.
• The natural history of the condition should be understood.
• There should be consensus over which patients to treat.
• The screening programme should be economically viable in terms of
overall costs of medical care.
• Case finding should be a continuous process.
UK abdominal aortic aneurysm screening
• In the UK, AAA screening is being gradually introduced, with the
timescale for national coverage to be completed by the end of 203.
• The NHS AAA screening programme invites men for screening in the
year they reach the age of 65yrs.
• Men aged over 65yr can request a scan from their local programme.
• Attendees undergo abdominal ultrasound scan to detect an AAA.
• Patients with an aortic diameter of less than 30mm will be discharged;
those with an aortic diameter of 30mm or more will enter a local AAA
surveillance programme.
• Local programmes will continue to monitor AAA diameter until it
reaches the threshold for surgical intervention, at which time patients
will be referred to a vascular surgeon for a discussion regarding the risks
and benefits of AAA repair.
12 CHAPTER  Epidemiology of vascular disease

Sensitivity and specificity

The efficiency of a screening test is of utmost importance. For an effective
screening test the disease should be easily detectable, and both those with
and without the disease should be identified correctly. This is described by
the sensitivity and specificity of the test.
• Sensitivity is the ability of the test to correctly identify the disease in
patients who have the disease.
• Specificity is the ability of the test to correctly identify patients who do
not have the disease.
• The positive predictive value (PPV) is the proportion of positive test
results that are truly positive.
• The negative predictive value (NPV) is the proportion of patients with a
negative test who do not have the disease.
See Table .2 for a summary.

The AAA screening programme achieves a sensitivity and specificity of

almost 00%. Ultrasound aneurysm screening has a PPV and NPV approach-
ing 00%; therefore, patients without the condition are rarely misclassified
as having an AAA, and patients with the condition are rarely misdiagnosed.
However, in up to 3% of patients ultrasound screening is not possible when
the subject is seen because the abdominal aorta is obstructed by bowel gas,
inhibiting visualization.
Population benefits
The aim of any screening programme is to decrease the morbidity and mor-
tality associated with the condition. Mortality from elective AAA surgery is
much lower than from aortic rupture (whether or not emergency surgery is
undertaken. Therefore, AAA screening leading to elective repair expected
to prevent significant numbers of AAA ruptures and deaths.
• The accepted diameter at which AAA’s are deemed suitable for repair
is 55mm: over this size, the yearly risk of rupture becomes greater than
the risk of surgical intervention in a healthy individual.

Table .2 The calculation of sensitivity, specificity, and predictive values

for clinical tests
Screening True disease classification of apparently well population
result Diseased persons Persons without disease
Positive True +ve (with disease False +ve (without disease but
and +ve test) +ve test)
Negative False –ve (with disease True –ve (without disease
but –ve test) and –ve test)
Total Total unknown cases of Total persons without the
disease disease
Sensitivity = true +ve/total unknown cases of disease.
Specificity = true –ve/total persons without disease.
Positive predictive value = true +ves/(true +ves + false +ves).
Negative predictive value = true –ves/ (true –ves + false –ves).
 Screening for vascular disease 13

• As more patients are identified to have an (asymptomatic) AAA by

the screening programme, overall mortality rates from AAA should
decrease, although it will inevitably lead still to death in a small number
of patients.
• Data from the MASS trial suggested that one life will be saved per 240
men invited to the screening programme (number needed to treat), and
one extra death will occur for every 2080 men invited to the screening
programme (number needed to harm).
• The MASS trial showed that aneurysm-related mortality was significantly
reduced in a screened male population aged between 65 and 74yrs, with
a 53% reduction in those who attended for screening
• Over 4yrs, the MASS trial showed that the incremental cost effective
ratio for screening was £28,400 per life-year gained (£36,000 per
quality-adjusted life year). This falls to approximately £8000 per life year
gained at 8yrs.
• This compares favourably with other existing screening programmes,
such as breast and cervical cancer.
Limitations of aneurysm screening
As screening targets asymptomatic individuals it has important ethical differ-
ences from clinical practice. AAA screening has the potential to save lives.
Patients whose aneurysm is 55mm or greater in diameter when screened
will be offered intervention (open repair or endovascular abdominal aortic
aneurysm repair (EVAR) to prevent rupture), whilst those will small aneu-
rysms can be entered into a surveillance programme to monitor aneurysm
expansion with the intention that surgical intervention will be undertaken
when warranted. However, screening has limitations:
• False positive results cause increased stress and anxiety to patients, and
further unnecessary investigations.
• False negative results give the patient a false sense of security, which
may delay final diagnosis in later life
• Aneurysm screening occurs in the 65th year of life. As the age of
the population increases, and cardiovascular risk factor modification
improves, some patients may develop AAA’s after this age, and may
therefore not be detected.
• Recent papers have highlighted that the epidemiology of AAA may
be changing. The incidence at age 65 may be lower than previously
reported, which suggests that screening should be performed at an
older age.
• The incidence of AAA differs between different populations and ethnic
groups. Extrapolations regarding the incidence of AAA in different
populations (and, hence, the benefits of screening) should be made
with caution.
• Interventions performed to treat AAA only prevent potential rupture of
the AAA. Future morbidity or mortality from other causes is unaffected.
Hence some patients will undergo treatment which carries costs and
potential risks yet does not extend their lifespan.
14 CHAPTER  Epidemiology of vascular disease

Additional screening
In the UK the only vascular NHS national screening programme is for
abdominal aortic aneurysms. However, there are several other systems
designed to reduce vascular risk factors, as well as commercial services
offering vascular screening.
• The NHS Health Check programme aims to help decrease vascular risk
through preventing heart disease, stroke, diabetes, and renal impairment
through 5-yearly checks between the ages of 40–74yrs.
• Smoking cessation advice is mandatory during any consultation.
• Many private hospitals and clinics advertise vascular screening, including
aortic and carotid ultrasonography, blood testing for vascular risk.
Further reading
Ashton HA, Buxton MJ, Day NE, Kim LG, Marteau TM, Scott RA, Thompson SG, Walker NM,
Multicentre Aneurysm Screening Study Group. The Multicentre Aneurysm Screening Study
(MASS) into the effect of abdominal aortic aneurysm screening on mortality in men: a randomised
controlled trial. Lancet. 2002; 360: 53–9.
Ashton HA, Gao L, Kim LG, Druce PS, Thompson SG, Scott RA. Fifteen-year follow-up of a ran-
domised clinical trial of ultrasonographic screening for abdominal aortic aneurysms. Br J Surg 2007;
94: 696–70.
Choke E, Vijaynagar B, Thompson J, Nasim A, Bown MJ, Sayers RD. Changing epidemiology of
abdominal aortic aneurysms in England and Wales: older and more benign? Circulation 202;
25: 67–25.
Thompson SG, Ashton HA, Gao L, Scott RA. Multicentre Aneurysm Screening Study Group.
Screening men for abdominal aortic aneurysm: 0 year mortality and cost effectiveness results
from the randomised Multicentre Aneurysm Screening Study. Br Med J 2009; 338: b2307.
UK Screening Portal. UK Screening Portal. Available at: M www.screening.nhs.uk
Wilson. JMG, Jungner G. Principles and practice of screening for disease. Geneva: World Health
Organization 968. Available at: M http://www.who.int/bulletin/volumes/86/4/07–0502BP.
pdf

