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All you need to know about

Vascular Surgery

A GUIDE FOR MEDICAL STUDENTS,

EARLY YEAR DOCTORS AND
ALLIED HEALTHCARE PROFESSIONALS
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ISBN 978-1-3999-7402-8 EDITED BY FOREWORD

First Edition Mr Patrick Coughlin Consultant Vascular Surgeon. Leeds Teaching Hospital NHS Trust
Mr Lasantha Wijesinghe Consultant Vascular Surgeon. Member of Council RCS England

Vascular surgery involves the medical and surgical management of

Publishers AUTHOR ACKNOWLEDGEMENT
Vascular Society of patients with diseases of the arteries, veins and lymphatics. I am
Great Britain & Ireland, Dr Mujahid Abdalla Specialist Registrar Mr Ian Massey Clinical Lead Prosthetist, biased but, in my humble opinion, vascular surgery is the greatest
c/o Executive Business in Radiology. Royal Stoke University Hospital Artificial Limb and Appliance Centre, surgical specialty. The surgery is technically challenging and exciting
Support Limited, City Mr Julien Al Shakarchi Consultant Rockwood Hospital and involves life and limb saving operations for peripheral arterial
Wharf, Davidson Road, Vascular Surgeon. Worcestershire Royal Mr Ciaran McDonnell Consultant disease, carotid artery disease and aortic aneurysms. The medicine
Hospital Vascular Surgeon. Mater Misericordiae
Lichfield, Staffordshire,
University Hospital, Dublin
is also important as our patients are often frail with multiple
WS14 9DZ Mr Chris Ashmore Clinical Research co-morbidities. In addition much of our practice is evidence based
Fellow. Leeds Teaching Hospital NHS Trust Mr Lewis Meecham Consultant Vascular
Email: admin@ Surgeon and active vascular research helps us make the right treatment
vascularsociety.org.uk Dr Leanne Atkin Consultant Nurse
Professor Arun Pherwani Keele decisions for our patients.
Specialist. Mid Yorkshire Teaching NHS Trust
University School of Medicine
Mr Marc Bailey Associate Professor.
© Vascular Society of University of Leeds Mr Harj Rayt, Consultant Vascular The surgical specialities are often only covered briefly in
Great Britain & Ireland Surgeon. Glenfield Hospital, Leicester undergraduate courses and so this book hopes to give you an
Dr Tom Baker Core Surgical Trainee.
2023. All rights reserved. Dorset and Wiltshire Vascular Network
Mr David Russell Consultant Vascular introduction to vascular surgery and inspire budding doctors to
Surgeon. Leeds Teaching Hospital NHS Trust
Mr Henry Bergman Research Fellow. consider training in this brilliant surgical specialty. This beautifully
Dr Fatemeh Sakhinia Consultant illustrated and easy to read book has been written for medical
Cambridge University Hospital NHS Trust Radiologist. Royal Stoke University Hospital
No part of this publication Mr David Bosanquet Consultant Miss Becky Sandford Consultant
students, doctors in the early stages of their career as well as
may be reproduced, stored Vascular Surgeon. Aneurin Bevan University Vascular Surgeon. St. Thomas's Hospital, allied healthcare professionals who are looking to gain a greater
Health Board London understanding of vascular surgery.
in a retrieval system or
transmitted in any form by Miss Victoria Bristow Vascular Nurse Professor Rob Sayers Professor of
Specialist. Cambridge University Hospitals Vascular Surgery. Glenfield Hospital,
any means, electronic, NHS Trust
I would like to thank everyone who has helped bring this book to
Leicester
mechanical, photocopying, Mr Aminder Singh Research Fellow.
fruition by contributing chapters, editing and illustrating skills – it has
Mr Patrick Coughlin Consultant Vascular
recording or otherwise Surgeon. Leeds Teaching Hospital NHS Trust Cambridge University Hospital NHS Trust been a real team effort to provide this important free resource.
without the prior Dr Than Dar Academic Clinical Fellow. Miss Kaji Sritharan Consultant Vascular
permission of the Leeds General Infirmary Surgeon. Department of Vascular Surgery, Please enjoy reading or dipping into as a quick reference guide.
Liverpool University Hospitals NHS
publisher. Dr Maram Dawish Surgical Trainee. Foundation Trust.
Vascular Surgery Department, University
Hospital of Wales, Cardiff Mr Fabio Stocco Academic Clinical Miss Rachel Bell MS FRCS
Fellow. Leeds General Infirmary. Consultant Vascular Surgeon
Care has been taken to Miss Claire Dawkins Consultant Vascular
Surgeon. Newcastle Upon Tyne Hospital NHS
Millie Sucharitkul Medical Student. President of the Vascular Society of Great Britain
confirm the accuracy of University of Edinburgh.
the information presented.
Foundation Trust and Ireland
Mr Jon De Siqueria Academic Clinical Dr Penny Sucharitkul Academic
However, the editor, Lecturer. Leeds Teaching Hospital NHS Trust Foundation Trainee. Bristol Royal Infirmary.
contributors, and publisher Mr Conor Dooley Specialist Registrar in Mr Chris Twine Consultant Vascular
are not responsible for Vascular Surgery. Mater Misericordiae Surgeon. Bristol Royal Infirmary.

errors or omissions or for University Hospital Dublin. Miss Mary Weisters Consultant Vascular
Dr Ismay Fabre Core Surgical Trainee. Surgeon. Dorset and Wiltshire Vascular
any consequences from Network
Welsh Deanery
application of the
Miss Rachael Forsythe Consultant Mr Chandana Wijewardena Consultant
information contained Vascular Surgeon. Cambridge University
Vascular Surgeon. Edinburgh Royal Infirmary
within this book. Hospital NHS Trust
Mr Sam Galea Higher Surgical Trainee.
Dr Rosannah Williams Clinical Fellow,
Oxford
Swansea University Health Board.
Dr Georgios Koufopoulos Clinical
Fellow in Vascular Surgery. Liverpool
Miss Emma Wilton Consultant Vascular
University Hospital NHS Foundation Trust Surgeon. Oxford University Hospital NHS
Foundation Trust
Dr JY Kwan Academic Clinical Fellow.
Leeds Teaching Hospital NHS Trust Dr Andrew Winterbottom Consultant
Interventional Radiologist. Cambridge
Mr Tristan Lane Consultant Vascular University Hospital NHS Trust.
Surgeon. Cambridge University Hospitals
NHS Trust Dr Natalie Yonan Foundation Doctor.
Newcastle Upon Tyne Hospital NHS
Mr Thomas Lyons Higher Surgical Foundation Trust.
Trainee. Worcestershire Royal Hospital
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INTRODUCTION CONTENTS

The many contributors to this volume share a love for vascular Foreword ........................................................................................................................................ i
surgery; its many complexities, its joys, its anatomical range, its beauty
and its frustrations. We are unified by the desire to make the lives of
vascular patients better, to relieve their pain and to save life and limb. Introduction ................................................................................................................................. ii
To do this we rely on the expertise of other professionals, our teams.
It is therefore intentional that while this book has a surgical emphasis Theme 1: Overview of vascular surgery
for Foundation doctors and medical students, it is also aimed at those 1. Vascular Anatomy - Chapter 1 ................................................................................................. 4
professionals such as specialist nurses, surgical care practitioners
2. Vascular Anatomy - Chapter 2 ................................................................................................ 6
and therapists without whom our work would be impossible and not
3. Biology of vascular disease ..................................................................................................... 8
half as rewarding.
4. Venous imaging .................................................................................................................... 10
The management of vascular disease and the typical vascular patient 5. Arterial imaging ..................................................................................................................... 12
have changed over the years. We now deal with more elderly 6. Strategies for revascularisation ............................................................................................. 14
comorbid patients but have a wide array of endovascular treatments
available. However, the basics of vascular surgical care remain rooted
in compassion combined with scientific knowledge and technical skill. Theme 2: Peripheral arterial disease and lower limb disease
7. Best medical therapy ........................................................................................................... 18
Though the numbers of infrarenal aneurysms and carotid stenoses 8. Intermittent claudication ........................................................................................................ 20
suitable for surgery may have decreased in some populations, the 9. Chronic limb threatening ischaemia ...................................................................................... 22
global prevalence and mortality associated with peripheral arterial 10. Diabetic foot disease ............................................................................................................. 24
disease has increased substantially. The scourge of diabetic vascular 11. Lower limb amputation ......................................................................................................... 26
disease is upon us. Likewise, venous disease in all forms demands
greater expertise and resources. Trauma and vascular injuries
secondary to interventional medical procedures seem to increase Theme 3: Diseases of the aorta
annually. The need for enthusiastic, committed young people from 12. Abdominal aortic aneurysm ................................................................................................. 30
all backgrounds to train in vascular surgery is clear. 13. Ruptured abdominal aortic aneurysm ................................................................................... 32
14. Type B aortic dissection ........................................................................................................ 34
If you are determined to follow another medical specialty, this book
15. Thoracic and arch aneurysmal disease ................................................................................ 36
will be a good reference when you come up against a vascular
problem. If you are thinking about a career in vascular surgery but
are still not sure, we hope these chapters will kindle a love for it. Theme 4: Venous disease
If you are already drawn to this brilliant discipline then we hope you 16. Varicose veins and chronic venous disease .......................................................................... 40
enjoy the book and will share it widely.
17. Venous leg ulceration ........................................................................................................... 42
18. Deep venous disease ............................................................................................................ 44

Mr Lasantha Wijesinghe Mr Paddy Coughlin

Consultant Vascular Surgeon Consultant Vascular Surgeon Theme 5: Miscellaneous
Member of Council RCS Member of Council VSGBI 19. Carotid artery disease ........................................................................................................... 48
England 20. Thoracic Outlet Syndrome and Vasospastic disease ............................................................ 50
21. Management of patients with renal disease .......................................................................... 52
22. Acute limb ischaemia ............................................................................................................ 54
23. Mesenteric and other visceral disease .................................................................................. 56

Acknowledgements ................................................................................................................. 58

ii 1
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THEME 1

OVERVIEW OF VASCULAR SURGERY

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1
internal carotid artery
VASCULAR ANATOMY – CHAPTER 1 has no branches in the
neck. The external
Thorax
The sympathetic chain runs along the length of the vertebral column and consists of pre- and
Than Dar, Rob Sayers
l
carotid artery gives off
post-ganglionic fibres and sympathetic ganglia. It is a fundamental part of the sympathetic
eight branches that
nervous system, and allows nerve fibres to travel to spinal nerves that are superior and inferior to
primarily supply the
the one in which they originated.
face.
l The stellate ganglion lies on the neck of the first rib at the thoracic inlet. It provides the majority of
l The internal jugular
the sympathetic nerve signals to the head, neck, arms and aspects of the upper chest. During
vein exits the cranial
endoscopic thoracic sympathectomy, a treatment to manage hyperhidrosis, the sympathetic trunk
Vascular surgeons operate all over the body, therefore detailed knowledge of the cavity through the
must be divided below the ganglion to avoid Horner’s
jugular foramen to Scalenes:
vascular anatomy and surrounding structures is important in understanding vascular descend in the carotid
syndrome, recognised as a triad of ptosis, miosis, and - Posterior
ipsilateral facial anhidrosis. The aortic arch begins and - Middle
pathologies, procedures, and complications. sheath. - Anterior
ends at the angle of Louis which lies at the T4/5
Several cranial nerves Divisions of brachial plexus
l vertebral disc level. Its three main branches are the
are closely related to brachiocephalic, left common carotid, and left Phrenic nerve
the carotid arteries subclavian arteries. Subclavian: - Artery
- Vein
during their course. l It continues as the descending thoracic aorta in the
l Damage to cranial posterior mediastinum giving off the bronchial,
Head Anterior nerve IX mediastinal, oesophageal, pericardial, superior
communicating (glossopharyngeal) phrenic, intercostal and subcostal arteries.
l Blood supply to the brain arises from the internal carotid and artery Anterior
vertebral arteries. The internal carotid arteries are divisions of
cerebral produces impairment
artery l The brachial plexus and subclavian vessels can be
the common carotid arteries. in the gag reflex and
compressed when they exit the thorax to cause
Posterior swallowing. Damage to
The internal carotid artery enters the cranial cavity through the communicating Middle
thoracic outlet syndrome. This can be due to Pectoralis
l
cranial nerve XII minor
carotid foramen and runs a tortuous intracranial course to artery cerebral compression from the anterior scalene muscle, a
artery (hypoglossal), which Axillary: - Artery
bifurcate into its terminal branches, the anterior and middle cervical rib or due to compression between the
innervates the - Vein
cerebral arteries. clavicle and the first rib. Features include upper
muscles of the tongue,
limb paraesthesia, claudication and weakness.
l The territory of the anterior cerebral artery includes the midline produces tongue
Anterior
of the frontal lobe and superior and middle portions of the choroidal deviation towards the
parietal lobe. A stroke in this artery commonly affects the artery side of the lesion.
contralateral lower limb. l Cranial nerve X
l The territory of the middle cerebral artery includes the motor (vagus) gives off Upper limb
and somatosensory cortices. A stroke in this artery commonly Basilar
Posterior branches to the
artery
cerebral
pharyngeal plexus
l Knowledge of the anatomy of the upper limb is helpful to appreciate the steps in
produces such deficits in the face, trunk and upper limbs. artery
that innervate the procedures such as embolectomies and formation of renal dialysis fistulas.
l The vertebral artery arises from the first part of the subclavian Pontine
arteries pharyngeal l The axilla acts as a conduit for neurovascular structures to enter the upper limb. It contains
artery in the superior mediastinum. It ascends through the
constrictors for the axillary artery, vein, lymph nodes and the brachial plexus.
transverse foramina of the cervical vertebrae to enter the cranial
Anterior Vertebral swallowing. The The axillary vein lies medial to the artery. It is formed by the basilic and brachial veins.
cavity through the foramen magnum. It goes on to supply the spinal artery
l
muscles of the larynx
posterior part of the brain, cerebellum, brainstem and spinal artery
are supplied by the
cord. Features of a stroke in this artery include ataxia, dizziness l The axillary artery is a continuation of the
recurrent laryngeal
and nystagmus. Axillary subclavian artery beginning at the outer border of
except cricothyroid,
The vertebral arteries form an anastomotic connection with the internal carotid
artery the first rib. It is divided into three parts based on
l which is innervated
arteries at the base of the brain, known as the Circle of Willis. This rich anastomosis between the anterior and its relation to pectoralis minor.
by the external
posterior circulations to the brain allows cerebral perfusion to be preserved if an artery becomes occluded. branch of the l In the arm, it continues as the brachial artery at the
superior laryngeal inferior border of teres major. One of the branches
nerve. A superior is profunda brachii which runs with the radial nerve
Profunda in the spinal groove of the humerus.
laryngeal nerve palsy brachii artery
produces a hoarse The cubital fossa is a triangular region in the elbow.
Neck voice, reduced vocal
l

Brachial It is bound laterally by brachioradialis and medially

l It is important to be aware of the many major frequency range, and artery by pronator teres to form a distal apex. The base
Internal neurovascular structures in the neck that will be increase risk of goes across the two humeral epicondyles. Beneath
carotid artery encountered specifically during a carotid aspiration. the deep fascia of the forearm, the following
endarterectomy. The ansa cervicalis is structures can be seen from lateral to medial:
External l
carotid artery l The carotid artery lies within the carotid sheath formed by the C1-3 bicipital tendon, brachial artery and median nerve.
alongside the internal jugular vein and vagus nerve in nerve roots. It l The brachial artery divides into the radial artery
the anterior triangle of the neck which is bound innervates the laterally and ulnar artery medially. They continue in
infrahyoid muscles Ulnar artery
Vertebral posteriorly by the anterior border of the Radial artery the forearm to form the deep and superficial
artery sternocleidomastoid, anteriorly by the midline of the involved in speech and palmar arches that supply the hand.
Superior neck and superiorly by the mandible. swallowing. It can sit
thyroid The main superficial veins in the upper limb are the
artery on top of the carotid l
Right l The right common carotid artery arises from the basilic and cephalic veins which can be seen on
subclavian artery and may need
artery Common brachiocephalic artery. The left common carotid artery the ulnar and radial aspects of the forearm
to be divided to
carotid artery arises directly from the aortic arch. In some cases, it respectively.
facilitate carotid
can arise from the brachiocephalic artery, which is Palmer Arch
surgery.
Brachiocephalic referred to as a bovine arch.
artery
l The common carotid arteries bifurcate at C3-4 level
into the internal and external carotid arteries. The

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2 VASCULAR ANATOMY – CHAPTER 2