Primary and secondary prevention

of vascular disease
Background
• By definition, all patients with occlusive vascular disease have
atherosclerosis.
• Individuals with PAD have a 2–6-fold increased risk of death due to
coronary heart disease. They are ~4 times more likely to suffer a stroke
or transient ischaemic attack than those without PAD.
• Secondary cardiovascular prevention, which may include both lifestyle
modification and medical treatment, should be an integral part of the
management of all patients with atherosclerotic disease.
• The aim of such treatment is to slow the progression of PAD and
to reduce the incidence of cardiovascular events, such as myocardial
infarction and stroke.
• The need for effective medical management of patients with PAD is
enshrined in guidelines such as that issued by the American College
of Cardiology and American Heart Association (ACC/AHA) in 2005
on the management of PAD. Whilst aneurysmal and occlusive arterial
vascular disease are distinct entities, many patients with aneurysmal
 Primary and secondary prevention of vascular disease 15

disease also have significant atherosclerotic disease. The ACC/AHA

guidelines recommend that atherosclerotic risk factors should also be
actively managed in patients with abdominal aortic aneurysms.
• Other guidelines with recommendations for cardiovascular 2°
prevention in patients with known or suspected atherosclerotic disease
include the Joint British Societies’ Guidelines on the Prevention of
Cardiovascular Disease in Clinical Practice (2005), the SIGN Guidelines
on Risk Estimation and the Prevention of Cardiovascular Disease
(2007), the WHO Guidelines on the prevention of Cardiovascular
Disease (2007), and the AHA/ACC guidelines for 2° prevention for
patients with coronary and other atherosclerotic vascular disease (Smith
et al. 20). These all make similar, but not identical recommendations.
The following recommendations are based on the Joint British Societies’
Recommendations ( JBS2).
Smoking cessation
• All patients should be advised to stop smoking, not only because on
the impact on perioperative risk, but also because death, myocardial
infarction, and amputation are significantly more frequent in patients
with PAD who continue smoke.
• Medical advice and regular follow-up achieves cessation rates of
approximately 5%. With nicotine replacement therapy this increases to
approximately 6%.
• A smoking cessation programme is best managed in conjunction with
the primary care physician or the support of a specialist clinic.
Diet
As with smoking cessation, dietary change is more likely to be achieved with
professional support from a dietician or the primary care physician. The
JBS2 guidelines recommend the following:
• Aim to maintain body mass index at between 20 and 25kg/m2.
• Avoid central obesity (defined as a waist circumference in white
Caucasians > 02cm in men and 88cm in women, or a waist
circumference in Asians of > 90cm in men and 80cm in women).
• Maintain fat intake at ≤30% of total energy intake.
• Keep saturated fat intake at ≤0% of total fat intake and cholesterol
intake at <300mg/day.
• Eat at least five portions of fresh fruit and vegetables a day.
• Consume ≤00mmol/day of salt, i.e. <6g of sodium chloride or <2.4g
sodium/day.
• Limit alcohol consumption to 2 units a week for men and 4 units a
week for women.
Exercise
• Regular physical activity (e.g. fast walking) of at least 30min/day should
be taken.
• It has to be recognized that exercising to this intensity may not be
feasible in patients with intermittent claudication or ischaemic rest pain.
However, exercise should form part of the management of intermittent
claudication. A regular supervised exercise programme can increase the
speed, distance, and duration of walking.
16 CHAPTER  Epidemiology of vascular disease

Blood pressure
Raised BP should be controlled.
• Goals are:
• <40mmHg systolic and <85mmHg diastolic in non-diabetics.
• <30mmHg systolic and <80mmHg diastolic people with established
atherosclerotic disease, diabetes, and chronic renal disease.
• Concerns that antihypertensive therapy may worsen claudication or
critical limb ischaemia (by reducing perfusion pressure) are usually
unfounded. Most patients are able to tolerate anti-hypertensive
treatment without a worsening of symptoms.
Lipids and statins
Blood cholesterol concentrations should be controlled in people with ath-
erosclerotic disease. This may require changes to diet with or without drug
treatment.
Optimal targets are:
• Cholesterol <4.0mmol/L with a low density lipoprotein (LDL)
cholesterol of <2.0mmol/L.
• A 25% reduction in total cholesterol and a 30% reduction in LDL
cholesterol.
• The target depends on whichever gets the person to the lowest
absolute value.
All patients should receive dietary and lifestyle advice directed towards
cholesterol reduction. The prescription of a statin is also indicated in most
patients presenting for vascular surgery.
Statins
• Studies in acute coronary syndrome suggest that early treatment
with a statin after an acute coronary event reduces the incidence of
subsequent cardiovascular events, when subsequent compliance is good.
• All patients should be treated with a statin from the time of
presentation with an acute cardiovascular event. They should be
followed up regularly to ensure that treatment is continued regardless
of the initial cholesterol level.
• Most patients presenting for elective vascular surgery will already be
on treatment when seen by the anaesthetist. However, patients with
an indication for statin therapy may present in pre-assessment. It is
inappropriate to initiate lifelong therapy without appropriate follow-up
and, therefore, the patient should be referred to their general practitioner
with a request to start treatment with a statin if appropriate.
• Before starting treatment it is important to confirm that the patient
is statin-naive and that they have not previously discontinued statin
treatment because of adverse effects.
• Important considerations:
• Untreated hypothyroidism should be excluded.
• Dose reduction may be required in severe renal impairment.
• Specialist advice should be sought in patients with hepatic
impairment.
 Primary and secondary prevention of vascular disease 17