Harj Rayt, Than Dar2
Lower limb
l The external iliac artery continues as the common femoral artery in the femoral
triangle, which is bound superiorly by the inguinal ligament, laterally by sartorius,
and medially by adductor longus.
l The common femoral artery branches into the profunda femoris and superficial
femoral arteries. The superficial femoral artery continues its course anteromedially
in the subsartorial (adductor) canal. It emerges at the adductor hiatus of adductor
Vascular surgeons operate all over the body, therefore detailed knowledge of the magnus to become the popliteal artery.
l The popliteal fossa is a diamond
vascular anatomy and surrounding structures is important in understanding vascular shaped space behind the knee. It
Common
femoral artery
Common
femoral artery

pathologies, procedures, and complications. is bound by the hamstrings Saphenofemoral

Profunda
superiorly and the two heads of femoris artery
junction
gastrocnemius inferiorly. Its Great
contents include the popliteal vein saphenous vein
Superficial
and artery, tibial, sural, and femoral artery Profunda
common peroneal nerves, and femoral vein
lymph nodes. Superficial
Popliteal
Clinical notes l At the inferior border of popliteus, artery
femoral vein
Abdomen and pelvis Suprarenal the popliteal artery divides into the Perforator veins
Superior aorta May-Thurner Anterior
l The abdominal aorta is a retroperitoneal mesenteric
l
anterior tibial artery and tibial artery Popliteal vein
artery syndrome tibioperoneal trunk. The anterior
structure that begins at T12 as it descends Coeliac artery
- branching tibial artery passes through the Tibioperoneal Saphenopopliteal
from the diaphragmatic crura to L4, where it into hepatic / This is characterised trunk junction
bifurcates into the common iliac arteries. splenic and by the presence of an interosseous membrane between
left gastric anatomical variant in the tibia and fibula IN THE Peroneal artery
l The abdominal aorta gives rise to paired Short saphenous
which the right ANTERIOR COMPARTMENT down Posterior tibial
visceral, unpaired visceral, and parietal vein
common iliac artery the leg. It crosses the ankle joint to artery
branches.
compresses the left become the dorsalis pedis artery,
l The coeliac trunk arises at T12 to supply the common iliac vein which lies lateral to the extensor hallucis longus tendon. It joins the lateral plantar
foregut from the lower third of the oesophagus against the lumbar artery in the foot to complete the plantar arch.
to the second part of the duodenum. It gives Inferior mesenteric spine. The resultant
Gonadal arteries artery l The tibioperoneal trunk divides into the posterior tibial and peroneal arteries.
off three branches: the left gastric, splenic, and reduction in blood The posterior tibial artery descends deep to gastrocnemius and soleus IN THE
common hepatic arteries. flow increases the POSTERIOR COMPARTMENT. It passes behind to the medial malleolus through
l The superior mesenteric artery arises at L1 to Common iliac
Internal iliac risk of deep vein the tarsal tunnel before dividing into the medial and lateral plantar arteries. The
artery
supply the midgut from the second part of the artery thrombosis. peroneal artery passes behind the fibula and descends IN THE LATERAL
duodenum to two thirds along the transverse COMPARTMENT of the leg.
colon.
External iliac l Nutcracker
artery The main superficial veins in the lower limb are the great and small saphenous
syndrome l

l The inferior mesenteric artery arises at L3 to veins.

supply the hindgut from the distal third of the This is characterised
by compression of l The great saphenous vein runs anterior to the medial malleolus. It ascends medially
transverse colon to two thirds along the
the left renal vein, up the lower limb, close to the saphenous nerve, to drain into the femoral vein in
rectum.
typically between the the groin. The small saphenous vein runs posterior to the lateral malleolus. It
l The common iliac arteries bifurcate at the abdominal aorta and ascends posteriorly up the leg, close to the sural nerve, to drain into the popliteal
sacroiliac joints to become the internal and superior mesenteric vein.
external iliac arteries. artery. Clinical l The deep veins follow the course of the major arteries in the lower limb, for
l Change text to: The inferior vena cava begins symptoms of this example the femoral vein and artery accompany each other in the femoral sheath.
at L5 where the common iliac veins unite. It syndrome can include In the presence of deep vein thrombosis, flow can be directed into the superficial
ascends in the abdomen to the right of the Portal haematuria and veins via the perforating veins.
vein
abdominal aorta to enter the diaphragm at T8. abdominal or flank
Splenic vein pain.
l The renal vein on the left is longer than the Renal vein
right, generally drapes over the aorta and l Varicocele
receives drainage from multiple tributaries Inferior
including the left gonadal vein, whereas the
Superior This is a scrotal
mesenteric vena cava
swelling due to dilated Clinical notes
right gonadal vein drains directly into the vein
inferior vena cava. veins in the
Inferior Common iliac vein l Surface landmarks
mesenteric pampiniform plexus.
vein As the left testicular The common femoral artery lies at the mid-inguinal point, halfway between the anterior
Internal vein drains into the superior iliac spine and the pubic symphysis. This is important in locating the common femoral
iliac vein left renal vein, a left- artery for endarterectomies or endovascular procedures.
sided varicocele
External
iliac vein should raise l Acute compartment syndrome
suspicion of left-sided Intermuscular septa divide the leg into four compartments: anterior, lateral, superficial
renal cell carcinoma posterior, and deep posterior. The swelling or bleeding that ensues after trauma or ischaemia
as it can spread increases the pressure within these compartments, which can lead to compression of their
along the course of contents. This is a limb threatening condition that requires emergency four compartment
the renal vein. fasciotomy to relieve the pressure.

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Aneurysmal development

3 BIOLOGY OF VASCULAR DISEASE

Fabio Stocco, Marc A Bailey Aneurysm: Defined as
a progressive, focal,
In genetically susceptible
patients, environmental
BOX 1
THE STRUCTURE OF
BLOOD VESSELS
permanent dilatation of factors such as smoking,
an artery (>1.5x normal). hypertension and
Clinically sequelae are atherosclerosis cause
rupture with a high a dysfunction and
WHAT CAUSES VASCULAR DISEASE? associated mortality rate or weakening of the
l Vascular disease encompasses pathology of the circulatory system (blood vessels) and the consequences less commonly thrombosis aortic wall.
of coagulation. This includes diseases of arteries (aorta, peripheral, or carotid), veins, lymphatic channels or embolism.
and both arterial and venous thrombosis / embolism. Elastin and collagen are lost and the media degenerates. The wall loses tensile strength and
l Common risk factors for vascular disease are genetics, modifiable factors (e.g., smoking, high cholesterol, dilates forming an aneurysm (aorta >3 cm). AAA grow at ~2 mm per year. As size increases so
high blood glucose, high blood pressure), trauma or infections. does the wall shear stress and eventually the aorta will rupture. Elective repair is therefore
offered when the AAA is large (>5.5 cm) to remove the risk of rupture.
l The most common cause of vascular disease is atherosclerosis, which describes the build-up of a
cholesterol-laden fatty plaque inside the artery wall causing narrowing of the lumen and reduced blood
supply to target organs – in the leg arteries this causes intermittent claudication.
Neointimal
Thrombosis hyperplasia
ATHEROSCLEROSIS 1. Tunica intima
Thrombosis describes the clotting of blood in the arterial or (NIH) (endothelium): the inner
venous circulation. It can be triggered by (i) hypercoagulability,
Several factors drive chronic endothelial injury that triggers formation of Following revascularisation layer of the blood vessels
(ii) vascular wall pathology or (iii) altered blood flow (known as
atherosclerosis: (e.g. angioplasty, bypass graft), is a single cell layer of
Virchow’s triad).
treatment failure is a major endothelial cells that is
• Hyperlipidaemia • Hypertension • Haemodynamics • Smoking Arterial injury (including surgery) or atherosclerotic plaque clinical problem. NIH describes anti-thrombitic and in direct
• Toxins • Viruses • Immunity rupture can lead to exposure of subendothelial proteins: the the unwanted pathological contact with flowing blood.
von Willebrand factor binds to platelet glycoproteins leading vascular remodelling response Implicated in vascular
to platelet aggregation and thrombus formation. Reduced following revascularisation, diseases.
Endothelial injury results in endothelial dysfunction and increased blood flow due to lumen narrowing via atherosclerotic plaque, leading to re-stenosis and
permeability. Monocytes adhere to the dysfunctional endothelium and NIH or stasis in diseased veins is an important driver of 2. Tunica media (middle or
eventually occlusion.
migrate into the intima. They differentiate into macrophages. thrombosis in vascular surgery. Genetic thrombophilia medial layer): primarily
(e.g. Factor V Leiden) increases the risks of thrombosis. Endothelial injury leads to consists of vascular smooth
stimulation of VSMC proliferation muscle cells, elastin and
COAGULATION CASCADE and migration. This causes collagen. The thickest layer
Within the intima macrophages are activated. Vascular smooth muscle cells INTRINSIC release of inflammatory and more prominent in
(VSMC) are recruited by factors released from activated platelets, EXTRINSIC cytokines and synthesis of new arteries than veins. Provides
XIIa XII
macrophages and the generally inflamed vascular wall milieu. extra-cellular matrix. This support for the vessel,
TISSUE FACTOR FROM
DAMAGED TISSUE XIa XI causes thickening of the intima, propagates the pulse wave,
TF VIIa VII narrowing the lumen with a allows contraction / dilation
IXa IX
fibrous plaque in a similar way to regulate blood flow and
VIIIa VIII
The VMSC de-differentiate and adopt a macrophage like phenotype. These to atherosclerosis. The altered blood pressure. Implicated
X Xa flow in the treated segment of in vascular diseases.
activated cells and invading macrophages engulf cholesterol (foam cells)
Va V artery (or bypass graft) increases
releasing further inflammatory cytokines; a positive feedback loop.
PROTHROMBIN THROMBIN the risk of thrombosis and graft 3. Tunica adventitia
occlusion / failure. (outermost layer): contains
FIBRINOGEN FIBRIN connective tissue with
varying amounts of elastic
The VSMC proliferate and synthesise collagen and abnormal extracellular
and collagenous tissue.
matrix. Extracellular lipids are engulfed. The lesion grows with a lipid rich
Venous disease Mainly fibroblasts. Attaches
core and a protective fibrous cap made of VSMC. Arterial thrombosis
Chronic venous hypertension (CVH) is a the vessel to the
occures when there is rupture of the fibrous cap
common disorder of the lower extremities surrounding tissue and
which can manifest as varicose (dilated and provides general support.
tortuous) veins or deep venous insufficiency.
Peripheral arterial disease It is caused by dysfunctional valves causing Varicose vein + inflamed
incompetent valve
l Atherosclerotic plaque causes arterial lumen narrowing and reduced end organ venous reflux, increasing the venous pressure + reflux
perfusion. An example of this is in peripheral arterial disease (PAD): this causes in the leg. Deep venous obstruction,
reduced blood flow to the limbs, most commonly the legs, which can cause secondary to venous thrombosis, can also
intermittent claudication or chronic limb threatening ischaemia. cause CVH.
l Acute thrombosis occurs where there is disruption of the plaque fibrous cap Venous reflux can be caused by dysfunction
exposing its thrombogenic lipid core resulting in the development of intraluminal of pressure-sensing in the vein wall which
thrombosis. This can either occlude the lumen (commonly a cause of acute leads to pathological vascular remodelling
myocardial infarction) or result in embolic disease more distally (a common cause of stroke). and inflammation.
l An embolism is a blockage of a blood vessel caused by material that has travelled from a more distant source. Further, following a deep vein thrombosis
This is usually a blood product but can also be caused by fat / air or amniotic fluid. The most common source (DVT) the thrombus formation can damage
is cardiogenic (e.g. atrial fibrillation [AF] or left ventricle [LV] thrombus) or peripheral (e.g. unstable plaque or the valves in the deep veins. The pooling of blood in abnormal superficial veins makes them prone to
aneurysmal mural thrombus). In the venous circulation it can cause a pulmonary embolism and the common thrombosis: thrombophlebitis describes thrombosis and inflammation of superficial veins, whereas deep
source is a DVT. veins are subject to DVT that can lead to pulmonary embolism (PE), which can be so severe to be fatal.

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UPPER LIMB VENOUS IMAGING

4 VENOUS IMAGING
Mujahid Abdalla, Fatemeh Sakhinia, Arun Pherwani
Radiography
(conventional x-ray)
Computed Tomography (CT) and Magnetic Resonance (MR) Venography
These modalities are useful in differentiation of equivocal cases of TOS and can provide
additional anatomic detail required for surgical planning.
Anatomical abnormalities
potentially causing thoracic MR imaging is the preferred modality for investigation of suspected TOS and is particularly
outlet syndrome (TOS) such preferred to CT given its lack of ionising radiation (especially beneficial in the generally younger
as prominent cervical ribs, affected patient population). However, absolute or relative contra-indications to MR (e.g.
WHAT IS VENOUS IMAGING? fracture callouses or incompatible implanted device, severe dialysis-dependent renal failure, claustrophobia) may
compressive tumours can often preclude use of this modality. In such cases, CT with intravenous contrast is then the preferred
l Vascular surgeons commonly see patients with disorders of the veins. be demonstrable on chest, imaging modality (see below) or time-of-flight non-contrast MR imaging.
l The majority of problems affect the veins in the legs but there are also recognised issues with the veins in shoulder or spine radiographs.
MR imaging is acquired with gadolinium-based intravenous contrast material. The intravenous
the arms. catheter should be placed on the asymptomatic arm in order to minimise T2* artefact caused by
l Imaging is key to providing an accurate diagnosis of patients with venous disorders. concentrated gadolinium contrast that may obscure the axillosubclavian vasculature on the
Plain film AP thoracic inlet symptomatic side. Several series of images are then performed with the upper limbs adducted
and abducted to allow detection of positional stenoses of the vessels.
CT is excellent for assessment of bony anatomy and therefore detection of anomalous ribs or
LOWER LIMB VENOUS IMAGING FOR DEEP AND SUPERFICIAL VENOUS DISEASE fractures that may predispose to TOS. The investigation of TOS with CT is typically acquired
with intravenous iodinated contrast material and, as with MR imaging, the intravenous catheter
Continuous-wave Doppler ultrasound Computed Tomography (CT) and should be placed on the side opposite to the symptoms in order to prevent streak artefact from
This is utilised as a non-invasive initial screening test Magnetic Resonance (MR) Venography dense contrast material.
for chronic disease of the superficial lower limb veins. These modalities are most useful in the evaluation of the
It involves using a pencil ultrasound probe and is a more proximal veins and their surrounding structures but Intravascular ultrasound (IVUS)
relatively inexpensive examination. Acoustic signals can also depict abnormal superficial veins (varicose veins)
are used to render venous blood flow and IVUS allows for detection of stenotic or obstructive disease of the venous system.
relatively well. They allow for accurate assessment of
incompetence of the great saphenous vein can be intrinsic venous obstruction or extrinsic venous it probably has a similar sensitivity in identifying upper limb venous lesions that are occult on
detected. However, this method is less accurate in compression. venography or conventional ultrasound.
diagnosing incompetence of the lesser saphenous
vein or the deep venous system due to anatomical Optimal imaging with these modalities necessitates the
variations and operator-dependent differences. injection of intravenous contrast material with appropriate Conventional
timing of image acquisition to coincide with venous filling, in contrast Pre op venography
order to obtain a ‘venogram’. Both CT and MR venography
Colour-flow Duplex ultrasound can be used to delineate complex venous anatomy, such as Left Cervical rib, venography
This is another non-invasive modality and is relatively iliofemoral venous obstruction, prior to intervention. Right prominent These techniques are
simple to perform. It facilitates functional and Transverse process invasive and involve
morphological examination of both the deep and the injection of
Intravascular ultrasound (IVUS) contrast material
superficial venous system. In particular, deep vein
thrombosis (DVT) of the lower limb can be diagnosed This technique involves the use of a catheter-based ultrasound intra-arterially or
with high accuracy via dynamic venous compression probe to image peri-luminal vascular anatomy in order to intravenously in order
detect stenotic or obstructive disease of the venous system. Colour-flow Duplex to visualise vessels
using the ultrasound probe itself.
IVUS appears to be superior to venography in the estimation
ultrasound using x-rays via
In addition, the dynamic assessment capabilities of fluoroscopy. They
ultrasound can aid in identification of the anatomical of morphology and severity of central venous stenosis as well In cases of suspected vascular
as in visualising detailed intraluminal anatomy. This superior TOS, colour-flow Duplex can be used to Venoplasty
level of venous incompetence. This is done through demonstrate extrinsic
utilisation of a tilt table (or standing the patient up) as detection of stenosis severity has resulted in increased venous ultrasound is a highly sensitive after
percutaneous interventions for the treatment of chronic lower and specific imaging modality. It is compression of the decompression
well as manual calf compression by the operator(s) to upper limb veins.
induce venous reflux. Simultaneous venous waveforms limb venous disease. In particular, IVUS has been shown to also non-invasive and inexpensive
be ideal for identifying pelvic venous lesions (namely iliac) that and is the initial imaging test of Venography is Standard and
traces can be rendered using the pulse-wave function particularly useful in
on most modern ultrasound machines to register are occult on conventional ultrasound or venography. choice. cutting balloon
venous TOS when
venous reflux digitally. This technique permits functional dynamic imaging
There are Conventional contrast venography and morphological examination of is required to
however both the deep and superficial demonstrate
Contrast venography allows for direct visualisation of the
Venous duplex scanning diagnostic venous system. As in the lower occlusion of upper
venous system via either an ascending or descending
of the popliteal fossa. limitations with limbs, DVT can similarly be limb veins on
approach.
this modality in diagnosed with high accuracy in hyperabduction and
assessment of Ascending venography is defined as injection of contrast in the upper limbs via dynamic as part of intervention
the pelvic veins the veins of the dorsum of the foot and subsequent compression of the veins using with lysis for acute
due to their deep visualization of contrast travelling cephalad in the deep the ultrasound probe. Extrinsic DVT and post
location. Also, in venous system of the lower limb. This provides detailed causes of upper limb venous operative venoplasty.
some cases, it is imaging of venous anatomy that can help guide surgical compression from adjacent Post op venography
not possible to interventions and can also aid in distinguishing primary from anatomical structures may also
definitively secondary disease. be diagnosed, especially when
assess the deep Descending venography involves proximal injection of imaging with dynamic
veins of the lower contrast with the patient in a semi-vertical position (using a assessment, i.e. imaging in real
leg due to tilt table) and requesting the patient to perform the Valsalva time during active/passive
variations in manoeuvre. It is most useful in identifying reflux in the movement of the upper limb.
individual patient common femoral vein and at the saphenofemoral junction,
anatomy. but may be used to assess other locations also.

10 VENOUS ImAGING 11
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l It is not user

5
dependent but Magnetic Resonance Angiography (MRA)
ARTERIAL IMAGING appropriate protocols
MRA is a further imaging modality that can provide cross-sectional imaging of arteries within the body.
need to be in place for
Patrick Coughlin accurate image
acquisition
l It is able to provide
information on every
artery within the body
WHAT IS ARTERIAL IMAGING? including those within
l Imaging of the arterial tree is key to confirming an accurate diagnosis and determining an optimal treatment the thorax and
strategy. abdomen
l It provides precise
l The imaging strategy used will be determined by the access to the imaging modalities below and often
anatomical detail
more than one imaging modality may be used in patients. including assessment
of the lumen, arterial
wall and extra-arterial
anatomy
CT angiography The disadvantages
Arterial Duplex CTa allows the cross-sectional imaging l Exposure to radiation
Duplex is a non-invasive ultrasound imaging modality technique that of arterial vessels throughout the body
using the injection of contrast material l Small risk of contrast
incorporates two modes of ultrasound - Doppler and B-mode. The
to evaluate the arterial tree. allergy
B-mode aspect obtains an image of the vessel being studied with the
Doppler aspect able to measure speed and blood flow. CTa has a number of advantages l Small risk of contrast
nephropathy in
l It is non-invasive patients with chronic
l It is rapid to perform and tends to be kidney disease
available 24 hours per day, 7 days l CT angiography may
per week in most hospitals. overcall the degree of MRA has a number of advantages:
stenosis in patients
l It is non-invasive
with lower limb PAD
l It does not require exposure to ionising radiation
l It can be challenging
to accurately l It is not user dependent but does require appropriate protocols for image acquisition
determine the l It has the potential for non-contrast examination but commonly the use of contrast is still required
presence and severity
of atherosclerosis in MRA does also have a number of disadvantages:
the infrapopliteal l It is not as quick as CT angiography for image acquisition
arteries in patients
l There are a number of MRI contraindications around implanted medical devices – specifically
with significant medial
Duplex is commonly the first line arterial investigation. pacemakers and defibrillators (although newer devices are increasingly becoming MRI compatible)
artery calcification
It is specifically used for: (e.g. patients with l MR angiography tends not to be available 24 hours per day / 7 days per week within the UK
diabetes mellitus and MRA may not be able to see and capture images of calcium deposits within the arterial tree
l Assessment of carotid disease l
renal failure)
l Investigation of upper and lower limb arterial disease – considered
as first line imaging by NICE for lower limb PAD.
l It has significant benefits in those patients who require surveillance Intra-arterial digital subtraction angiography (IADSA)
following intervention (e.g. post infrainguinal bypass surgery or
stenting, surveillance of EVAR, etc) due to the repeated IADSA is still deemed to be the “gold standard” method of angiography.
requirements of such investigations This involves direct puncture into an artery (usually the common femoral artery) and insertion of a sheath following
There are a number of advantages to its use: this. IADSA is rarely used in isolation as a diagnostic imaging modality but most commonly as a bridge to some form of
concomitant endovascular intervention. In most cases, duplex or cross-sectional angiography would provide the detail
l The ultrasound machine is portable and the imaging modality is needed to plan an endovascular intervention.
non-invasive
IADSA is used diagnostically either to determine the quality of a distal target infrapopliteal artery when there is
l It does not requires use of contrast / nephrotoxic agents uncertainty of its quality to support a femoro-distal surgical bypass or to accurately determine the blood supply in the
l The use of both Doppler and B-mode allows for a more precise foot.
estimation of the degree of significance of the arterial disease The advantages of IADSA are:
l It allows for visualisation of the entire artery (including the wall) and l Comprehensive evaluation of the lower limb PAD
not just the lumen, providing information on plaque characterisation
l There are no real issues with medial artery calcification
l It is low cost
l It is able to provide detailed anatomy of the arterial supply to the foot which can be important in patients with
There are some disadvantages to its use: diabetes
l Operator dependence with a learning curve associated with The disadvantages of IADSA are:
performing these scans
l Contrast is required and so patients with CKD may be susceptible to contrast nephropathy
l Challenges in assessing intra-abdominal vessels, especially in
more obese patients l The procedure is invasive with associated risks
l The procedure requires the use of radiation

12 13
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6 STRATEGIES FOR REVASCULARISATION

Penelope PJ Sucharitkul, Christopher P Twine
BOX 2
Complications

Vascular surgery comes with

risks, and highly co-morbid
patients
WHAT IS REVASCULARISATION?
l Site infection – open surgery
l Revascularisation is a surgical procedure which aims to restore blood flow to an area of the body where carries higher risks of post-
the arteries have been blocked, usually by atherosclerosis operative infection.
l Restoring blood flow can prevent amputation and save lives as well as healing wounds, reducing pain and l Bleeding – arterial bleeding in the
increasing quality of life leg commonly requires further
surgical intervention.
l This can be achieved with ‘endovascular’, ‘open’ or ‘hybrid’ surgical operations
l A patient’s disease can often be treated by more than one operation type. Choosing the best option l Occlusion – clot in bypass and
risks of having to re-intervene.
requires balancing a number of factors and careful shared decision making
l Cardiovascular events – patients
are at high risk of myocardial
Endovascular intervention in action in the IR Suite. infarction and must be
Endovascular revascularisation commenced on best medical
BOX 1 management (smoking cessation,
l ‘Endo’ comes from the Greek word, éndon, diabetic control, high intensity
meaning within.
Patient selection
statin therapy, antihypertensive
l A minimally invasive approach to revascularisation,
l Vascular patients are often elderly and co-morbid with and antiplatelet therapies) to try
‘Endovascular’ refers to image guided surgery other medical problems such as diabetes, previous and mitigate this risk.
where a wire is threaded into the artery and myocardial infarction or stroke.
l Hospital associated infections –
through the blockage. Devices such as balloons l Patients may experience various complications after a long stays in hospital can result in
and stents are passed over the wire and used to revascularisation operation (see Box 2). exposure to resistant organisms.
re-open the blocked or narrowed artery. l Endovascular surgery is generally lower risk than open l Amputation – occlusion of the
l An ‘Angioplasty’ is always performed during an or hybrid surgery. Depending on the artery affected
bypass may result in amputation.
endovascular intervention, this describes the and pattern of atherosclerosis, it may not be as durable
process of opening up the blocked or narrowed as open surgery. l Death – mortality in this cohort
artery. remains high, despite intervention.
l Open surgery has higher short term risks to the
l It is often performed under local anaesthetic, using patient. It may be more durable than endovascular or
ultrasound to access the artery with a needle. hybrid surgery in the long term. Support for patients
l Multiple devices may be used for one endovascular l If a patient has a pattern of atherosclerosis suitable for The Circulation Foundation is a UK
intervention, the choice is different for each artery endovascular or open surgery, many factors need to be based vascular charity which provides
treated considered to make the best decision on which option information and support for patients
l Not all patterns of disease are suitable for to choose. with vascular diseases,
endovascular surgery but, as technology and l A more medically fit patient may benefit more from https://www.circulationfoundation.
devices advance, so do the indications. open surgery, whereas a more comorbid patient may org.uk/
l Generally, endovascular surgery is lower risk for benefit more from endovascular treatment. However,
the patient in the short term but may not be as this varies depending on the artery.
durable as open or hybrid surgery in the long term. l Patients undergoing arterial intervention will be Surgeons undertaking a lower limb bypass.
l A more co-morbid patient (see Box 1) may benefit discussed at a multi-disciplinary team meeting
more from the lower risk nature of endovascular comprising surgeon, radiologists, anaesthetists and
intervention. other team members because of the complex nature
of the decision making.

Open revascularisation Hybrid revascularisation

complications, such as swelling due to reduced
l ‘Open’ refers to procedures where a surgical incision venous outflow. l Hybrid procedures combine an open operation with an endovascular operation.
is made to access the artery. l All patterns of disease may be treated by open l A theatre with suitable imaging and operative capacity is needed to perform a hybrid operation.
l This requires large cuts in the skin and needs a surgery, so patient selection (see Box 1) and shared
general anaesthetic or ‘block’ such as a spinal decision-making understanding the benefits and l X ray equipment is needed to perform a hybrid procedure. This is operated by a radiographer, emphasising the need for a
anaesthetic. risks is very important. team approach.
l Less diseased arteries before and after the blockage l Open revascularisation procedures are higher risk l These procedures were previously conducted via an open approach, or with separate endovascular and open components,
are exposed and a tube or ‘conduit’ is sewn to each. for the patient in the short term but may be more but with new imaging equipment and theatres, these can now be performed with reduced invasiveness for the patient.
The blood travels through the conduit and bypasses durable in the long term. l A common hybrid operation is a common femoral endarterectomy with iliac stenting where blockages in the common
the blockage, thus restoring blood flow to the foot. femoral artery are removed using open surgery, then the blood flow to this area from the aorta is opened with balloons and
l Patients who are less comorbid may be suitable for
l The conduit is usually taken from the leg, where a open surgery (see Box 1), while those with multiple stents.
healthy section of vein, for example the saphenous comorbidities may be better suited to endovascular
vein, is harvested for the bypass. This carries its own treatment.

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THEME 2

PERIPHERAL ARTERIAL DISEASE

AND LOWER LIMB DISEASE
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MECHANISM OF ACTION OF COMMON ANTIPLATELETS AND ANTICOAGULANTS FOR

7
MECHANISM OF
BEST MEDICAL THERAPY TREATMENT OF ATHEROSCLEROTIC DISEASE
ACTION
Natalie Yonan, Claire Dawkins Fibrinogen Fibrin - Clopidogrel
DABIGATRAN

Thrombin Clopidogrel is an
Prothrombin
RIVAROXABAN CLOPIDOGREL
GDPIIa/IIIb inhibitor of the

Ac
adenosine

tiva
APIXABAN TICAGRELOR
WHAT IS BEST MEDICAL THERAPY?

tes
FXa ADP Platelet diphosphate (ADP)

p la
To reduce progression of PAD but also morbidity related to cardiovascular disease, particularly cerebral and aggregation P2Y12 platelet

tele
ASPIRIN
FX

ts
UNFRACTIONATED receptor, which inhibits
cardiac ischaemic events, all patients diagnosed with PAD should be initiated on: HEPARIN
P2Y12

FVIIa: TF LMWH platelet aggregation.

l Antiplatelet therapy – usually clopidogrel 75mg (FXa only) Thromboxane A2
WARFARIN Platelet This is an irreversible
l Statin – usually atorvastatin 80mg Decreases process, thus platelets
vitamin K
There should also be optimisation of hypertension and diabetes management. dependent
Progression of a plaque are affected for their
Through platelet activation
synthesis of FII, lifespan, approximately
Atherosclerosis
Alongside medical management it is important to give appropriate lifestyle advice: VII, IX and X Atherothrombosis
7 days.
Components of
l Smoking cessation – through counselling, medications such as nicotine replacement treatment, and Endothelial damage arterial thrombi -
fibrin and platelets
smoking cessation programmes.
l Encourage exercise (including through supervised exercise programmes), healthy diet and weight loss.
Antiplatelet therapy and anticoagulation Management of hypertension
Patients with PAD should be commenced on antiplatelet Hypertension, with resultant increased pressure and damage to vessel
therapy. Clopidogrel 75 mg daily is the antiplatelet of choice walls, is another risk factor for PAD. NICE guidelines recommend a
WHY IS BEST MEDICAL THERAPY IMPORTANT? in peripheral arterial disease with evidence (CAPRIE trial) target blood pressure of <140/90 mmHg (<150/90 if over 80 years of
Peripheral arterial disease (PAD) is most commonly caused by atherosclerosis, the causative factor also demonstrating a greater relative risk reduction for major age). The recommended approach is shown in Figure 1.
in coronary and cerebrovascular disease. Patients with PAD have a higher risk of having a stroke or a vascular events in clopidogrel when compared with aspirin.
There is discussion regarding use of ACE inhibitors in the absence of
myocardial infarction, with a 2-3 times risk of cardiovascular mortality compared with the control Proton pump inhibitors (PPI) are often prescribed for gastro- hypertension, for reduction of cardiovascular disease; however, there
population. Optimising cardiovascular risk factors is therefore paramount in patients with PAD to protection; however, caution is needed with omeprazole and are no current guidelines recommending this.
reduce cardiovascular morbidity and mortality. esomeprazole due to interactions with clopidogrel.
Evidence (VOYAGER PAD, COMPASS) has shown low dose FIGURE 1: SUMMARY OF MANAGEMENT OF
rivaroxaban (2.5 mg) with aspirin (75 mg) is of benefit in HYPERTENSION (NICE)
patients with peripheral arterial disease and stable
RISK FACTORS FOR PERIPHERAL ARTERIAL DISEASE, SPLIT MECHANISM OF ACTION cardiovascular disease. In practice this may be used for high
INTO MODIFIABLE AND NON-MODIFIABLE risk patients under specialist vascular input and bleeding risk
- Statins
must be considered.
MODIFIABLE Anticoagulation is commonly used for patients with embolic or
Statins are competitive inhibitors of thrombotic events. Intravenous heparin is often used in the
HYPER- 3-hydroxy-3-methylglutaryl coenzyme
SEDENTARY SMOKING LIPIDAEMIA short term for its immediate action, ease of control and
HYPER- A (HMG-CoA), which is a step in the
LIFESTYLE
TENSION reversibility. This is often changed to Low Molecular Weight
synthesis of cholesterol. Heparin (LMWH) after 24-48 hours to reduce the requirement
l This impacts lipid metabolism, for monitoring and improve flexibility. Longer term warfarin or
DIABETES RISK and importantly reduces low- DOACs can provide appropriate anticoagulation orally, with
OBESITY DOACs being many patients' choice although these are used
MELLITUS FACTORS density lipoprotein cholesterol
FOR PAD (LPL-C) levels. off-label for the treatment of arterial thrombus.

PMH OF FAMILY
l There is also an associated anti-
CARDIO OR HISTORY inflammatory response, thought Management of diabetes
CEREBRO- OF PAD
to be due to their inhibition of
VASCULAR CKD Close diabetes management, for both type 1 (T1DM) and
DISEASE isoprenoids, which helps with
type 2 (T2DM) diabetes mellitus, with tight glycaemic control
plaque stabilisation
EX INCREASING reduces the risk of macro and microvascular complications.
SMOKER AGE
The aim of treatment is usually a HbA1c <48mmol/L (6.5%) A = Angiotensin converting enzyme inhibitor or Angiotensin receptor blocker,
Important recommendations when for both T1DM and T2DM. For those with T2DM, this is C = Calcium channel blocker, D = Thiazide like diuretic
NON-MODIFIABLE
initiating a statin: initially through lifestyle advice, but often requires https://www.nice.org.uk/guidance/ng136/resources/visual-summary-pdf-
medication. 6899919517
l Measure non-fasting lipid profile prior
to starting. Repeated at 3 and 12 Anti-diabetic drugs:
Lipid modification months, with the aim to lower
l Metformin – first line for T2DM
Dyslipidaemia is a strong risk factor for the development of PAD non-HDL-C by >40%. Symptomatic relief
alongside cardiovascular disease. First line lipid modification therapy l Combination therapy – DPP-4 inhibitors, pioglitazone,
l Measure non-fasting lipid profile In patients with PAD where revascularisation is not possible or ill-advised,
of choice is 80mg Atorvastatin daily. sulfonylurea, SGLT-2 inhibitors are all options and
prior to starting. Repeated at 3 and vasodilators may offer some improvement to select patients. Iloprost
In patients who have cholesterol levels within the normal range, there escalate from dual to triple therapy
12 months, with the aim to lower infusions can offer some improvement in patients with unmanageable
is still benefit to statin therapy with further reduction of lipid levels and non-HDL-C by >40%. l Insulin – only treatment for T1DM, and for poorly symptoms. Naftidrofuryl oxylate can be used for a 3-6 month trial in
the anti-inflammatory effect of statins. controlled T2DM following initial therapies. patients with claudication. Treatment should be discontinued if no
l Important drug interaction:
If statins are contraindicated then alternative treatment can be Clindamycin. Statins should always be All patients with PAD should be screened for diabetes, improvement is seen. Cilostazole, Pentoxiphylline and Inositol nicotinate
considered, for example, ezetimibe in primary hypercholesterolaemia. stopped prior to commencement. initially with HbA1c measurement. are not recommended.