• Several statins are metabolized by the cytochrome P450 system and,

therefore, may interact with drugs including amiodarone, diltiazem,
verapamil, and macrolides.
• Five statins are currently available in the UK
• Atorvastatin.
• Fluvastatin.
• Pravastatin.
• Rosuvastatin.
• Simvastatin.
• Financial considerations may inform the choice of first-line treatment
and local guidance should be consulted.
• Treatment is generally begun with intermediate doses, e.g. simvastatin
40mg. The dose may be reduced or the drug changed in patients who
cannot tolerate this.
• High dose treatment, e.g. with atorvastatin 40–80mg or simvastatin
80mg is reserved or those with very high initial cholesterol, progressive
disease despite lipid lowering strategies, or following recent acute
coronary syndrome.
Adverse effects of statins
• Myositis (uncommon):
• Clinical manifestations range from muscle cramps and myalgia,
through to life-threatening rhabdomyolysis. Adverse effects of statins
on skeletal muscle are infrequent.
• Pooled data from randomized controlled trials suggest an incidence
of myositis and of rhabdomyolyis of 70 and 20, respectively, per
00,000 patients treated for 5yrs. The pooled incidences of these
complications in the placebo group were 50 and 4 per 00,000
patients per 5yrs.
• Rhabdomyolysis is primarily associated with cerivastatin, which is no
longer available.
• A meta-analysis reported that in the perioperative period a greater
than 0 fold increase in serum CK was seen only slightly more
frequently in patients who received statin than those who received
placebo (0.7% versus 0.3%).
• The adverse effects of statins on muscle are generally reversible if
the drug is discontinued. If myositis is suspected the statin should be
discontinued at once.
• Disordered liver function (infrequent):
• Usually manifest as increased hepatic transaminases.
• Usually occurs in the first year after starting treatment.
• Incidence is <% of patients.
• Routine monitoring of liver function is no longer required in
patients starting standard doses of simvastatin or pravastatin, but
is still recommended in the drug information for higher doses and
other statins.
• If transaminases increase to >3 times the upper limit of normal, the
statin should be discontinued. Specialist advice should be sought in
the case of lesser elevations.
18 CHAPTER  Epidemiology of vascular disease

Perioperative statin therapy

Statins should be continued throughout the perioperative period.
• Preoperative statin therapy is associated with 59% reduction in the risk
of mortality after vascular surgery (.7% compared with 6.%).
• Acute statin withdrawal is associated with worse outcome in patients
with acute coronary syndrome. There is evidence of a similar
effect in vascular surgery patients with one study showing a 2-fold
increase in troponin release when statins were discontinued in the
perioperative period.
Other drugs
Other lipid-lowering drugs should be considered if the total cholesterol and
LDL cholesterol targets are not achieved. These include fibrates, bile acid
sequestrants, cholesterol absorption inhibitors, nicotinic acid, and omega-3
fatty acids.
Blood glucose and diabetes
The optimal fasting glucose in people with cardiovascular disease, including
vascular surgical patients, is ≤6.0mmol/L.
• If the non-fasting glucose is <6.mmol/L the fasting glucose does not
need to be checked.
• If the fasting glucose is ≥ 6.mmol/L then the fasting glucose should be
measured.
• If the fasting glucose is 6. – 6.9mmol/L, but not diagnostic of diabetes
(≥ 7.0mmol/L) then it should be repeated or an oral glucose tolerance
test (OGTT) should be performed.
• A fasting glucose between 6.–6.9mmol/L on second testing indicates
impaired fasting glycaemia (IFG).
• Repeated fasting glucose concentrations ≥7.0mmol/L indicate diabetes.
• If symptoms of diabetes are present (such as thirst, polyuria, and weight
loss), a single fasting glucose of ≥7.0mmol/L indicates diabetes.
• Impaired glucose tolerance (IGT) can only be diagnosed by an oral
glucose tolerance test with a 2-h glucose concentration between 7.8
and .0mmol/L. A 2-h glucose concentration of ≥.mmol/L is
diagnostic of diabetes.
• For people with either IFG or IGT the aim is to prevent progress to
diabetes through lifestyle intervention. If the person has diabetes tight
glycaemic control is recommended with target of a fasting or pre-
prandial glucose of 4.0–6.0mmol/L and an HbAc <6.6%
Cardioprotective therapies
Antithrombotic therapy
Aspirin
• Aspirin 75mg od is recommended for all people with atherosclerotic
disease. If aspirin is contraindicated clopidogrel 75mg od may be
prescribed.
• Aspirin withdrawal is associated with:
• A worse outcome in patients with acute coronary syndrome.
• A significant increase in the risk of cardiac events after
non-cardiac surgery.
 Primary and secondary prevention of vascular disease 19

• No increase in significant surgical bleeding.

• Therefore, aspirin should not be withdrawn from vascular surgery
patients in the perioperative period.
Warfarin
Anticoagulation should be considered in cases of:
• Atrial fibrillation with moderate risk of embolic events (aged 60–75yrs
without additional risk factors).
• High risk of embolic events (aged >75yrs with other risk factors, such as
hypertension, diabetes, or left ventricular dysfunction).
• Target INR is 2–3.
• Patients at risk of systemic embolization, e.g. significant LV dysfunction,
LV aneurysm, or a history of paroxysmal tachyarrhythmia.
Beta-blockers
• The POISE study of perioperative high dose metoprolol did not support
prophylactic beta-blockade for all patients with established cardiac
disease undergoing non-cardiac surgery.
• However, some patients with cardiovascular disease have a primary
indication for beta-blockade. These include:
• Heart failure.
• Previous myocardial infarction (MI), especially large infarction or MI
complicated by heart failure or ventricular arrhythmias.
• The POISE trial raised concerns about hypotension associated with
perioperative beta-blockade.
• The withdrawal of beta-blockers in the perioperative period is
associated with a significantly increased risk of cardiac events.
• Therefore, beta-blockers should be continued through the perioperative
period (with intravenous (IV) substitution if necessary) unless there is
significant hypotension.
• If it is deemed appropriate to reduce or discontinue beta-blockade the
patient should be regularly monitored and any tachycardia managed
appropriately.
ACE inhibitors
• ACE inhibitor or an angiotensin II receptor antagonist therapy are first
line therapy in hypertension for people aged <55yrs except for Black
people of African or Caribbean origin.
• ACE inhibitors reduce cardiovascular risk by lowering BP.
• They may also have a direct effect on atherosclerosis, by effects on
endothelial function, decreasing plasma concentrations of type  tissue
plasminogen activator, increasing the release of tissue-type plasminogen
activator and changing the fibrinolytic balance.
• The importance of these effects in reducing cardiovascular risk is
uncertain.
Perioperative management
• Discontinuation of aspirin or statin therapy after MI increases the
risk of re-infarction. Similar considerations probably apply in the
perioperative period.
• Discontinuation of aspirin therapy for cardiovascular prevention before
surgery increases the risk of perioperative MI.
20 CHAPTER  Epidemiology of vascular disease