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What is the differential diagnosis?

FIGURE 2: ANKLE BRACHIAL

8 INTERMITTENT CLAUDICATION
Paddy Coughlin
PRESSURE INDEX (ABPI)
MEASUREMENT
Exertional leg pain is not uncommon. Other conditions
to consider are:
l Spinal stenosis: the neurogenic claudication symptoms are usually
BOX 1
Supervised
Exercise
caused by ischaemia or mechanical compression of nerve roots. Pain
may not only be present on walking but also on standing and on upright Programme
exercises. A key discriminator is its relationship to posture with lumbar For IC, enrolment in a
flexion reducing the pain (e.g. leaning forward or lying down) supervised exercise
WHAT IS INTERMITTENT CLAUDICATION (IC)? l Entrapment syndromes: primarily popliteal artery entrapment syndrome programme (SEP) is
where the popliteal artery undergoes muscular compression during effective and improves
l The classical symptom of IC is that of muscular pain, usually cramp-like in nature, that is precipitated by exercise. This is usually caused by an aberrant gastrocnemius anatomy symptoms, increases
walking and relieved by rest. The pain usually comes on quicker if walking up hill and is usually seen in younger patients (<40 years of age). walking distance and
The muscle group(s) affected are those downstream of the significant arterial disease. As the superficial improves quality of life. It
l l Compartment syndrome: this condition occurs due to a marked increase
femoral artery is the most common site of significant PAD, the calf is the usual symptomatic muscle. The has also been proven to
in tissue pressure within the confinement of a closed fascial space during
be cost-effective. The ideal
thigh (and calf) can be affected when the arterial disease is proximal to the profunda femoris artery and the exercise – commonly the calf. It tends to present in athletes. Other
SEP takes place 3 times a
buttock affected when the disease occurs proximal to the internal iliac artery. If there is significant aortic symptoms may include numbness / tingling in the dermatomal
week for a minimum of 3
disease then both legs can be affected and in men this can also cause impotence (Leriche’s syndrome) distribution of the nerve running through the compartment or weakness
months duration. Exercise
of the affected muscle.
l Pain results from ischaemic neuropathy involving small unmyelinated sensory fibres (types A delta and C) programmes commonly
l Venous claudication: thought to be an exercise induced pain resulting use a mixture of walking
and from local intramuscular acidosis from anaerobic metabolism (lactate buildup)
from venous outflow impairment which leads to an intense ‘squeezing’ and lower limb strength
type pain throughout the affected leg. There is usually a history of exercises.
previous deep vein thrombosis (commonly of the iliofemoral veins).
SEP is more effective than
How to diagnose l Osteoarthritis unsupervised exercise
FIGURE 1: ASSESSMENT OF LOWER LIMB PULSES programme. However, in
intermittent
the UK, there are a lack of
claudication appropriate numbers of SEP
Management of intermittent claudication for IC. As such, although
History
Optimal management of cardiovascular risk to Femoro-popliteal disease home-based walking therapy
l Muscular pain brought on l n

reduce overall cardiovascular morbidity and is not as effective as SEP, it

by walking and relieved by If revascularisation is needed and there is
mortality (see chapter 7). is a useful alternative when
pain. The initial claudication stenotic disease or a short occlusion, then compared to walking advice
and maximal walking The natural history of the leg in intermittent endovascular revascularisation is first line –
l
alone.
distances tend to be very claudication is relatively benign (75% of usually with balloon angioplasty.
reproducible Alternative exercise therapies
patients with symptoms either staying the same For more extensive atherosclerotic disease including cycling / strength
Examination or improving their walking distance) and this then, where possible, a surgical bypass with training / upper arm
should influence the management of such autologous vein is preferable, although in
l Assessment of lower limb ergometry may be an
patients. The indication for treatment is whether higher risk patients then an endovascular
pulses (Figure 1). alternative when walking
the symptoms negatively affect the patient’s approach may be appropriate.
Ankle brachial pressure therapies are not an option
l quality of life.
index (ABPI) measurement for patients.
l Supervised Exercise Programme (SEP) – see Box 1
(Figure 2) Peroneal Posterior
Anterior tibial
l Pharmacotherapy
Imaging
tibial
n NICE guideline suggests consideration of ABPI VALUES AND MANAGEMENT
l Imaging should only be naftirorfuryl oxalate only when SEP has
undertaken if uncertainty of not led to satisfactory improvement and
diagnosis or if planning for ABPI value Interpretation Recommendation
Arcuate
the patients prefers not to undergo
revascularisation. Its aim is Dorsalis
revascularisation. Naftidrofuryl acts as a >1.4 Arterial calcification Manage claudication in primary care initially.
to provide a “roadmap” of pedis
vasodilator. Review the clinical benefit If foot / leg wounds or evidence of CLTI needs urgent
the site and severity of the Plantar
after 3–6 months and stop the medication
referral to vascular specialist.
lower limb atherosclerosis arch
if no benefit. 0.9 – 1.4 Normal Nil
l First line arterial imaging is Revascularisation strategies:
l 0.8 – 0.9 Some minor arterial Risk factor modification.
usually an arterial duplex disease Manage claudication in primary care initially.
(combination of doppler n Aorto-iliac disease Patients are able to have compression bandaging therapy
and ultrasound) with CT In the case of short stenosis/occlusion with these ASBPI readings.
The femoral pulse is located – It can be palpated midway between the
or MR angiography useful (<5 cm) of iliac arteries, endovascular
anterior superior iliac spine and pubic symphysis, just inferior to the 0.5 – 0.8 Moderate arterial Risk factor modification.
cross-sectional imaging therapy gives good long-term patency
inguinal ligament disease Manage claudication in primary care initially.
when planning with a low risk of complications. If foot / leg wounds or evidence of CLTI needs urgent
revascularisation referral to vascular specialist.
In cases of ilio-femoral lesions, a hybrid
Patient should not have compression therapy applied
procedure is indicated, usually endart- with these ABPI readings.
erectomy or bypass at the femoral level
ABPI = Highest ankle pressure <0.5 Severe arterial Risk factor modification.
combined with endovascular therapy of
Higher arm systolic pressure iliac arteries, even with long occlusions. disease Manage claudication in primary care initially.
If foot / leg wounds or evidence of CLTI needs urgent
ABPI: 0.9-1.4. Normal value. Pressure usually higher in arm than leg. If the occlusion extends to the infra-renal referral to vascular specialist.
ABPI <0.9: Diagnostic for PAD. If value is <0.5 this is suggestive of severe PAD. aorta, covered endovascular reconstruction Patient should not have compression therapy applied
ABPI >1.4: suggestive of a non-compressible vessel. This is commonly found in patients with diabetes mellitus and / or renal failure of an aortic bifurcation can be considered. with these ABPI readings.
and is caused by calcification in the wall of the artery which makes it resistant to collapse by the blood pressure cuff. Open surgery (aortobifemoral grafting) can
also be considered.

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INTERMITTENT CLAUDICATION 21
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9 CHRONIC LIMB THREATENING

ISCHAEMIA
BOX 2
Non-invasive haemodynamic tests
BOX 3
Peripheral Arterial Disease Quality Improvement
Framework (PAD-QIF)
Ankle pressure (AP) and ABPI
Kaji Sritharan, Georgios Koufopoulos l Measurement of ankle pressure (AP) and the calculation of ABPI l The PAD-QIF aims to reduce unwanted variation in the delivery of
is recommended as the first-line non-invasive test. services for people with PAD and describes the care pathways,
workforce and facilities required to improve outcomes for patients
l AP <50 mm Hg or ABPI <0.4 is typically seen in severe PAD, BUT with PAD.
a significant proportion of patients, particularly those with CKD
and diabetes, will have incompressible blood vessels due to It advocates equitable access for people with PAD to timely
WHAT IS CHRONIC LIMB THREATENING ISCHAEMIA?
l

calcification, leading to artifactually elevated readings. revascularisation. Patients with CLTI who are admitted to hospital,
l Chronic Limb Threatening Ischaemia (CLTI) is the advanced stage of peripheral arterial disease (PAD). It should be treated within 5 days; non-admitted patients with CLTI
l If this is suspected, toe pressures (TP) and toe-brachial index should be treated within 2 weeks.
occurs due to the presence of severe PAD, whereby the blood supply to the foot is insufficient for the needs
(TBI) or other haemodynamic measurements, should be
of the tissues. This results in a combination of rest pain, gangrene or lower limb ulceration which is present considered.
for a duration of 2 or more weeks; and associated with one or more haemodynamic abnormalities.
Admitted patient - severe chronic limb threatening ischaemia and/or foot sepsis
Toe pressures (TP) and toe-brachial index (TBI)
l Rest pain is discomfort within the forefoot which typically occurs at night when the foot is elevated in the
bed. The pain will often wake the patient from their sleep and is l TP is measured by placing an appropriately sized mini-cuff
relieved by hanging the affected limb off the bed. This is because around the base of the great toe. This is attached to a standard
gravity helps blood flow to return to the ischaemic leg. manometer. A photoplethysmographic or continuous-wave
Doppler flow detector is then used to determine when flow
returns while the inflated cuff is slowly deflated. Immediate 2 days 5 days

The digital arteries are relatively spared from calcification and TP Non-admitted patient - stable disease, such as mummified toes
How to diagnose CLTI
l

is therefore less often affected by incompressibility, unlike AP.

History
l TBI <0.7 is abnormal and a TP <30 mmHg is associated with
l Pain in the feet which disrupts sleep and is relieved by hanging severe PAD.
the foot from the bed.
Several other non-invasive tests also exist but are not recommended
l Ulceration or gangrene. Same day 1 working day 7 days 14 days
for routine use.
Examination
l Pale foot with evidence of tissue loss.
Imaging l Every patient should receive a multi-specialty assessment,
l Foot pulses are not palpable. including shared decision-making over treatment options. The
l Imaging is performed for the purposes of evaluating the pattern core members of the multi-disciplinary team are shown below.
l Positive Buerger’s test with a Buerger’s angle of less than 20 BOX 1 of PAD which will help when planning intervention.
degrees (see Box 1).
Buerger’s test l First line arterial imaging is usually an arterial duplex CORE MEMBERS
l Assessment of haemodynamics (see Box 2) and
Buerger's test assesses the adequacy of the (combination of doppler and ultrasound) with CT or MR
documentation of the WIfI score should also be performed Formal lower limb MDT meeting
arterial supply to the leg. It has two parts: angiography providing useful cross-sectional imaging for
(see Chapter 10). Vascular surgeon - at least two
planning revascularisation. In some cases, invasive diagnostic
1. Assessment of elevation pallor digital subtraction angiography (DSA) can be helpful for Interventional radiologist - at least two
With the patient supine, raise both legs at the Vascular specialist nurse
Wlfl score planning surgery.
Vascular anaesthetist
same time to an angle of 45 degrees and hold for
The WIfI system is based on three key factors: Consultant in care of elderly and frailty
l
one minute. Observe the colour of the feet and the
Wound, Ischaemia, and foot Infection. Prognosis Clinical vascular scientist
angle at which they become pale. Pallor is a sign of MDT administrator
l The composite WIfI score, which is calculated by adding the ischaemia and it occurs when the peripheral l CLTI is associated with premature death, with a mortality rate
Wound, Ischaemia, and Infection sub-scores, is a predictor of the arterial pressure is not sufficient to overcome the of 20% to 25% in the first year after presentation, mainly due
likelihood of amputation, limb salvage and wound healing and can effects of gravity. In a limb with a normal to cardiovascular events.
identify those patients who may benefit from revascularisation. circulation, the toes and sole of the foot will remain l The 5-year all-cause mortality for patients with CLTI is as high Revascularisation strategies
pink, even when the limb is raised by 90 degrees. as 70% and this is greater than that for some cancers.
The poorer the arterial supply, the less the angle to l Improvement of the blood supply to the foot can be
Rutherford classification which the legs have to be raised for them to achieved by using minimally invasive angioplasty
become pale. A vascular angle of less than 20 Management techniques, open surgery (endarterectomy or bypass
l The Rutherford classification is a commonly used system to degrees indicates severe PAD. operation) or a combination of angioplasty and open
l Optimal management of cardiovascular risk factors will reduce
categorise the severity of PAD. It includes both a clinical surgery, so-called hybrid interventions.
2. Assessment for reactive hyperaemia. cardiovascular mortality and morbidity .
descriptor and an objective assessment of haemodynamics
Then ask the patient to hang their legs down over Left untreated, the estimated overall risk of limb loss in CLTI is
l CLTI usually occurs as a result of arterial disease at
using ankle pressures (AP) and toe pressures (TP). l

the side of the bed. Gravity will help blood flow to approximately 25% at 1 year. However, the risk of amputation multiple levels. The level(s) of arterial disease within
l Rutherford categories 4 to 6 characterise CLTI (shown below). return to the ischaemic limb and the foot will the lower limb (iliac, common femoral, superficial
remains high even in those who have undergone a successful
slowly turn pink and soon after red (so-called revascularisation. femoral, popliteal and tibial) arteries, the nature
Rutherford Stage Clinical Presentation ischaemic rubor or sunset foot). This occurs due (occlusion versus stenosis) and the extent of disease
l Patients who present late and with the greatest degree of tissue (i.e. length of lesions), along with the fitness of the
0 Asymptomatic to the dilatation of the arterioles in an attempt to
loss are at the highest risk of major amputation. patient and WlfI score, will influence which strategy is
1 Mild intermittent claudication remove the metabolic waste products that have
built up in a reactive hyperaemia. The foot then l Early revascularisation will prevent limb loss, and the delays to best employed.
2 Moderate intermittent claudication
returns to its normal colour. treatment can be prevented by developing well organised In some patients, primary amputation or palliation may
3 Severe intermittent claudication l
networks with clear referral pathways. be the management strategy of choice. For example,
4 Ischaemic rest pain If possible, examine both legs at the same time, as
The effectiveness of non-revascularisation therapies, such as, those patients with significant co-morbidities or limited
5 Minor tissue loss the changes are most apparent when one leg has a l

spinal stimulation, pneumatic compression, prostanoids, and life-expectancy, complex or no options for
6 Major tissue loss normal circulation.
hyperbaric oxygen, is not yet established. revascularisation, extensive tissue loss or infection.

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FIGURE 1: SHOWING CORRECT USE OF SEMMES-WEINSTEIN MONOFILAMENT TO TEST FOR GLOVE AND

10 DIABETIC FOOT DISEASE

Chris Ashmore, Dave Russell
STOCKING DISTRIBUTION OF DIABETIC SENSORY NEUROPATHY, AS DETAILED IN IWGDF 2023 PRACTICAL GUIDELINES

WHAT IS DIABETIC FOOT DISEASE?

l Diabetic foot disease is a common complication of diabetes mellitus (DM). It is a constellation of pathologies
which includes neuropathy, ulceration, peripheral arterial disease, neuro-osteoarthropathy, gangrene and
infection.
l Diabetic foot ulceration describes any disruption of the epidermis of the foot. The severity of an ulcer can
vary depending on the site, size, depth and degree of infection or ischaemia.

Epidemiology Clinical assessment Imaging Management

l Of the 5 million adults with DM, 10–25% will l Assess the patient holistically, obtaining clinical observations, a full l All patients with a deep ulcer or suspected Charcot foot should have an X-ray to All patients with a diabetic foot ulcer (DFU)
develop a diabetic foot ulcer in their lifetime. vascular examination and a neurologic examination of the foot. assess for fractures, deformity and osteomyelitis. should have a referral made to a specialist
Where diagnostic uncertainty persists, MRI of the foot can be considered. multidisciplinary diabetic foot service
l 50–80% of lower limb amputations are l All ulcers can be assessed using the SINBAD system. This l
within 24 hours.
attributable to diabetes. Survival following a provides a structured approach to ulcer assessment and can l Vascular imaging should be reserved for patients who are likely to require intervention.
diabetic foot ulceration is 60% at 5 years, facilitate communication between healthcare professionals. Mechanical offloading
and 50% at 2 years following a major lower 1. Site. Describe the location of the ulcer with reference to the Wlfl score l This is the mainstay of management
limb amputation. dorsal or plantar surface, digital, interdigital, forefoot, midfoot for all DFUs
or hindfoot. l The WIfI score is a classification score for diabetic foot disease based on the presence
and severity of the wound, distal ischaemia and foot infection.
l Offloading techniques can be
Aetiology of diabetic foot ulcers 2. Ischaemia. Full assessment of lower limb pulses. Insonation divided into orthotic and surgical
Diabetic foot ulcers are classified as of foot vessels with a handheld doppler and quantifying l It is used to predict the risk of amputation and the benefit from revascularisation .
l
n Orthotic footwear can shift
neuropathic, neuroischaemic or ischaemic. metrics of arterial pressure (such as ABPI, toe pressures or The score is not added but is reported by each component e.g.WIfI: 2,0,1, with a stage
l
weight away from the affected
transcutaneous pressure of oxygen). of risk calculated using a scoring matrix or App.
l Identify the specific aetiology of a foot ulcer by area of the foot.
considering the following: 3. Neuropathy. 10 g Semmes-Weinstein monofilament See below.
l
n Non-removable devices are
assessment of intact plantar skin is used to describe the
Diabetic sensorimotor neuropathy. superior to removable devices,
n presence and distribution of neuropathy (see Figure 1).
Caused by advanced glycation end products largely due to patient
and microvascular disease of the vasa 4. Bacterial infection. Diagnosis made by the presence of two compliance.
signs of infection (redness, swelling, heat, pain, purulent Diagrammatic representation of the Wound, Ischaemia and foot Infection (WIfI) staging
nervosa. This leads to foot deformity (clawed Plantar ulcers should be treated
system
n

toes, prominent metatarsal heads) and loss discharge). Osteomyelitis should be suspected in a positive
with below knee casts/walker
of protective sensation (LOPS) in the foot, probe to bone test.
boots unless contraindicated.
compounding traumatic or pressure damage 5. Area. Measure the surface area of the ulcer.
n Surgical techniques include
which may lead to skin breakdown. 6. Depth. Using a sterile probe, describe the depth of the ulcer achilles tendon lengthening,
with reference to the skin, subcutaneous tissues, muscle or WOUND
n Peripheral arterial disease (PAD). flexor/extensor digital tenotomy,
Arises due to hyperglycaemia, oxidative bone. 0: No ulcer ISCHAEMIA metatarsal head resection, joint
stress-induced endothelial dysfunction and l The presence of fever, tracking cellulitis, lymphangitis, abscess, 1: Superficial ulcer, arthroplasty, or metatarsal
atherosclerosis. Impaired tissue perfusion no gangrene 0: TP >60 mmHg osteotomy.
purulent discharge, rapidly progressing necrosis or crepitus
results in aberrant wound healing or 2: Deep ulcer or gangrene 1: 40-59 mmHg
indicate that urgent surgery may be needed. Soft tissue infection
ischaemic necrosis. in toes 2: 30-39 mmHg
Toe pressures 3: Extensive ulcer or 3: <30 mmHg l Superficial soft tissue infection can
n Precipitating event. Epidermal ulceration extensive gangrene generally be treated by systemic
can be caused by macrotrauma, such as
l Diabetes causes medial arteriosclerotic calcification resulting in
incompressible vessels and a falsely elevated ABPI in people antibiotics covering Gram positive
standing on a nail, or repeated microtrauma organisms. Need for intravenous
due to foot deformity. with diabetes and LOPS.
antibiotics or hospital admission
l Toe pressures measure the pressure required to occlude digital depends on the extent of infection
arteries and are less affected by LOPS. and presence of systemic
Prevention
l If the toe pressure value is <40 mmHg, the wound is less likely symptoms.
l All people with diabetes should be screened FOOT INFECTION
to heal without revascularisation. l Surgical debridement, if required,
for diabetic foot ulcers. The frequency of 0: No infection
screening, ranging from annual to monthly should be performed urgently as
1: <2 cm cellulitis ‘time is tissue’.
check-ups, can be determined using the Toe Pressure 2: >2 cm cellulitis / pus
IWGDF Risk Stratification Score. (mmHg) Interpretation 3: Systemic symptoms
l Strategies for ulcer prevention include the >60 No significant or mild arterial disease
provision of structured foot care education,
40–59 Moderate peripheral vascular disease
advice or the provision of appropriate
footwear, and the treatment of any modifiable 30–39 Severe peripheral vascular disease
risk factors.
<30 Critical ischaemia

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Amputation technique

11
The MDT
LOWER LIMB AMPUTATION l An MDT approach should be applied to all 1. Dissection through skin an underlying fascia
Ismay Fabre, Rosannah Williams, Ian Massey, David Bosanquet patients.
2. Muscle groups are identified and transected approximately 1–2 inches
longer than the planned level of bone cut to ensure adequate tissue
coverage for the residual limb.
3. Major arteries and veins should be identified, dissected, ligated and
GOALS OF AMPUTATION SURGERY transected.
l Removal of all compromised, necrotic or grossly infected tissue. 4. The major nerves should be identified and sharply transected to reduce
l Achievement of primary healing the risk of neuroma formation.
l Create a functional residual limb to preserve independent ambulatory ability in capable patients 5. The bone/s are then transected and filed to ensure no sharp edges.
l Pain relief 6. Closure is done in layers, including the fascia, subcutaneous tissue and
Amputation surgery should be performed to preserve life or preserve quality of life. skin. Some surgeons may also use myodesis (suturing muscles to drill
holes in the bone), or myoplasty (suturing agonistic to antagonostic
muscles) to provide more stability and better soft tissue coverage.
l Revascularisation and limb salvage should be
considered in all patients.
Indications for lower limb amputation Patient-centered care and shared decision
Rehabilitation
l

making is crucial.
l Acute or chronic limb ischaemia
l Infection
Trauma
Steps in fitting a prosthetic limb
Risks of amputation
l

l Malignancy 1. Physiotherapy and Occupational therapy work with

Pain: Post-operative pain is common; many centres will place a perineural the patient to ensure fitness for a prosthetic limb.
l A “non-functional” limb nerve catheter during MLLA to deliver local anaesthetic directly to the
2. The Prosthetist makes a ‘mould and model’ of the
Symptom management in palliation (in cases nerves. Acute pain team review is recommended after surgery.
l
residual limb. This may be with plaster, fibreglass or
where life cannot be saved, quality of death Phantom Limb Pain or Sensation: The feeling that the removed limb digital imaging.
should be considered) remains attached, commonly pain or itching. Management is with
3. A socket is created around the model.
neuropathic analgesics.
4. The socket is sometimes set up on a ‘diagnostic
Infection: Surgical Site Infections (SSI) are a leading cause of morbidity
prosthesis’ to asses function and comfort before the
Levels of amputation and mortality after amputation. Vascular patients are often high risk due to
definitive socket is made.
common co-morbidities such as diabetes and smoking.
How do you decide what level to perform a lower limb amputation? 5. Multiple appointments may be required to ensure the
Wound healing problems & need for debridement or more
To determine the level of amputation the surgeon must balance the goals of amputation surgery, particularly the likelihood prosthesis is optimised to the individual.
proximal amputation: Failure of primary wound healing is a common
of primary healing creating a functional residual limb. problem after amputations of an ischaemic limb due to poor perfusion, 6. Once the prosthesis is functionally optimised, an
The higher the amputation level is, the higher the likelihood of primary healing (due to higher chances of sufficient blood seroma, haematoma and SSI. Wound complications occur in 12-34% of external finish can be added as deemed appropriate
supply), but the functionality of the residual limb is lower. BKA and 6-16% of AKA. for each patient.

The optimal site is the lowest amputation level that will heal, therefore providing maximum rehabilitation potential. Non-healing wounds may require debridement or revision of amputation.
Revision could be at the same level, or revision to a higher level. Rates of
conversion from BKA to AKA is 9-28%.
CLASSIFICATION OF AMPUTATIONS Hemipelvectomy Mortality: The 5-year mortality after major amputation varies from Factors improving rehabilitation potential
30-70%; it is higher for AKA than BKA.
PRIMARY vs SECONDARY
Hip Other: All patients undergoing surgery are at risk of developing chest
l Medical optimisation. Cardiovascular optimisation is
important as energy expenditure of ambulation
Amputation undertaken as Amputation undertaken disarticulation infections post-operatively and thromboembolism including DVT, PE, increases <40% after a BKA, and <70% after AKA.
primary operation when there when limb salvage, i.e. CVA and MI. Early mobilisation and VTE prophylaxis reduce this risk.
is no option for limb salvage, revascularisation efforts, l Creation of a dynamic residual limb with muscle
or in a palliative setting for have failed. stabilising procedures and good soft tissue coverage
Transfemoral /
symptoms management creates a more balanced, functional residual limb to
above knee FACTORS THAT INCREASE RISK OF
amputation interact with the prosthetic.
WOUND COMPLICATIONS
l Good wound care ensures a healthy interface for
Major Lower Limb
Amputation vs Minor Amputation Through knee
amputation
Pre-operatively Peri-operatively Post-operatively
l
interaction with a prosthetic.
Early mobilisation with physiotherapy improves long
Hip Disarticulation Trans-metatarsal
Diabetes l BKA have a higher Development of term outcomes.
amputation
l l

Transfemoral Amputation rate of primary infection, seroma or

l Smoking l Safe discharge planning with occupational therapy.
Knee Disarticulation Digital Amputation Transtibial / healing failure than haematoma
Transtibial Amputation below knee
l Renal failure AKA. This is likely l Psychology, counselling and support groups should
l Compartment
Ankle Disarticulation amputation
High body mass due to AKA level be offered to all patients and their family, as undergoing
l
Syndrome
index amputations an amputation is a life changing event.
Minor amputations are often performed in combination with having a more l Poor wound care
Syme l Anaemia reliable perfusion
l Regular assessment with prosthetist is important as
revascularisation procedures for distal necrosis to ensure healing of amputation
the residual limb may evolve over time, requiring
the amputation site. If possible, they are preferable as they can preserve l Poor perfusion status.
re-fittings.
foot function.

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THEME 3

DISEASES OF THE AORTA

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12 ABDOMINAL AORTIC ANEURYSM

Conor Dooley, Ciarán McDonnell

Pre-operative
CT scan of an
WHAT IS ABDOMINAL AORTIC ANEURYSM? infrarenal
abdominal
l An aneurysm is defined as a localised swelling of an artery which exceeds 50% of it’s normal diameter.
aortic
aneurysm

Diagnosis
l AAAs are usually asymptomatic until they are either rupturing or in imminent danger of doing so.
l The majority are detected coincidentally either during a routine clinical examination or on abdominal imaging such
as ultrasound or CT being performed for some other reason.
Complications of aneurysm repair
l An ultrasound-based screening programme to detect AAA in males aged 65 or over operates in the UK and in
many other countries. Open Surgical Repair is characterised by three major physiological insults: Laparotomy, Aortic Cross Clamping and Ischaemia-
Reperfusion Injury, none of which occur during EVAR. This is reflected in differences between the complications of the two types
of procedures.
Surgical management
Complications of OSR Complications of EVAR
Natural history and rationale for treatment The principle of surgery is to exclude the
aneurysm from the circulation by insertion Apart from the obvious potential complication of bleeding Persistent blood flow within the aneurysm sac (endoleak) is a
The natural history of aortic aneurysms is continuous from the suture line, there are many others: unique complication of EVAR. Endoleaks are classified
of a synthetic graft inside the aneurysm
enlargement, leading ultimately to rupture with depending on their source:
sac. This prevents the aneurysm from
catastrophic bleeding.
expanding and ultimately rupturing,
Elective surgical repair is the only option to prevent this. SURGICAL INSULT
causing catastrophic internal bleeding. TYPE NATURE OF LEAK RELEVANCE
The purpose of surgical repair is therefore to prevent The difference between the two types of Laparotomy - Ileus
death from rupture, which still carries a 75–80% aneurysm surgery – Open Surgical - Bowel/ureteric/viscus injury I Loss of the sealing zone at High velocity blood flow within
mortality risk, relatively unchanged over the last 40 Repair (OSR) and Endovascular the proximal or distal ends the AAA. Requires urgent
- Laparotomy wound dehiscence
years. of the aneurysm treatment.
Aneurysm Repair (EVAR) is related to or later incisional hernia
how the graft is introduced. - Respiratory complications
Aneurysm diameter is the best predictor of rupture risk, II Persistent back bleeding Usually low velocity and very
secondary to impaired
with current guidelines stating that when an AAA Open Surgical Repair (OSR) respiratory movement due
from lumbar arteries or often self-limiting.
reaches a maximal diameter of 5.5cm then elective inferior mesenteric artery
to pain
repair should be considered in asymptomatic cases. l Open Surgical Repair is performed back into the aneurysm sac
via a laparotomy, most commonly a
AAAs less than 5.5cm in diameter are usually just kept Aortic Cross - Increase in cardiac afterload with
Separation of the High velocity flow within the
longitudinal midline incision but cardiac complications, M.I., C.C.F., III
under surveillance with regular ultrasound scanning. Clamping components of the graft AAA which requires urgent
sometimes via a transverse incision. arrhythmia etc.
within the aneurysm sac attention
The aorta is clamped proximal and
distal to the aneurysm which is then Ischaemia- - Hypotension
Due to porosity of the Described in the earlier phase
- Myocardial depression IV
Any Symptomatic AAA should be considered for urgent repair opened and a synthetic graft (usually Reperfusion graft material of endograft development –
made from Dacron or PTFE) is then - Cardiac irritation and
irrespective of AAA sac size. Symptoms include lower back or Injury rarely if ever seen now.
Arrhythmias
abdominal pain with no other identifiable cause or a palpable sutured into the normal aorta above
- Acute lung injury
tender AAA on examination. and below. The clamps are released - Acute renal failure V Expansion of the aneurysm Controversial. May require graft
and blood flow to the lower torso sac with no demonstrable explantation and conversion to
restored. endoleak open repair if continuous.

Endovascular Aneurysm Repair (EVAR)

Application of the aortic clamp renders the lower torso Iatrogenic arterial injury can occur as a consequence of the
l This is performed by means of relatively ischaemic, and when blood flow is restored this endograft being introduced through the iliac arteries.
introducing a stent (endograft) usually washes out various metabolites into the systemic
through the femoral arteries. The stent circulation which can cause a systemic inflammatory
consists of a metal exoskeleton with type response. WHICH METHOD OF REPAIR –
synthetic graft material stitched onto
Loss of blood flow through the inferior mesenteric artery OPEN OR ENDOVASCULAR?
it and is usually scrunched-up within
a long narrow tube (a sheath) which can sometimes produce large bowel ischaemia.
Not surprisingly, the lesser surgical insult of EVAR is reflected in a lower 30-day
is introduced into the lumen of the Late complications which can occur are pseudoaneurysm mortality (1.8%) compared to OSR (4.8%). This survival advantage is not
femoral vessels over a guidewire and formation at the anastomotic sites, and the development maintained, however, with longer term survival being similar. The potential for
passed up into the aneurysm sac of an aorto-enteric fistula, where the exposed aortic the development of endoleak at any stage postoperatively requires lifelong
under X-ray guidance. When the stent suture line erodes through overlying bowel wall, follow up with serial imaging (usually annual ultrasound +/- xray) of EVAR
is in the correct position it is uncovered producing catastrophic (and almost invariably fatal) patients whereas this is usually not necessary in those undergoing OSR. There
and expands, sealing the aneurysm at bleeding. Hernias and adhesive small bowel obstruction is also a higher reintervention rate in those treated with EVAR vs. OSR. The
the proximal and distal ends and are further recognised complications. decision as to which procedure to undertake is usually made by the surgeon in
containing blood flow within the consultation with the patient, taking into account the individual anatomical and
endograft and not within the aneurysm physiological factors unique to each case.
sac.

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Surgical management

13 RUPTURED ABDOMINAL AORTIC

ANEURYSM
OPEN SURGICAL REPAIR – DIFFERENCES FROM ELECTIVE OPEN SURGERY

THE 30 MINUTE RULE:

Conor Dooley, Ciarán McDonnell A patient with a suspected rAAA should be
assessed, scanned and transferred to
theatre within 30 minutes.