• In the context of vascular surgery, the risks of perioperative infarction

outweigh any risk of bleeding associated with continuing aspirin, and
the drug should therefore be continued up to the day of surgery and
restarted as soon as possible after surgery.
• Some evidence suggests that, in patients on statin therapy, the risks of
perioperative MI are increased if the statin is not restarted on the first
or second postoperative day. Therefore, statins should be restarted as
soon as possible after surgery. As statins have to be given by the enteral
route, this may require the administration of the drug in liquid form via a
nasogastric tube (NGT).
• Some evidence shows that intraoperative hypotension is more common
in patients given an ACE inhibitor or angiotensin II receptor blockers
within 2–24h before anaesthesia and surgery. Therefore, many
practitioners omit the immediate preoperative dose of these drugs.
Because of the risk of post-operative hypotension, the timing for
restarting these drugs after surgery is a matter for clinical judgement.
Further reading
Joint British Society. JBS 2: Joint British Societies’ guidelines on prevention of cardiovascular disease in
clinical practice (JBS2). Heart 2005; 9(Suppl. 5): –52.
Scottish Intercollegiate Guidelines Network. Risk estimation and the prevention of cardiovascular
disease; a national clinical guideline. Scottish Intercollegiate Guidelines Network (Edinburgh:
SIGN). 2007. Available at: M www.sign.ac.uk
Smith SC Jr, Benjamin EJ, Bonow RO, et al. AHA/ACCF secondary prevention and risk reduction
therapy for patients with coronary and other atherosclerotic vascular disease: 20 update: a
guideline from the American Heart Association and American College of Cardiology Foundation.
Circulation. 20; 24: 2458–2473.
World Health Organization. Prevention of cardiovascular disease; guidelines for assessment and manage-
ment of cardiovascular disease. Geneva: WHO 2007 World Health Organization.

Vascular databases
Outcome data for vascular surgery are collected in a number of national
and international databases. These are used for two main purposes:
• To generate epidemiological data.
• To monitor the performance of vascular units.
Both of these functions are relevant to the vascular anaesthetist:
• The epidemiological data from large databases informs clinical practice.
• There is an increasing recognition that outcome from vascular surgery
depends on all aspects of care including anaesthetic care.
• It has been shown in at least one vascular unit that anaesthetists with a
specialist interest in vascular anaesthesia achieved better outcomes.
• Some vascular databases now include data on anaesthetic care and
anaesthetists are recognized as equal partners in initiatives to improve
vascular care, such as the UK Quality Improvement Programmes for
aortic surgery and amputation.
General databases
Data pertinent to vascular practice have been obtained from large national
databases that include, but are not limited to vascular surgery.
 Vascular databases 21

American College of Surgeons National Surgical Quality Improvement Program

(ACS NSQIP (USA))
• A United States national voluntary programme that collects data on all
types of surgery, including vascular surgery.
• It generates risk-adjusted data allowing comparison of the performance
of different surgical units.
• The ACS NSQIP risk model is complex and requires considerable data
collection. Because of this, at least one simpler risk adjustment model
has been proposed (the Surgical Mortality Probability Model).
• Analyses of vascular surgery data from ASC NSQIP suggest that general
anaesthesia for carotid endarterectomy is an independent risk factor for
perioperative MI and that general anaesthesia for EVAR is associated
with increased length of stay and an increased incidence of pulmonary
complications compared with spinal anaesthesia or local anaesthesia
with monitored anaesthesia care.
United Kingdom Hospital Episode Statistics (HES) database
• Contains centrally collected data on activity in National Health Services
(NHS) hospitals.
• Analyses of these data for vascular surgery demonstrated volume-
outcome relationships for aortic and other vascular surgeries. Units that
undertake more procedures tend to have better outcomes.
• In the UK this has led to a national initiative to centralize vascular
services so that they are based around a limited number of
larger centres.
Specific vascular databases
These have yielded valuable epidemiological data to inform clinical practice.
The EUROpean Collaborators on Stent/graft Techniques for aortic Aneurysm
Repair (EUROSTAR) registry
This a database of endovascular procedures undertaken at hospitals in
Europe for the repair of aortic aneurysms.
It currently includes data from over 30 centres and over 7,000 across
Europe and a MEDLINE search identified 60 publications relating to the
registry. Data from the EUROSTAR registry indicate that:
• Endoleak and a requirement from 2° interventions remains a problem
with EVAR.
• After 8yrs approximately half of patients who underwent repair
with first generation stent grafts remained alive and had not required
conversion to open aneurysm repair.
The M2S Medical Imaging Repository
• M2S is a commercial company that provides medical imaging services
to hospitals around the world and has provided the core imaging
laboratory services for some endovascular device trials.
• Data from large M2S database have been used to study compliance with
EVAR device guidelines and post-EVAR aneurysm sac enlargement.
22 CHAPTER  Epidemiology of vascular disease