WHAT IS RUPTURED ABDOMINAL AORTIC ANEURYSM?

l The patient is prepped and draped while awake before the
l A ruptured abdominal aortic aneurysm is a surgical emergency where the integrity of the abdominal aorta induction of general anaesthesia. Rapid sequence induction is
is compromised due to a breach within the aortic wall leading to leakage of blood out of the circulation. performed, followed by an immediate midline laparotomy.
(muscular relaxation from the anaesthetic can cause a loss of
l The aneurysmal nature of the aorta means that the aortic wall is weak.
tamponade of the retroperitoneal haematoma and therefore this
l This is a life threatening emergency reflected in the fact that a ruptured abdominal aortic aneurysm carries time needs to be limited)
a mortality rate in excess of 70%. l The aortic neck is dissected and clamped, once proximal control
has been achieved, time is given to the anaesthetic team to CT scan showing evidence of retroperitoneal
replace fluids and blood products and stabilise the patient. haematoma in a patient with a ruptured AAA
Aortic repair with a synthetic graft is then performed in a similar
Presentation Management approach to an elective repair.
The classical presentation of rAAA is Unstable patient Endovascular Repair (EVAR)
a triad of:
Patients who present haemodynamically unstable and have a known l If the aorta has suitable anatomy, then an endovascular repair
aneurysm or suspected rupture should be taken immediately to the may be performed preferentially under local anaesthesia and
1. Back / abdominal pain operating theatre for repair. mild sedation (although general anaesthesia can be performed).
2. Hypotension Patients need to be haemodynamically stable to permit an
Stable patient endovascular repair of a rAAA as the capacity to achieve rapid
3. Pulsatile abdominal mass Patients who arrive haemodynamically stable and conscious have arrest of aortic bleeding by application of an aortic cross clamp
sufficient time to be further assessed with imaging (CT angiogram). such as in an open repair, does not exist. In the case of significant
Two large IV cannulas should be placed for medication, fluids and blood hypotension an intra-aortic balloon placed in the proximal aorta
However only 30–50% will present
products. may aid with haemodynamically stability but makes the EVAR
with all three symptoms. Symptoms more challenging to perform.
can differ depending on the site of Co-morbid patient
rupture. Posterior wall rupture is EVAR – differences from Elective Surgery
Patients who are elderly, who have significant co morbidities and who
usually contained via the are unlikely to survive the operation should be considered for palliation. l It is preferable that repair is achieved using a bifurcated device Post-op
retroperitoneum and causes This is after discussion with the patient, if possible, family members and where possible. However, in certain circumstances, an EVAR can CT scan of
compressive symptoms on medical / anaesthetic teams. be performed using an aorto uni-iliac type graft. This allows an EVAR
surrounding nerves causing pain. blood flow into one iliac artery only while the other one is blocked
An anterior wall rupture (‘free rupture’) using a special vascular occluder. The leg supplied by this vessel
Investigation is then revascularised using a fem-fem crossover bypass. This
enters the peritoneal cavity and
usually presents with sudden collapse method is generally faster than the standard bifurcated EVAR
Ultrasound Can be performed at the bedside in the device and thus allows for more rapid control of bleeding if
and death. l

Emergency Department required.

l Can effectively assess the patient’s aorta size
Alternative presentation (e.g. if the Aorta is normal then a rAAA can be
ruled out)
of rAAA:
l NOT reliable to exclude a rupture Abdominal Compartment Syndrome (ACS) A Study to Know
l Flank/Groin/Scrotal Pain
A significant complication that can manifest after a ruptured aortic
l Haematuria CT Angiogram l The gold standard form of imaging
aneurysm repair. Abdominal compartment syndrome is defined as organ The IMPROVE Trial - The
l Collapse l Can be performed rapidly and is available in dysfunction with abdominal hypertension (>25 mmHg). This may present Immediate Management of
most Emergency Departments quickly with elevated peak airway pressures, decreased tidal volumes and Patients with Rupture: Open Vs
confirming the diagnosis
increased difficulty ventilating the patient as well as decreased urine output Endovascular Repair
l Added benefit of assessing suitability for due to acute renal failure. Abdominal pressures can be estimated via
endovascular repair (EVAR) bladder pressure measurements. There should be heightened vigilance Multicentre trial that randomised patients with a
Common misdiagnoses
for ACS after endovascular cases as these patients do not have the diagnosed rupture to either EVAR if anatomically
of rAAA: retroperitoneal haematoma evacuated during the procedure as would suitable or Open repair
l Renal Colic routinely happen during an open repair. l No difference in mortality between the two
Permissive hypotension groups
l Diverticulitis Management
A key element in managing a patient with rAAA allowing a relatively low l EVAR was associated with a shorter length of
l Perforated Viscus Conservative measures include nasogastric decompression, muscle
systolic blood pressure of 80–100 mmHg by avoiding large amounts of stay in ICU and hospital
relaxants, abdominal TAP blocks and, if these do not work, operative
fluid resuscitation. Aggressive fluid replacement can disturb the
decompression laparotomy. In these cases, the abdomen is left open with l Patients who underwent EVAR were also more
tamponade that has formed at the rupture site and risks of re-rupture of
a sterile abdominal dressing to protect the cavity and is closed later. likely to be discharged directly home
the contained retroperitoneal hematoma with catastrophic bleeding.

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Investigations n Connective tissue disorders – Marfan covering the left subclavian for

14
Blood pressure: patient is usually Syndrome, Ehlers-Danlos Syndrome revascularisation at a later date may be
TYPE B AORTIC DISSECTION
l

hypertensive, a hypotensive patient with n Congenital malformations – bicuspid acceptable.

symptoms of dissection should be aortic valve, coarctation of the aorta
l Open repair of TBAD is rarely performed
Millie Sucharitkul, Rachael Forsythe investigated for rupture in the acute setting due to the
l Improvement of pain upon blood significantly higher risk of complications
pressure control is a strong indicator for Differential diagnosis than TEVAR in this typically elderly, frail
aortic dissection l Chest X-ray and ECG may be used to and comorbid population. Open repair is
l D-dimer: studies show the potential of exclude other cardiac pathologies more commonly required for younger
WHAT IS AORTIC DISSECTION? D-dimer to aid diagnosis of aortic presenting with acute chest pain patients with aneurysmal change as a
dissection. A raised level in conjunction (e.g. cardiac tamponade, myocardial result of TBAD.
l A tear in the innermost layer of the aorta allowing blood to flow between the intimal and medial layers of the with typical symptoms is sensitive in l Acute complicated TBAD – initial control
vessel wall. This creates a ‘false lumen’, causing the layers to separate. infarction, pulmonary embolism)
detecting dissection. l Other acute aortic syndromes should of blood pressure and heart rate with
l Dissections arising in the ascending aorta or arch proximal to the left subclavian artery (Type A aortic Imaging also be considered upon presentation anti-impulse therapy, followed by surgical
dissection; TAAD) are surgical emergencies requiring immediate intervention by a cardiac surgery team. l Contrast CT Angiography (CTA) is l Confirmation on CTA rules out other intervention (typically TEVAR) to exclude
diagnostic – images acquired show pathologies the false lumen and restore blood flow to
l Dissections arising distal to the left subclavian artery (Type B aortic dissection; TBAD) are managed by the longitudinal division of the aortic wall compromised organs.
vascular surgery team. They do not always require immediate surgical intervention, but should be managed forming a double-lumen. Cardiac gating
l Acute uncomplicated TBAD – managed
initially in a critical care environment. TBAD can be complicated by retrograde TAAD dissection and a joint allows synchronisation of images to the
Management of TBAD medically in the first instance, but
management approach may be required. cardiac cycle l The aims of initial management for TBAD requires close surveillance to ensure
are to prevent or treat rupture of the aorta early detection and treatment of
l TBAD is one of three ‘Acute Aortic Syndromes’ alongside Intramural Haematoma and Penetrating Aortic complications. Early TEVAR (± neck
PREOPERATIVE SAGITTAL CTA OF and organ malperfusion. This starts with
Ulcer. The principles of management are similar for these pathologies revascularisation) may be required
TBAD immediate control of blood pressure and
l TBAD most commonly presents with acute severe chest pain, inter-scapular pain or signs of end-organ involvement of critical care teams during the subacute phase if there is
evidence of high risk features.
ischaemia such as abdominal pain, lower limb ischaemia or paralysis l The INSTEAD trial 5 proposes a
Location of entry ‘complication-specific’ approach, whereby
l Fatal complications include rupture of the aorta and visceral malperfusion leading to ischaemia of tear (yellow
cross) optimal medical management (through Lifelong surveillance
abdominal organs strict BP control and close surveillance) is
Dissection flap
preferred in the event of an uncomplicated
l Follow-up CTA should be scheduled
(red arrow)
dissection. Management with TEVAR at regularly – for example, at 1 month,
A. True Lumen;
this stage provides no significant survival 6 months, 1 year, and yearly thereafter.
Clinical classification of type B B. False Lumen;
This includes all patients diagnosed with
C. Innominate benefit to patients.
ANATOMICAL CLASSIFICATION OF AORTIC DISSECTION aortic dissection Artery; aortic dissection, irrespective of means
D. Left Carotid
Acute, subacute and chronic Artery; of management. This is due to the high
Most widely adopted classification systems are detailed TBAD is defined by the time from
E. Left Surgical management incidence of aneurysmal change following
Subclavian
below: symptom onset to clinical presentation. Artery l Thoracic Endovascular Aortic Repair diagnosis or treatment of dissection.
Stanford - Type A: Entry tear proximal to left subclavian artery, (acute: 1–14 days, subacute: 14–90 days, (TEVAR) has emerged as the preferred
Type B: Entry tear distal to left subclavian artery. chronic: >90 days). surgical option for patients with 3D RECONSTRUCTED CTA OF TBAD
PREOPERATIVE TRANSVERSE CTA complicated TBAD. Stent grafting to
DeBakey – Type 1: Entry tear in the ascending aorta, extending Uncomplicated versus complicated OF TBAD
A patient with an uncomplicated TBAD cover the intimal entry tear and stabilise
throughout, Type 2: Entry tear in the ascending aorta, isolated to
has not sustained a rupture and/or has the vessel wall prevents life-threatening
ascending aorta, Type 3A: entry tear in descending aorta, distal
no features of end-organ malperfusion. sequelae. TEVAR requires adequate
extent above diaphragm, Type 3B: entry tear in descending
A complicated aortic dissection refers to proximal and distal sealing zones
aorta, distal extent below diaphragm.
a dissection that has ruptured or caused (>20 mm) and may necessitate
SVS/STS – Type A: Entry tear in Zone 0, Type B: Entry tear in revascularisation of the neck vessels to
end-organ malperfusion and/or displaying
Zone 1 onwards. Distal extent also denoted by zones. B1,7 create a suitable length of proximal aorta
at least one of the high risk features:
indicates entry tear in Zone 1, dissection extending to Zone 7. Entry tear on which to land the stent graft. Most
l Refractory pain and/or hypertension (blue arrow) commonly, this is a left carotid-
l Visceral ischaemia and malperfusion, subclavian bypass. In an acute setting,
A. True Lumen;
even if solely radiological B. False Lumen
l Entry tear >10 mm
l False lumen diameter >22 mm PRE (1) AND POST (2) TEVAR
Aortic diameter >40 mm ANGIOGRAM OF TBAD
l l Transthoracic and transoesophageal
l Retrograde dissection echocardiography can both be used to 1 2
l Entry tear at lesser curve visualise the proximal aorta and, as
l Bloody pleural effusion such, is used mostly for TAAD.
l False lumen thrombosis Transoesophageal echocardiography is
more sensitive.
Diagnosis of aortic dissection
History Risk factors for aortic dissection
l Sudden onset, severe, tearing pain in the l Hypertension, most common cause
chest or between scapulae l Abrupt significant increase in blood
Diagram showing a type B Type A aortic dissection with l Radiation to limbs, suspect involvement pressure: heavy weight-lifting, use of The true lumen (A) and false The false lumen no longer fills
aortic dissection with an entry an entry tear within the of brachiocephalic or iliac arteries drugs with sympathomimetic effects lumen (B) both fill with with contrast. The origin of the
contrast. The left subclavian subclavian artery has been 5 days postoperatively
tear distal to the left ascending aorta and the l Radiation to abdomen, suspect (e.g. cocaine, ecstasy) artery (orange arrow) and covered by the stent graft –
subclavian artery. dissection extending down mesenteric ischaemia l Existent aortic aneurysm carotid-subclavian bypass hence the bypass. Therefore, The TEVAR stent graft is shown clearly, along with
in to the descending thoracic (yellow arrow), are similarly the subclavian does not fill
l Symptoms of other end organ l Certain conditions can predispose visualised. proximally (orange arrow).
the coiled origin of the subclavian artery (seen as
arota dysfunction: lower limb paraesthesia or The corrugated pattern of the
a white patch) and patent left carotid-subclavian
individuals to development of aortic TEVAR graft stent can be seen bypass (*)
paralysis dissections: along the aorta.
l Syncope and sweating

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Clinical Features l If the patient presents with

15
symptoms then there is an
THORACIC AND ARCH ANEURYSMAL History urgent need to exclude BOX 1
Most patients are rupture of the aneurysm. Indications and considerations for repair
DISEASE
l

asymptomatic and the Family History Indications for ascending aortic repair:
aneurysm is detected as an
Family history of dissection,
Becky Sandford incidental finding often l

aneurysm, connective tissue

l 5.5 cm as a general threshold for surgical intervention for
following a chest xray (CXR) non-syndromic/non-bicuspid aortic valve patients
or cross-sectional imaging disorder, or sudden death at a
young age may be present.
l Any aneurysms that have a growth rate greater than 0.5 cm/
(CT or MRI). year are considered for surgical repair.
l A CXR will commonly show Examination
l The size limit is reduced to 4.5–5.0 cm for syndromic
WHAT IS THORACIC AND ARCH ANEURYSMAL DISEASE? one or all of the following: l Findings may be normal in aortopathy
n widening of the the absence of aortic rupture.
l Aneurysms of the aortic arch and descending thoracic aorta may arise as a result of different underlying mediastinum
Indications for arch / thoracic descending aortic repair
l Patients may be hypotensive /
pathology tachycardic if there is an l Aneurysms >60 mm should be considered for repair
n enlargement of the aortic
l Both are more common in men than women, and rupture of a thoracoabdominal aneurysm affects 10–15 knob aortic rupture. l In patients with CTD, a lower threshold of 50 mm may be used
per 100,000 person years displacement of the Investigations
n Symptomatic patients should be considered for urgent aortic
l They may be associated with connective tissue disorders (CTD) such as Marfans or Loeys-Dietz syndrome trachea from the midline l If there is a clinical suspicion repair
or related to an underlying vasculitis If patients are symptomatic of thoracic aortic pathology
l
Risks of repair need to be balanced with risks of aortic rupture
they classically present with then a CT angiogram should
l Occasionally such aneurysms may be mycotic in nature when deciding optimum management plans.
chest pain or back pain which be undertaken.
is usually interscapular.

Connective Tissue Disorders

Management options
Marfan syndrome
Open surgery
A genetic disorder that affects connective tissue and can cause pathological processes to occur across multiple
l Often more suitable for younger patients and
systems in the body. MS is caused due to a mutation in one of the genes that makes fibrillin (FBN1) which leads to
those with connective tissue disorder or those
a weakened connective tissue. It is autosomal in nature and in 75% of cases is inherited (in the remaining 25% it without good endovascular options due to the
occurs due to a new mutation). Such patients are at risk of developing cardiac valvular issues and are also at risk aortic arch anatomy.
of aneurysmal degeneration of the ascending aorta and the arch of the aorta.
l Needs collaboration with cardiac surgeons and
Loeys–Dietz syndrome facilities for cardiopulmonary bypass.
An autosomal dominant condition that can affect a number of genes that encode transforming growth factors. l Higher complication risks associated with such an
approach. Risks of open surgery need to be TEVAR with a left subclavian
The condition can present with premature arterial aneurysm formation or dissection (even can happen in children). artery fenestration
balanced against benefits.
Vascular Ehlers–Danlos syndromes (vEDS)
Endovascular surgery
vEDS is one of a number of syndromes classified as Ehlers Danlos syndrome. vEDS is the most severe of the l The development of more complex endovascular
causes. It is commonly caused by mutations in the COL3A1 gene which results in extremely fragile tissues in techniques has meant that more patients can be l Can incorporate branches for the left subclavian,
general but specifically blood vessels. Patients commonly present with early aneurysmal formation (with rupture) treated this way. left carotid and innominate arteries in some
or arterial dissection. Treatment is challenging due to the arterial fragility. cases. BOX 2
l Often more suitable for atherosclerotic aneurysms
in older patients.
Prevention of
Hybrid intervention
complications
l Usually incorporates branched or fenestrated graft Combination of open arch surgery and endovascular
Anatomy l The location of the aneurysm reflects the complexity of treatment options design to maintain perfusion to visceral vessels management of the thoracic aortic aneurysm. Spinal cord ischaemia from covering
l Important to understand which great vessels may be affected and the aortic arch the spinal arteries can occur after
l The frozen elephant trunk (FET) technique is a
and thoracic aorta can be split into zones (The Ishimaru's classification scheme – thoracoabdominal aneurysm repair.
relatively new technique that involves surgical
see Table 1) CT angiogram showing repair of the aortic arch which then facilitates an Spinal cord perfusion = Mean
l Thoracoabdominal aneurysms are described according to the Crawford classification endovascular stenting of the endovascular repair of the descending thoracic Arterial Pressure – intraspinal
system, with Type II aneurysms being the most extensive and carrying the greatest aortic arch with a fenestration aorta. It is increasingly used in more complex pressure
risks involved with repair. of the brachiocephalic trunk aortic pathologies where there is a lack of a
with a carotid-carotid and left proximal landing zone for a thoracic endovascular Increasing MAP is vital to maintain
carotid to subclavian bypass. stent graft. spinal cord perfusion
TABLE 1: SHIMARU'S CLASSIFICATION Spinal Cord protection relies on strict
l The proximal part of the FET consists of a
0 Involves the origin of the innominate artery standard aortic graft that has multiple branched physiological parameters, e.g.:
grafts coming of the main body which can be l Hb >100 g/L
1 The origin of the left common carotid artery (LCCA) anastomosed to the individual arch vessels
(there is also often a branch that can facilitate
l Sats >96%
2 The origin of the left subclavian artery distal body perfusion at the time of surgery) The l MAP >90 mmHg
distal part of the graft is a self-expandable stent l CSF drainage can also be
3 The proximal descending thoracic aorta down to the graft that is positioned in the descending thoracic considered in high risk cases
T4 vertebral body aorta which can provided a stable landing zone
for a subsequent TEVAR.
4 The remainder of the thoracic aorta

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THEME 4

VENOUS DISEASE
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FIGURE 1: C2 DISEASE –
Compression strength can range from light Differential diagnoses for

16
(liners at 10 mmHg) to strong (European
VARICOSE VEINS AND CHRONIC VARICOSE VEINS
Class 4 stockings >49 mmHg). Herbal
venous disease
Varicose veins are easy to identify; however,
medication such as red vine leaf extract
VENOUS DISEASE and horse chestnut extract can also be
recommended to the patient. These
the additional signs and symptoms seen
with varicose veins may be caused by other
conditions.
Victoria Bristow, Tristan Lane medications have been shown to reduce
signs and symptoms of chronic venous Lower limb oedema
insufficiency. Occurs without venous insufficiency from the
Superficial venous disease following causes:
In instances where conservative
l Lower limb dependency / immobility / lack
WHAT ARE VARICOSE VEINS AND WHAT IS CHRONIC VENOUS DISEASE? management has failed, or the patient is of activation of the foot and calf muscle
symptomatic including having episodes of pumps.
l Varicose veins are common and are the visible component of superficial venous disease. Up to 40% of the superficial venous thrombosis, bleeding, l If unilateral, rule out causes of extrinsic
population are affected to a lesser or greater extent. skin changes or active ulceration, there are iliac vein compression (e.g. malignancy)
l Deep venous disease is due to either incompetence or obstruction of the deep veins which is often FIGURE 2: C4 DISEASE – several methods of treatment. l Heart failure commonly causes bilateral
secondary to deep vein thrombosis (DVT). CHRONIC SKIN CHANGES NICE guidelines recommend the following leg swelling.
treatment preference order for truncal veins Lymphoedema should be considered.
l Chronic venous disease is where chronic venous hypertension has led to permanent skin damage which l
(great saphenous, small saphenous or
increases the risk of skin ulceration. l Obesity leads to relative venous
anterior accessory saphenous vein):
hypertension and subsequent oedema.
1. thermal treatment (radiofrequency
Leg pain
ablation or endovenous laser treatment)
How is venous disease diagnosed? Clinical directed imaging l Aching legs can also be a sign of
2. chemical ablation (ultrasound guided peripheral arterial disease. In which case
Venous disease is diagnosed with three key components: Imaging should be undertaken with a venous foam sclerotherapy)
insufficiency duplex ultrasound scan to assess an ankle brachial pressure index (ABPI) of
1. Clinical history 3. open surgery (high tie and stripping). less than 0.8 would be indicative of the
for superficial and deep venous reflux. Duplex
2. Clinical examination means the use of colour imaging to show flow The tortuous veins that remain can be presence of peripheral arterial disease
in addition to the picture (B-mode) image. treated with phlebectomies (performed which may need further investigations and
3. Clinically directed imaging – venous duplex ultrasound and
using open surgery by hooking the veins out risk factor modification.
rarely magnetic resonance venography and direct invasive
venography through small skin incisions) or ultrasound l Leg pain can also be related to spinal
guided foam sclerotherapy. disease. The symptoms of spinal disease
Clinical history often include neuropathic pain, they often
Positioning The vast majority of varicose vein
A detailed clinical history should be undertaken that differ from those with venous disease by
for a venous FIGURE 3: C6 DISEASE – procedures can be completed under local
includes: having a positive sciatic stretch test on
duplex VENOUS ULCERATION anaesthetic and most patients can have
clinical examination.
l Symptoms should be discussed with a focus on any pain, swelling, ultrasound some type of treatment. This is one of the
itching of the legs and risk factors identified such as prolonged most common procedures performed in the Skin changes
periods of standing. It is important to also gauge what the NHS. l Skin rashes, psoriasis and eczema can
individual’s biggest concern is? mimic chronic venous skin changes.
Deep venous disease
l Family history – focussing on thrombotic conditions. Superficial vein thrombosis (SVT)
The management of deep venous disease
l Past medical history – any previous deep vein thrombosis (DVT) heavily depends on patients' symptoms. l This condition has historically been known
or central venous access? The deep venous system may be as superficial thrombophlebitis.
l Current medication including anticoagulants, hormonal therapies. obstructed or incompetent. Incompetent l It typically, presents as a painful and
Incompetent deep venous systems are managed tender lump or cord, with redness and
l Previous surgical history – any previous varicose vein procedures?
saphenofemoral conservatively as described above. heat, located in an area of pre-existing
Has the vein previously been used in other procedures e.g.,
junction with gross Obstruction is primarily caused by DVT, varicose veins, particularly along the
coronary artery bypass grafts (CABG) or arterial bypasses? reflux demonstrated
and this may lead to post-thrombotic course of the great saphenous vein (GSV).
Clinical examination by colour duplex
ultrasound. syndrome, the severity of which can be l Misdiagnosis as an infective process is
An examination should be performed assessing the legs bilaterally for scored with the Villalta score. Those who common and frequently results in the
visible varicosities, leg oedema and skin changes. The Clinical- are asymptomatic are managed unjustified use of antibiotics.
Etiology-Anatomy-Pathophysiology (CEAP) classification can be used conservatively with compression hosiery
to give an objective number of the severity of chronic venous disease Management of venous disease l Diagnosis is made clinically and with the
and anticoagulation, this is the vast
(Table 1). With progressive venous hypertension, skin changes will use of a venous duplex scan.
Treating venous disease has been shown to majority of patients.
develop. l Any SVT <3 cm from the saphenofemoral
offer significant benefits to patients at low In those with severe symptoms due to junction (SFJ) should be treated as a DVT.
Lower limb pulses should also be checked to rule out any peripheral cost with good expectations of a positive obstruction, this can be acute or chronic.
arterial disease. result. Acute DVT can be treated with thrombus • If the SVT is >3 cm from the SFJ and
removal, which is most effective in the first >5 cm in length, then the patient should
There are many options: be anticoagulated for 6 weeks.
14 days post event, often followed by
TABLE 1: CEAP CLINICAL STAGES Conservative management stenting of a narrowing in the vein. • In any other circumstances then
Conservative management of venous Chronic deep venous occlusion that affects symptomatic treatment should be
C0 C1 C2 C3 C4 C5 C6 the ilio-caval system may be amenable to considered. This is usually is in the form
disease is heavily reliant on patient
No signs of Telangiectasia Varicose Limb swelling Venous skin changes Healed Active compliance with compression hosiery or deep venous stenting. This is complex and of non-steroidal anti-inflammatory agents.
venous or thread veins- (haemosiderin, venous venous compression wraps. Patients often find specialised limited to experienced centres All patients are entitled to a specialist vascular
disease veins (Figure 1) atrophie blanche, ulceration ulceration these garments difficult to apply and wear. to achieve good results. review and assessment, but treatment is
lipodermatosclerosis) (Figure 3)
NICE guidance does not recommend this dependent on funding according to current
(Figure 2)
approach in patients where intervention is local guidance.
an option.

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within the deep veins (reflux disease – which is not amenable to l The choice of which compression system is based on a

17
treatment – or occlusive disease). number of factors, the therapeutic reason for compression
VENOUS LEG ULCERATION l Table 1 highlights the classic characteristic between a venous (to aid healing or prevent recurrence), the amount of reducible
and arterial ulcer, however, in many patients the differential oedema, the levels of exudate and the patients desire to be
Leanne Atkin features may not be so pronounced able to self care. Where indicated patients should be
considered for superficial venous intervention (see Chapter
l Where the ulcer is chronic and failing to heel despite treatment 16). There is strong evidence to support a strategy of treating
then one should consider malignant transformation and a biopsy superficial venous reflux in the context of an active / healed
of the ulcer edge should be performed. venous ulcer.
WHAT IS VENOUS LEG ULCERATION? n The ESCHAR study. This study showed that once a
l A leg ulcer is defined as a wound on a lower limb, below the knee but above the level of the malleolus with Treatment venous ulcer was healed, superficial venous intervention
chronic venous insufficiency (CVI) the most common cause. CVI is the failure of the veins to carry blood l Strong compression therapy (>/= 40 mmHg at the ankle) is the reduced the episodes of recurrence at 4 years in patients
cornerstone of effective management of patient a venous leg wearing compression stocking from 31% to 56%.
back to the heart appropriately resulting in abnormal increase in pressure within the veins (chronic venous
hypertension). ulcer. n The EVRA study. This study looked at the effect of
Strong compression is known to decrease time to healing and superficial venous intervention in patients with an active
l CVI can occur due to problems in either the superficial or deep veins. The most common issue is failure of l
ulcer. It found that there was a reduction in healing time
reduce the risk of recurrence. Strong compression therapy
the valves to work in the veins causing reverse flow of the blood (reflux). Less common, venous obstruction from 82 days in the control group (compression only) to
can be applied in many ways – compression hosiery kits
usually due to thrombus can cause venous hypertension. (Figure 3), multilayer compression bandages (using 2 or 4 56 days in the treatment group (compression and venous
components) (Figure 4) and compression wrap systems intervention). Further in the treatment group wound
(Figure 5). They are all designed to provide 40 mmHg of healing was achieved in 85.6% of patients at 24 weeks
compression at the ankle. post treatment.
Introduction Assessment l If the iliac veins are occluded due to a previous deep vein
l Increased venous pressure l A holistic assessment of thrombosis then iliac vein stent insertion can be considered
FIGURE 1: the patient should include FIGURE 3: COMPRESSION HOSIERY KIT with the aim of reducing the degree of venous hypertension.
alters the balance of fluid in
the tissue and in the Visible varicose obtaining an appropriate l Patients with venous leg ulceration should heal within 12
capillaries resulting in fluid veins with medical history, Note the 2 different weeks, if failing to heal despite evidence-based care consider
being forced from the vein evidence of skin considering the patient stockings designed to provide
escalation to specialist services.
into the surrounding tissue staining and factors, the appearance strong level of compression
venous of the limb and wound (40 mmHg) at the ankle
causing oedema and a local
inflammatory process within ulceration assessment. TABLE 1: CLASSIC DIFFERENCES BETWEEN
the soft tissues. This leads l Other causes of VENOUS AND ARTERIAL ULCERS
to the changes of skin ulceration be considered
pigmentation skin Venous ulcer Arterial ulcer
including lower limb
(haemosiderin staining – peripheral arterial disease Patient factors High Body Mass Index History of arterial
Figure 1) and tissue fibrosis (PAD) which can occur problems in other
(lipodermatosclerosis – alongside venous vascular beds (e.g. stroke,
Figure 2). heart attack)
hypertension (i.e. mixed
Other factors can contribute ulceration). Previous history of a History of factors that
l FIGURE 4: 2 LAYER COMPRESSION BANDAGE SYSTEM
deep vein thrombosis (DVT) are associated with
to venous hypertension. l When lower limb arterial disease –
These include obesity and ulceration is present, the diabetes mellitus,
poor mobility. Other causes smoking, hypertension
arterial supply of the
of leg swelling (e.g. heart affected leg should be Immobility A history in keeping with
failure) may also contribute objectively assessed by intermittent claudication
to ulceration. (i.e. muscle cramps brought
both palpation of the on by walking and relieved
l Venous ulceration is a direct lower limb pulses and by by rest)
consequence of venous recording the patient's Limb related Presence of oedema
hypertension and is regarded ankle brachial pressure assessment
as ‘end stage’ of chronic index (ABPI) or toe Evidence of skin changes in Pain (although may be
keeping with venous absent in patients with
venous disease. pressure. This will confirm hypertension: diabetes due to neuropathy)
or refute the diagnosis of • Haemosiderin deposition
PAD and act as a guide • Venous eczema
for the suitability of • Erythema around gaiter
FIGURE 5: COMPRESSION WRAP SYSTEM area
compression therapy. • Lipodermatosclerosis
FIGURE 2:
If the ABPI is greater than • Evidence of varicose veins
Chronic oedema l

resulting in skin 0.8 then strong Shiny skin

fibrosis and skin compression therapy can A red foot (‘sunset foot’)
changes be safely applied.
Wound in gaiter area Wound on the foot
(lipodermatosclerosis) l All patients with venous Hairless skin
ulceration should have a
lower limb venous duplex Wound Flat Punched out
assessment
scan. This will determine Irregular Round
whether the venous High Exudate Often dry
hypertension is caused by
Evidence of granulation / Sloughy / necrotic tissue
problems within the sloughy tissue
superficial veins (i.e.
Develops over weeks Quick to develop
varicose veins – which is
amenable to treatment) or

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n Computed tomography venography l Persistent venous symptoms at 1 month

18 DEEP VENOUS DISEASE n Magnetic resonance venography l Residual thrombus on US

Treatment Investigation
Sam Galea, Emma Wilton Aims to reduce the risk of PE and l Venous duplex of lower limb with full
propagation of the DVT. Treatment also assessment of deep and superficial
aims to reduce the risk of developing PTS. systems
Iliac vein
Anticoagulation with the use of warfarin n DVT / chronic scarring / deep
l
stent in situ
venous reflux / superficial venous
WHAT IS DEEP VENOUS DISEASE? or direct oral anticoagulant
reflux
l Compression therapy as tolerated -
l Chronic venous disease is due to elevated ambulatory pressure within the lower limb leading to venous CT venogram/ MR venogram
check for pedal pulses l
hypertension.
l Limb elevation n Deep vein obstruction / fibrotic
l This can be due to either deep or superficial venous disease. scarring / collaterals / May–Thurner
l Early thrombus removal in selected syndrome (MTS) compression /
l The most severe outcome of chronic venous disease is the formation of a venous leg ulcer. patients with symptomatic iliofemoral malignancy
DVT
l Endovenous imaging
n Endovenous thrombectomy +/- iliac
vein stenting n Direct venography and intravascular
ultrasound – to confirm adequate
FIGURE 1: RIGHT LOWER LIMB ACUTE DVT o Mechanical thrombectomy inflow prior to undertaking venous
Aetiology
o Aspiration thrombectomy stenting in appropriately selected
Deep venous obstruction patients.
o Pharmacomechanical
l Acute - deep venous thrombosis (DVT) thrombectomy Treatment
l Chronic l Catheter directed thrombolysis +/- iliac l Compression therapy / limb elevation / DEEP VENOUS INCOMPETENCE
n Thrombotic vein stenting Exercise (DVI)
o Post-thrombotic syndrome (PTS) In severe cases of PTS endovascular Aetiology
n Non-thrombotic Chronic deep venous iliac vein stenting can be considered in
appropriately selected patients. For this DVI most commonly results from venous
o Non-malignant iliac vein and IVC outflow obstruction reflux due to faulty valve function developing
obstruction to be successful it is imperative to have
Post thrombotic syndrome (PTS) adequate inflow from the femoral / as a long-term consequence of DVT and
- Congenital
profunda vein. Patients undergoing recanalisation. It may also be due to primary
- May-Thurner syndrome (secondary to Aetiology
stenting will need to adhere to a post- valvular incompetence without previous
overlying crossing artery) / non-
The fibrinolytic pathway completely operative anti-coagulation and episode(s) of DVT. The prevalence of DVI is
thrombotic iliac vein lesion (NIVL)
dissolves acute thrombus but in 30–50% surveillance protocol which is tailored 10–15% and it is more common in women.
o Malignant iliac vein / IVC external
compression of patients this is incomplete and results to the individual’s risk profile. Clinical presentation
in some form of deep venous scarring
Deep venous incompetence Symptoms of chronic venous
e.g., synechia, residual obstruction and Non-thrombotic iliac venous
insufficiency (CVI):
l Valvular damage secondary to DVT valvular incompetence. This is termed outflow obstruction
post-thrombotic syndrome (PTS). It has a l Pain / ache in limbs / swelling of the
l Congenital Aetiology limb / oedema
significant impact on quality of life. PTS is
graded using the Villalta score. The risk of Non-thrombotic iliac vein lesions (NIVLs) l Venous skin changes / venous leg
PTS increases in proximal DVTs. Up to are due to extrinsic compression of the ulceration
10% of patients will go on to develop iliac vein, commonly between arterial
DEEP VENOUS OBSTRUCTION severe PTS with the formation of venous structures and the spine, without Investigation
leg ulceration over a 10-year period. associated thrombosis. It is present in up Duplex ultrasound
Acute DVT
l