VASCUNET
An international registry of vascular surgery conducted under the auspices
of the European Society of Vascular Surgery.
• The first VASCUNET report was published in 2007 and included data
on over 30,000 patients who underwent surgery over a 0-year period.
This report included data from six countries; Denmark, the UK, New
Zealand, Australia, Sweden, and Switzerland.
• Amongst the findings of this report were the observation that the
median age of patients undergoing aortic surgery was 72yrs and that
the age of patients undergoing aortic surgery had tended to increase
between 997 and 2006.
• It was also noted that there were fewer emergency operations, and
by inference, ruptures in more recent years.
• The second VASCUNET audit was published in 2008 and included
data from 0 countries reported marked differences in outcome from
AAA repair between countries. Mortality for open elective open aortic
aneurysm repair was higher in the UK than in any of the other nations
that submitted data and led to establishment of the national Abdominal
Aortic Aneurysm Quality Improvement Programme. (AAA QiP)
National vascular database
• The national vascular database (NVD) was established in 997 under
the auspices of the United Kingdom Vascular Society whose core
membership is vascular surgeons.
• Data are entered on a number of ‘index procedures’, including elective
AAA repair, carotid endarterectomy, and lower limb amputation.
• Currently used widely, but not universally, in the UK.
• Recent NHS guidance on commissioning vascular surgery requires that
both NHS Trusts and surgeons undertaking AAA repair submit data to
the NVD. This is likely to further expand data entry into the NVD.
• The recording of data into the NVD is also one of the key components
of vascular surgery quality improvement in the United Kingdom.
• The NVD is explicitly a collaborative venture and includes data fields
for preoperative data that may be collected by the anaesthetist and also
data fields for intra- and post-operative anaesthetic management. These
were developed in collaboration with the Vascular Anaesthesia Society
of Great Britain and Ireland (VASGBI) and all vascular anaesthetists are
encouraged to register for NVD access (M https://nww.nvdonline.nhs.
uk), to enter data for cases into the database.
Abdominal Aortic Aneurysm Quality Improvement Programme
• Not a national database itself, but arose from 2nd VASCUNET report
and links with other databases.
• Its aims are to improve outcome from AAA repair through several
initiatives, including:
• Expansion of data collection into the NVD—analysis of both these
data and data on vascular procedures from the UK HES.
• The development of best practice protocols for pre-, intra- and
post-operative care.
 Vascular databases 23

• Support for regional meetings involving all key stakeholders to

develop Regional Action Plans.
• Conducting patient focus groups to inform the development of the
AAA Quality Improvement Programme.
Useful information
ACS NSQIP. Available at: M http://site.acsnsqip.org/
United Kingdom Hospital Episode Statistics. Available at: M http://www.hesonline.nhs.uk
European Society of Vascular Surgery VASCUNET. Available at: M http://www.esvs.org/social/
vascunet
United Kingdom National Vascular Database. Available at: M http://www.vascularsociety.org.uk/
national-vascular-database.html
United Kingdom Abdominal Aortic Aneurysm Quality Improvement Programme. Available at:
M http://www.aaaqip.com/

Further reading
Edwards MS, Andrews JS, Edwards AF, Ghanami RJ, Corriere MA, Goodney PP, Godshall CJ, Hansen
KJ. Results of endovascular aortic aneurysm repair with general, regional, and local/monitored
anesthesia care in the American College of Surgeons National Surgical Quality Improvement
Program database. J Vasc Surg 20; 54: 273–82.
Glance LG, Lustik SJ, Hannan EL, et al. The Surgical Mortality Probability Model: derivation and
validation of a simple risk prediction rule for noncardiac surgery. Annl Surg 202; 255: 696–702.
Hobo R, Buth J, EUROSTAR collaborators. Secondary interventions following endovascular abdom-
inal aortic aneurysm repair using current endografts. A EUROSTAR report. J Vasc Surg 2006;
43: 896–902.
Leichtle SW, Mouawad NJ, Welch K, et al. Outcomes of carotid endarterectomy under general
and regional anesthesia from the American College of Surgeons’ National Surgical Quality
Improvement Program. J Vasc Surg 202; 56: 8–8.
Leurs LJ, Buth J, Laheij RJ. Long-term results of endovascular abdominal aortic aneurysm treatment
with the first generation of commercially available stent grafts. Arch Surg 2007; 42: 33–4.
 Chapter 2 25

Anatomy physiology and

responses to vascular
surgery

Cardiovascular 26
Pathophysiology of aortic clamping and unclamping 48
Respiratory 50
Anatomy relevant to regional anaesthesia 58
Physiology of cerebral blood flow 65
Renal 69
Coagulation and the response to major haemorrhage 75
Physiology of pain 8
26 CHAPTER 2 Anatomy physiology and responses

Cardiovascular
Embryological development
The cardiovascular system is the first organ system to develop and function
in the human embryo starting within 3 weeks of gestation (Fig. 2.). By
week 7 the heart resembles the adult heart, except for the patent foramen
ovale. Blood vessels originate from angiogenic cells differentiated from the
mesoderm (Fig. 2.2). They cluster and join together to form plexuses within
which vacuoles develop into lumens, bordered by endothelial cells, which
contain haemangioblasts containing haemoglobin.
Anatomy
The heart
See Figs 2.3 and 2.4.
• The adult heart is situated in the anterior mediastinum and weighs
200–400g.
• Two-thirds of its volume lies to the left of the midline.
• It is divided into left and right sides along its longitudinal axis by atrial and
ventricular septa.
• It is divided horizontally by a fibrous septum containing the 4 cardiac
valves, which separate the atria from the ventricles.
• Largely composed of muscular tissue (myocardium), attached to the
fibrous rings of the atrioventricular (AV) and arterial orifices.
• The heart musculature forms a syncitium of interconnecting cells. This
ensures contraction is coordinated to provide maximum efficiency.
• The myocardial conducting system is formed of specialized cardiac
myocytes which exhibit an increased length of action potential from the
sino-atrial (SA) node to the ventricular myocyte.
• Covered externally by pericardium and internally by endocardium.

Fig. 2. Embryological development of the heart.

Clusters of angiogenic cells join to form endocardial tubes, blood vessels and blood cell precursors
(). The heart tube begins beating, grows, and loops into the adult shape (2, 3).
 Cardiovascular 27

I
1 2

II

III

IV
3 4
V
VI
9
8
5

Fig. 2.2 Aortic arches. In early development there are paired dorsal aortae joined to
the aortic sac by six arches. The dorsal aortae become the descending aorta.
. External carotid artery. 2. Internal carotid artery. 3. Right subclavian artery. 4. Aortic arch. 5.
Vertebral artery. 6. Left subclavian artery. 7. Right pulmonary artery. 8. Left pulmonary artery. 9.
Ductus arteriosus

1. Superior vena cava

2. Aortic arch
3. Aortic root
1 2 4. Pulmonary trunk
5. Left pulmonary artery
6. Left atrium
7. Right atrium
5 8. Left ventricle
3 9. Interventricular septum
4 10. Right ventricle
6

10

Fig. 2.3 The heart and great vessels viewed from the front.
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½ lb. of sugar
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For the Filling.

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No. 85—FARINA TART.

7 eggs
¾ cup of sugar
½ cup blanched, ground, sweet almonds
15 bitter, blanched, ground almonds
1 grated lemon peel
¼ lb. of farina, good measure

Preparation: The yolks of eggs, sugar, lemon peel and almonds

are stirred 1 hour, the farina mixed in dry and lastly the beaten
whites of eggs. Butter a round, loose bottom pan, put the batter in
and bake slowly 1 hour.
 No. 86—BROWN SPICE CAKE No. 3.
2 cups of brown sugar
1 cup of butter
3 eggs
1 cup of milk
3 cups of flour
1 tsp. of cloves
½ tsp. of nutmeg
1 cup of chopped raisins
1 cup of chopped hickory nuts
3 tsps. of baking powder
1 tsp. of cinnamon

Preparation: Cream the butter with sugar and yolks of eggs,

add the milk, cloves, cinnamon, nutmeg, raisins, nuts, flour, baking
powder and whites of eggs. Butter a pan, put the batter in and bake
1¼ to 1½ hours in medium hot oven.

No. 87—SPICE CAKE No. 4.

½ cup of butter
½ cup of lard
1½ cups of dark brown sugar
2 eggs
½ cup of cold coffee
½ cup of sour milk
1 tsp. of soda
¾ tsp. of cinnamon
½ tsp. cloves
3½–4 cups of flour

Preparation: The butter, lard, yolks of eggs and sugar are

stirred to a cream, add the coffee, sour milk in which the soda has
been dissolved, cinnamon, cloves, flour and beaten whites of eggs.
Butter a pan, put the batter in and bake 1 hour or bake in 3 layers.

No. 88—SCOTCH TART.

¾ lb. of butter
1 lb. of sugar
½ lb. of finely cut raisins
9 eggs
Juice and rind of 1 lemon
1 lb. of flour
2 heaping tsps. of baking powder

Preparation: The butter is stirred to a cream, with yolks of

eggs, sugar, lemon juice and rind; add the flour and lastly the baking
powder and beaten whites of eggs. Butter a pan, put the batter in
and bake to a light brown color.

No. 89—LARD CAKE.

½ lb. pork lard
6 eggs
½ lb. of sugar
¼ lb. of corn starch
¼ lb. of flour
½ lb. blanched, ground, sweet almonds
20 blanched, ground, bitter almonds
1 heaping tsp. of baking powder

Preparation: Stir the yolks of eggs and sugar to a cream;

cream the lard and mix with the eggs and sugar. Now add flour and
almonds in spoonfuls and lastly the baking powder and beaten
whites of eggs. Butter a pan, put the batter in and bake to a nice
brown color.

No. 90—SEXTON’S CAKE.

½ lb. of butter
¼ lb. of sugar
½ lb. of extra fine flour
¼ lb. blanched, ground, sweet almonds
½ tsp. baking powder

Preparation: The butter is stirred to a cream; add the sugar,

ground almonds, flour and baking powder and stir 45 minutes.
Spread the batter ½ inch thick in small square muffin pans or in a
large square buttered cake pan, bake it to a light brown color and
leave it to cool a little before taking out of the pan, because it breaks
easily. After it has cooled off completely, dust with sugar or spread
frosting on.

No. 91—CHOCOLATE TART.

¼ lb. sweet chocolate
1 cup of water
¼ lb. ground almonds
¼ lb. of butter
3 eggs
1¼ cups of sugar
1½ tsps. of baking powder
2 cups of flour

For Filling.

1 pt. of whipped cream

 Preparation: Stir the butter, sugar and yolks of eggs to a
cream. Add the chocolate dissolved in water, unblanched, ground
almonds, flour and baking powder and the beaten whites of eggs.
Butter a round, loose bottom pan, put the batter in and bake in a
slow oven. Mix the whipped cream with sugar and vanilla and fill or
cover the tart with it before serving.

No. 92—ENGLISH BRIDE’S CAKE (FRUIT

CAKE).
1 lb. of butter
1 lb. brown sugar
10 eggs
1 lb. of flour
1 pt. of brandy
1 tbsp. ground cinnamon
2 lbs. finely cut citron
½ tbsp. of ground cloves
4 ground nutmegs
1 tsp. of baking soda
1 cup of molasses
10 lbs. of raisins
4 lbs. of currants
1 tbsp. of ground bark of nutmeg

Preparation: The butter is stirred to a cream with sugar and

yolks of eggs. Then work in ½ lb. of flour, the brandy mixed with the
spices and the molasses in which the soda is dissolved, the beaten
whites of eggs, then raisins, currants, citron and the other ½ lb. of
flour. The cake is baked 3 to 4 hours.
Remarks: This cake may be kept 20 years and longer and will
still be palatable. Wine is served with it.
 No. 93—GOOD TART DOUGH.
¼ lb. of butter
2 yolks of eggs
¼ lb. of blanched, ground almonds
¼ lb. of sugar
1 tbsp. of brandy
2 cups of flour
½ cup of cracker crumbs

Preparation: Cream the butter with sugar, egg yolks and

brandy, and add the flour. Roll out the dough and line a round, loose
bottom pan with it. Strew with ½ cup of cracker crumbs and ¼ lb.
blanched, ground almonds. Spread the fruit on the almonds. This
dough is very good for any kind of Fruit Tart.

No. 94—CHOCOLATE TART No. 2.

6 eggs
1 cup sugar
⅛ lb. chopped bitter chocolate
20 chopped almonds
½ cup of flour
1 heaping tsp. of baking powder

For Filling.

1 pt. of whipped cream

Preparation: Beat the whites of eggs to a stiff froth, add the

chopped bitter chocolate and almonds, then yolks of eggs and sugar,
and lastly the flour and baking powder. Bake in two layers. A little
before serving, spread whipped cream between the layers.
 No. 95—FILLED SAND TART.
Sand tart batter as in No. 82.
For Filling.

1 glass of fine fruit marmalade

For Frosting.

Rum frosting according to Chapter 20, No. 22

Preparation: The sand tart batter should be baked in 3 layers;

when cold, spread the fruit marmalade between the layers. Then
cover with rum frosting.

No. 96—TREE TART.

7 eggs
1 cup sugar
1 cup finest flour
Chocolate or sour filling

Preparation: Beat the yolks with a rotary egg beater, add ½

cup sugar and beat well again, then set aside. Beat whites to stiff
froth, add other ½ cup sugar. Mix both and add 1 cup flour
measured before sifting. Butter pans, dredge them with flour and
put the batter in. Bake in 8 layers in a slow oven. Spread chocolate
or sour cream filling as in No. 76, between the layers. You may also
cover with a frosting if you wish.

No. 97—FENCE TART.

First Layer.
 4 whites of eggs
3 yolks of egg
1 pinch of salt
⅓ tsp. cream of tartar
1¼ cups of sugar
1 cup flour

Second Layer.

⅓ or ¼ lb. bitter chocolate dissolved in ¼ cup hot water

1 cup of powdered sugar
1 tsp. of vanilla
½ package Knox gelatine dissolved in ¼ cup of water
1½ cups of cream
½ pt. whipped cream

Third Layer.

½ package Knox gelatine with pink coloring dissolved in ¼

cup of water
1 cup of powdered sugar
1½ cups of cream
½ pt. whipped cream
1 tsp. of vanilla

For the Covering.

1 pt. whipped cream

For the Fencing.

1½ doz, ladyfingers or macaroons

Preparation: The first layer. Whip whites of eggs to thin froth,

add salt and cream of tartar, then whip to a stiff froth, mix in the
sugar and then the yolks of eggs whipped to a cream. Mix the flour
in lightly and bake this batter in a buttered, round, loose bottom
pan. Loosen edge of layer and arrange ladyfingers or macaroons
around in circle. For the second layer. The dissolved bitter chocolate,
sugar, cream and vanilla are boiled for 2 minutes, stirring constantly;
stir in the dissolved gelatine, set the mixture in cold water and
continue stirring until it begins to thicken, then add the ½ pint of
whipped cream and spread the mixture over the baked layer. The
third layer is made exactly like the second layer only using the pink
coloring instead of the bitter chocolate; after the whipped cream is
added, spread the mixture over the chocolate layer.
Before serving, spread the 1 pint of whipped cream, to which
has been added a little sugar and vanilla, over the cake.

No. 98—FRUIT TART.

Apricot, Peach, Plum, Blueberry, Raspberry or
Strawberry Tart.
Prepare the batter according to No. 93, Good Tart Dough. Cover
with the desired fruit, either fresh or canned, sprinkle with sufficient
sugar, bake for 25 minutes. Before serving the cake, cover with
beaten cream or almond frosting, prepared according to No. 23,
Chapter 20 and then bake.

No. 99—SUNSHINE CAKE.

6 eggs
1 cup sugar
1 cup flour
1 even tsp. cream of tartar
Pinch of salt
½ tsp. vanilla
 Preparation: Beat the yolks of eggs first and add half the
sugar; beat the whites of eggs very dry and add remaining sugar;
beat well and add the vanilla, salt and the yolks of eggs; lastly, add
the flour and cream of tartar. Bake in a moderate oven one hour.

No. 100—LOVE CHOCOLATE CAKE.

¼ cup butter
1 cup sugar
1 egg
1 tsp. vanilla
½ cup sour milk
½ tsp. soda
2 squares bitter chocolate
½ cup hot water
1 large cup flour

Preparation: Cream butter and sugar; add the egg and vanilla;
add the milk in which the soda is dissolved; dissolve the chocolate in
a half cup boiling water, let cool and add; lastly, add the flour. Bake
in flat cake tin about 45 minutes.

No. 101—ANGEL FOOD.

Whites of 9 eggs
1 cup sugar
1 tsp. vanilla
1 cup flour
1 tsp. cream of tartar

Preparation: Beat the whites of eggs to a stiff froth; boil the

sugar with 4 tablespoons of water until all the sugar is dissolved;
beat the sugar syrup into the whites of the eggs; add vanilla and the
flour and cream of tartar. Bake slowly one hour.

No. 102—FRUIT CAKE.

1¼ cups sugar
½ cup butter
Yolks of 2 eggs
1 cup sour milk
1 tsp. baking soda
1½ cups flour
½ tsp. cloves
½ tsp. cinnamon
½ cup dates, raisins and citron
1 cup walnuts

Preparation: Cream the sugar and butter, add yolks of eggs,

cloves and cinnamon; dissolve the soda in the sour milk and add to
the rest; add the flour and mix well; lastly add the raisins, dates,
citron and walnuts. Bake about 45 minutes.

No. 103—CREAM PUFFS.

1 large teacup hot water
½ tsp. butter
1 teacup flour
4 eggs

Preparation: Stir the flour into the boiling water and butter. Set
aside to cool and, when cold, stir in the unbeaten eggs one at a
time. Drop in muffin tins and bake in a fairly hot oven. When baked,
fill with beaten cream, sweetened to taste and flavored with vanilla.
 No. 104—CREAM PUFFS.
1 cup boiling water
½ cup butter
1 cup pastry flour
3 eggs, beaten
Small pinch of soda

Preparation; Pour the water over the butter. As soon as it boils

and the butter is melted, stir in the flour and keep stirring until it
leaves the sides of the pan. Let cool, stir in the eggs and soda, drop
on the buttered pans and bake thirty minutes. Do not open the oven
door for twenty minutes for fear they will fall. Fill with whipped
cream, sweetened and flavored.

No. 105—YEAST DOUGHNUTS.

1 cup sugar
3 cups milk
Flour to make soft sponge
1 yeast cake
Mix and let stand over night

In the Morning Add:

1 cup sugar
½ cup butter
3 eggs
½ a nutmeg
½ tsp. soda
Flour to mix stiff

Preparation: Let rise, then roll and cut in shape desired, or roll
into long strips and twist into shape. Let rise again while the lard is
heating and then fry. Raised doughnuts require longer cooking.

No. 106—SOUR CREAM DOUGHNUTS.

5 tbsps. sour cream
1 cup milk
½ cup butter
2 eggs
Little salt
1 tsp. soda
¼ tsp. cinnamon
¼ tsp. nutmeg
1 tsp. baking powder
1 cup sugar
1¼ pts. of flour

Preparation: Stir butter, eggs and cream well, add all other
ingredients, roll and cut the dough, bake in hot lard to golden brown
color and sprinkle powdered sugar over.

No. 107—BLITZ-KUCHEN.
1 lb. sugar
½ lb. butter
8 eggs
1 lb. flour

Preparation: Stir sugar, butter and yolks of eggs together well,

add the stiffly beaten whites of eggs and flour. Bake in a long tin and
cover with sugar, cinnamon and chopped almonds. Cut and serve
while warm.
 No. 108—SPICE CAKE.
2 cups brown sugar
½ cup butter
2 eggs
2 egg yolks
½ cup sour milk
1 tsp. nutmeg
2 cups flour
1 tsp. cloves
1 tsp. cinnamon
1 tsp. soda

Preparation: Beat the sugar, butter and eggs together until

smooth; add the remaining ingredients. Bake in three layers and put
together with white frosting.

No. 109—WHIPPED CREAM CAKE.

Make a good sponge cake dough (see No. 29). and omit the
chocolate.
Filling.

1 pint whipped, sweet cream

1 pound blanched, chopped almonds
Vanilla
Sugar

Preparation: After the layers are baked, beat the cream stiff,
add sugar, vanilla and almonds; sweeten the cream and spread
between the layers and on top. This is the queen of all cakes.
 No. 110—WALNUT CAKE.
1 lb. walnuts (leave out 14 halves for the top)
1 cup powdered sugar
¾ cup crackers (rolled fine)
8 eggs
1 tsp. baking powder
1 cup powdered sugar

Filling.

2 cups milk
Corn starch to thicken
½ cup sugar
Vanilla
Yolks of 2 eggs

Preparation: Cream the yolks of eggs and the sugar; add the
beaten whites of the eggs; mix the rolled crackers, finely chopped
nuts and baking powder and add. Bake in three layers in a slow
oven.
Stir powdered sugar with a little water, spread on top of cake
and put on the walnut halves.

No. 111—ANGEL CAKE.

1 scant cup flour
1 scant cup sugar
1 tsp. baking powder
1 cup walnuts (cut)
1 cup dates (cut)
4 eggs
 Preparation: Cream the eggs separately, add sugar, walnuts,
dates, baking powder and flour. Bake in a buttered pan.
 CHAPTER 20.
FILLINGS AND FROSTINGS FOR
CAKES.

No. 1—VANILLA FILLING.

½ cup of sweet cream
3 eggs
1½ tsps. of vanilla
4 tbsps. of sugar

The preparation of the vanilla filling is the same as given in

Chapter 19, No. 29, Layer Cake with Chocolate.

No. 2—NUT FILLING No. 1.

1 tsp. of butter
½ cup of milk
2 tbsps. of flour
1 cup of sugar
½ cup of chopped nuts
1 egg

Preparation: The ingredients, excepting the white of egg, are

all mixed well. The mixture is cooked one minute, stirring constantly,
then cooled and the beaten white of egg mixed in.
 No. 3—RAISIN FILLING.
1 cup of sugar
¼ cup of water
1 cup of seedless chopped raisins
1 white of egg

Preparation: Water and sugar are stirred well, then boiled for
one minute and taken from the stove. The raisins and beaten white
of egg are mixed in and the filling spread on the cake, while still
warm.

No. 4—NUT FILLING No. 2.

1 cup of sugar
1 cup of finely chopped nuts
1 cup of sour cream

Preparation: The ingredients are mixed and cooked for several

minutes, stirring constantly.

No. 5—ALMOND FILLING.

2½ tbsps. of sugar
1 tbsp. of water
½ tsp. of vanilla
1 cup of blanched, ground almonds
Whipped cream, to taste

Preparation: The sugar, water and vanilla are boiled 1 minute

and spread on the cake while warm. The almonds are strewn on
immediately, then cover with the sweetened whipped cream.
 No. 6—LEMON FILLING.
½ cup of milk
4 tbsps. of sugar
1 tsp. of lemon extract
2 eggs
1 tsp. of flour

Preparation: This is given in Chapter 19, No. 33, Sponge Cake.

No. 7—WALNUT FILLING.

½ cup of chopped walnuts
½ cup of chopped seedless or seeded raisins
1 cup of sugar
¼ tsp. of vanilla
¼ cup of water

Preparation: The ingredients are mixed and boiled, stirring

constantly, then spread on the cake while still warm.

No. 8—CHOCOLATE FILLING.

¼ lb. of sweet chocolate
½ cup of sugar
1 tsp. of vanilla
2 tbsps. of water
3 whites of eggs

Preparation: The chocolate is dissolved in the water, vanilla

and sugar added and boiled 3 minutes while stirring constantly. Mix
in the beaten whites of eggs while the chocolate is still warm.
 No. 9—COCOANUT FILLING.
¼ lb. of cocoanut
2 whites of eggs
½ cup of sugar
1 tsp. of vanilla

Preparation: The whites of eggs are beaten to a stiff froth, the

cocoanut mixed in, then sugar and vanilla.

No. 10—BANANA FILLING.

4–5 bananas
¼ cup of sugar

Preparation: The bananas are peeled and sliced, mixed with

sugar and spread between the layers of the cake.

No. 11—DATE FILLING.

1 cup of dates
Juice and rind of 1 orange
2 tbsps. of water
½ cup of sugar

Preparation: The dates are chopped fine and mixed with

orange juice and grated orange rind, water and sugar and spread on
the cake.

No. 12—CHOCOLATE FROSTING No. 1.

 ⅛ lb. of sweet chocolate
¼ lb. of sugar
4 tbsps. of water
1 tsp. of vanilla

Preparation: Chocolate and sugar are dissolved in the water

and vanilla and cooked until it threads. Stir it a little while longer and
spread on the cake quickly, then put the cake into the oven again for
1 minute.

No. 13—CHOCOLATE FROSTING No. 2.

½ cup of butter
⅛ lb. of chocolate
2 cups of sugar
1 cup of boiling water
½ tsp. of vanilla

Preparation: The chocolate is grated, mixed with the other

ingredients, and boiled a few minutes, stirring constantly, until quite
stiff. Take off the fire, stir until nearly cold and spread on the cake
immediately.

No. 14—CHOCOLATE FROSTING No. 3.

½ lb. of confectionery sugar
2 heaping tbsps. of cocoa
1 tsp. of vanilla
3–5 tbsps. of water

Preparation: Sugar, cocoa and vanilla are mixed and the cold
water gradually stirred in, being careful not to take too much water
because the mixture must be thick. Spread on the cake at once. If
you wish, add ½ cup of blanched and chopped almonds.

No. 15—VANILLA FROSTING.

1 lb. of confectionery sugar
1 tbsp. of vanilla
Sufficient cream to make the frosting of proper consistency

Preparation: Vanilla is added to the sugar and the cream in ½

teaspoonfuls. Take only sufficient cream to make the frosting of
consistency to spread.

No. 16—LEMON FROSTING.

1 lb. confectionery sugar
Juice of 1 lemon
Cream, if necessary

Preparation: The lemon juice is mixed with the sugar and

stirred a while. If the frosting is too thick, add more cream.

No. 17—TUTTI-FRUTTI FROSTING No. 1.

1½ cups of sugar
1 tbsp. of cocoa or chocolate
1 tbsp. of butter
¼ cup of cocoanut
¼ cup of chopped walnuts
½ cup of milk
¼ cup of finely chopped raisins
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