Symptoms of PTS usually develop within to 70% of the asymptomatic population.

l Venous anatomy
The annual incidence of acute DVT is 1 per 1000 2 years of the DVT. This also adds a The compression results in intrinsic vein
people/year. significant healthcare burden. stenosis characterised by wall fibrosis or l Valve incompetence (reflux)
intraluminal webs / spurs. The most Retrograde blood flow with duration
Aetiology Clinical presentation n
common cause of a NIVL is commonly >1s in common femoral vein, femoral
l Unprovoked DVT – unknown cause; pose a higher Symptoms and signs: referred to as MTS. This is due to
Occurs when there is occlusion of the common vein and popliteal vein is pathological
long-term risk of recurrence. n
compression of the left common iliac vein
femoral vein and external iliac veins, completely l Aching / cramping / heaviness / Retrograde blood flow with duration
Provoked DVT - secondary to changes in any of the by the right common iliac artery. n
l
obstructing the outflow of all deep and superficial venous claudication >0.5s in superficial and perforator
domains of the Virchow Triad Clinical presentation
veins of the limb, as well as collaterals. l Pruritus veins is pathological
Clinical presentation l Asymptomatic
n Symptoms include sudden severe ischaemic l Limb swelling / skin discolouration / l Venous obstruction
Symptoms and signs (Figure 1): pain, massive congestion of the limb, cyanosis, venous ulceration l Symptoms of chronic venous disease Treatment
Pain in the leg sensory / motor disturbance, tachycardia and e.g., leg discomfort, limb swelling,
l
l Varicose veins This is focused on symptom control and
shock. It may also be complicated by massive PE, varicose veins and venous leg
l Swelling of the leg compartment syndrome and, potentially, lead to ulceration prevention of venous leg ulcer formation.
PTS risk factors
l Warm / hot skin of the leg venous gangrene. Compression therapy – compression
l Proximal DVT (2–3 times higher) l Pelvic venous insufficiency – pelvic pain l

l Red skin of the affected leg Pre-test probability score and dyspareunia bandaging/hosiery (see Chapter 17)
l Previous DVT
l Tenderness Wells DVT score Treatment l Exercise
l Obesity
l Venous claudication Investigation For symptomatic patients with NIVL, l Novel experimental therapies such as
l Pre-existing venous insufficiency endovenous valve creation/insertion of
l Phlegmasia cerulea dolens l Duplex ultrasound (including compression ultrasound) percutaneous iliac venous stenting is a safe
l Higher baseline Villalta score and effective treatment option compared neo-valve
n The most extreme clinical presentation of DVT l Cross-sectional imaging with medical management alone.

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THEME 5

MISCELLANEOUS
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Differential diagnosis

19 CAROTID ARTERY DISEASE

Maram Darwish, Lewis Meecham
Carotid arterial disease leading to TIA or
stroke can share symptoms with other
conditions, necessitating a careful evaluation
to establish an accurate diagnosis. Differential
Carotid endarterectomy (CEA)
This involves making an incision in the neck, exposing the carotid artery, and
removing the plaque causing the stenosis. It is considered the gold standard for
diagnoses may include temporal arteritis, revascularisation in patients with carotid arterial disease. CEA has been shown to
vertebrobasilar insufficiency, cervical spine significantly reduce the risk of stroke in symptomatic patients with significant carotid
pathology, cardiac sources of emboli, and stenosis. Complications may occur and include stroke, myocardial infarction,
other vascular disorders such as vertebral bleeding, infection, and cranial nerve injury. Patient selection is important and should
WHAT IS CAROTID ARTERIAL DISEASE? artery stenosis, intracranial arterial stenosis, consider factors such as age, comorbidities, and the presence of contralateral carotid
l Carotid arterial disease refers to the narrowing or blockage of the carotid arteries, which are responsible and vasculitis. Cardiac sources of emboli, occlusion.
for supplying blood to the brain. This is primarily due to atherosclerosis. such as atrial fibrillation or valvular heart
disease, are the most common and should be Carotid artery stenting (CAS)
l As the plaque evolves, it can lead to significant stenosis with a risk of plaque rupture or complete occlusion evaluated through electrocardiogram and
of the carotid arteries, disrupting blood flow to the echocardiography.
A less invasive alternative to CEA. It involves the placement of a stent into the
brain and increasing the risk of stroke. narrowed carotid artery to open it up and improve blood flow. CAS is typically
performed using a percutaneous approach in the groin. CAS is typically considered in
Management of carotid
patients who are at high surgical risk or have anatomical factors that make CEA
arterial disease challenging. An example of this is a patient who has had previous radiotherapy to the
Clinical presentation
The management of symptomatic carotid neck. CAS carries a higher risk of early stroke when compared to CEA with other
The vast majority of carotid artery disease is vascular disease involves both medical and associated risks including stent-related complications. However, it comes with less
asymptomatic. However, when symptoms do arise, surgical interventions. Medical management risks to the heart and a limited risk of any nerve injury. Careful patient selection and
they may include transient ischaemic attacks (TIAs), aims to control risk factors and reduce the operator expertise are crucial for optimal outcomes with CAS.
strokes or amaurosis fugax. TIAs manifest as risk of further sequelae of the disease. This
temporary episodes of neurological dysfunction, includes lifestyle modifications, and
such as sudden weakness or numbness in the face, pharmacological therapy.
arm, or leg, difficulty speaking, and visual disturbances
in the form of transient vision loss (amaurosis fugax) Surgical interventions are often considered
with resolution of symptoms within 24 hours of onset. for patients with significant carotid stenosis
(>50% NASCET criteria) in the form of Carotid plaque following endarterectomy
Strokes, on the other hand, result in more permanent
carotid endarterectomy (CEA) or carotid showing tight stenosis and area of
neurological deficits.
artery stenting (CAS). CEA involves the ulceration with adherent thrombus
surgical removal of plaque from the carotid
Diagnosis
artery, while §CAS involves the placement of
MRA showing
History a stent to widen the narrowed artery. Both
right internal
A detailed patient history is crucial in identifying procedures aim to reduce the plaque burden
l
carotid artery
symptoms associated with carotid arterial within the artery to the brain and reduce the
stenosis
disease. Symptoms of focal neurological deficits; risk of stroke. The choice between CEA and
arm/leg weakness, vision loss, facial droop, CAS depends on various factors, including
inability to speak, etc are all suggestive of a the patient's age, comorbidities, and
cerebrovascular accident occurring in the carotid anatomical considerations.
artery territory. Unilateral symptoms are a key Medical management
predominant sign. Cardiovascular risk factors This should involve lifestyle modifications
should also be addressed. and optimisation of medical therapy, known
resonance angiography (MRA) are also valuable as best medical therapy (BMT). This
Examination tools for further assessment and management includes smoking cessation and aggressive
l Neurological examination should also be planning. In the UK, two forms of imaging are control of hypertension, hyperlipidaemia,
performed to assess for any focal deficits. used to determine / confirm the stenosis prior to and diabetes. Antiplatelet therapy, such as
undergoing carotid artery intervention. clopidogrel or aspirin, should be prescribed
Imaging
to reduce the risk of thromboembolic events
l Duplex ultrasound is the and patients should have optimal lipid
initial imaging modality of TABLE 1 CAROTID ARTERY STENOSIS MEASUREMENT lowering therapy usually in the form of high
choice, providing CRITERIA ON DUPLEX ULTRASOUND intensity statin therapy (Atorvastatin 80 mg
information about the nocte). Management of asymptomatic carotid artery stenosis
degree of stenosis and
External Internal NASCET ECST Revascularisation strategies
plaque morphology. Carotid artery stenosis affects around 3% of individuals aged > 60 years
carotid carotid Revascularisation is considered in patients
NASCET (North American 30 65 and is responsible for up to 15% of all ischaemic strokes. While patients
artery artery with significant symptomatic carotid stenosis
Symptomatic Carotid 40 70 with asymptomatic carotid stenosis (defined as the presence of carotid
(>50% NASCET criteria). A decision on
Endarterectomy Trial) and 50 75 arterial disease but not having had a previous stroke or TIA) have a low
intervention is determined based upon the
ECST (European Carotid 60 80 risk of stroke with BMT, it is uncertain whether the benefits of carotid
risk of stroke versus the risk of intervention
Surgery Trial) criteria are 70 85 surgery outweigh the risks. The European Society for Vascular Surgery
and is determined by the degree of
used in assessing the 80 91 (ESVS) latest guidelines recommend that individuals with an
Estimated stenosis and time from event. Two main
degree of stenosis on position of 90 97 asymptomatic carotid stenosis of 60–99% and average surgical risk be
revascularisation approaches include carotid
duplex (see Table 1). carotid wall considered for carotid endarterectomy (CEA) only if they exhibit certain
endarterectomy (CEA) and carotid artery
Significant stenosis is characteristics associated with a higher risk of stroke. In high-risk patients
Approximate equivalent degrees stenting (CAS).
defined either as a 50% Common carotid artery who are not suitable for surgery, carotid artery stenting (CAS) may be
of internal carotid artery stenosis
NASCET or 70% ECST used in NASCET and ESCT The choice of procedure depends on indicated as long as the peri-procedural risk of stroke or death is less
stenosis. Computed according to recent direct various factors such as the patient's overall than 3% and the patient has a life expectancy of over 5 years.
comparisons
tomography angiography health, comorbidities, and individual risk
(CTA) and magnetic profile.

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FIGURE 1: CHEST X RAY SHOWING A RIGHT

Venous TOCS

20 THORACIC OUTLET SYNDROME AND

VASOSPASTIC DISEASE
CERVICAL RIB (WHITE ARROW) l

l
Primary subclavian vein thrombosis due to compression is also known
as Paget-Schroetter syndrome.
History: swelling of arm, pain worse with exercise, cyanosis, venous
claudication.
Chandana Wijewardena, Aminder Singh, Henry Bergman, l Examination: unilateral swelling of arm. Pulses should be present.
Rare cases can have signs of venous gangrene.
Andrew Winterbottom
l Diagnostic tests: Duplex ultrasound is first line followed by CT or MR
venography.
l Management: conservative management with arm elevation and a
compressive sleeve provides symptomatic relief in mild to moderate
WHAT IS THORACIC OUTLET COMPRESSION SYNDROME (TOCS)? cases. Pharmacological management with anticoagulation. Catheter
directed thrombolysis or surgical thrombectomy can be considered in
l The thoracic outlet, located between the thorax and the axilla, is the region where the subclavian artery, Diagnostic tests: Duplex ultrasound of arteries in
l
those with a severe presentation. Surgical resection of first rib would be
subclavian vein and brachial plexus travel from the thorax through to reach the upper limb. neutral and stress positions. Computed tomography (CT) required after initial management to prevent further episodes.
l TOCS includes a variety of symptoms due to compression of neurovascular structures within the thoracic with arterial contrast with arms up and down (dynamic
CT) positions can demonstrate arterial compression
outlet. Symptoms are related to the structure being compressed. Vasospastic disorders
(Figure 2). MR angiography.
l Common compression points include between scalene muscles, between clavicle and first rib and under l Due to vasospasm of digital arteries leading to reduced blood flow.
l Differential diagnosis: Can mimic Raynaud’s
pectoralis minor. A cervical rib is an important bony cause of TOCS. phenomenon.
Usually affects fingers.
l TOCS affects women more than men. l Initially digit colour turns white due to vasospasm, then blue from cyanosis
l Arterial TOCS with subclavian artery damage should be
and then red from reactive hyperaemia.
l Over 90% of patients have neurological symptoms such as pain or weakness from compression of nerve treated with surgery. If the cause of the compression is
roots of the brachial plexus. a cervical rib, this should be resected. If the compression l Predominantly affects females.
is proven to be between the 1st rib and the clavicle,
l Compression of the subclavian artery can lead to upper limb claudication or acute limb ischemia. resection of 1st rib is indicated. Depending on the Raynaud’s phenomenon
Compression of the subclavian vein can result in deep venous thrombosis. extent of the damage to the subclavian artery, arterial
reconstruction with patch repair or bypass graft may be
l The exact cause is unknown, but it is suggested abnormal red blood cell,
undertaken at the time of 1st rib or cervical rib resection white blood cell and platelet function lead to aggregation in the
identified, such as a cervical rib. microcirculation. Dysfunction in the peripheral nervous system can lead
Neurological TOCS Arterial TOCS to vasospasm alongside inflammatory conditions.
l History: commonest symptoms include pain, l Usually associated with compression of subclavian l Primary Raynaud’s phenomenon occurs on its own and it’s the most
FIGURE 2: VOLUME RENDERED CT ANGIOGRAM common type.
paraesthesia, and weakness. Location of artery from bony structures (clavicle and first rib) with
IN ARMS DOWN POSITION
paraesthesia is determined by which nerve time leads to arterial wall damage and post stenotic l Secondary Raynaud’s could be due to connective tissue disease, vascular
root is compressed. dilatation. disease, mechanical or environmental factors or drugs (Table 1).
a) with normal thoracic outlet and normal subclavian artery (white arrow).
l Examination: tenderness and paraesthesia l Clots formed within the post stenotic dilatation can Volume rendered CT angiogram l Diagnostic tests: hand cooling and pressure drop assessment or nail fold
in response to pressure over scalene muscles lead to distal embolisation. b) and curved plane reformat
c) in arms up position capillaroscopy. Blood tests to investigate secondary causes include full
may be present. Asking the patient to rotate l History: upper limb claudication or thromboembolic d-f) showing significant compression of the subclavian artery by the blood count, urea and electrolytes, erythrocyte sedimentation rate,
their head and tilt away from affected side disease-causing ischaemia. Severe cases may clavicle and 1st rib in the abnormal thoracic outlet (white arrow head). rheumatoid factor, and antinuclear antibodies.
may reproduce pain. Roo’s test involves present with digital gangrene. l Management: conservative with advice of using heating aids which can
abducting arm to 90oC in external rotation
Examination: full vascular examination. Look for help with symptom relief. Drug therapy with calcium channel blockers or
with finger clenching to reproduce l

signs of ischaemia such as ulcers or embolic changes. prostaglandins can be used to promote vasodilation. Sympathectomy and
symptoms.
surgery for more significant ischaemia is rarely required. In secondary
l Diagnostic tests: a scalene muscle block Raynaud’s, treatment of the underlying cause is essential.
with local anaesthetic leading to symptom
improvement suggests surgical treatment Demonstration of common compression points between
would be effective. A duplex ultrasound to (1) scalene muscles, (2) between clavicle and first rib and TABLE 1: SECONDARY RAYNAUD’S CAUSES
assess the subclavian artery and vein is (3) under pectoralis minor. Connective tissue Rheumatoid arthritis
required, as well as Xray for cervical rib disease Scleroderma
(Figure 1). Neurophysiology and MRI can Sjogren’s syndrome
Systemic lupus erythematosus
exclude alternative causes such as cervical
Takayasu’s arteritis
root compression.
Vascular disease Atherosclerosis
l Differential diagnosis: nerve compression Thromboangiitis obliterans (Buerger’s disease)
at cervical root (e.g. disc herniation) or in the Thromboembolism
upper limb (e.g. carpel tunnel) causing TOCS
neurological symptoms.
Mechanical or Jobs involving repeated actions or vibration
l Conservative management is first line with environmental Smoking
targeted physiotherapy and often significantly Trauma
improves symptoms in most patients. Drugs Beta blockers
l Surgery is offered to those failing conservative Chemotherapy
management. It involves resection of the Combined oral contraceptive pill
1st rib on the affected side and other bony 1. Anterior scalene 6. Subclavian vein 11. Acromion process
Ergot derivatives
2. Middle scalene 7. Subclavian artery 12. Humerus Interferon
abnormalities identified, such as a cervical
3. Posterior scalene 8. Clavicle 13. Pectoralis minor
rib. 4. Internal jugular vein 9. First rib 14. Axillary vein
Other Diabetes
5. Common carotid artery 10. Scapula 15. Axillary artery
Hypothyroidism
Malignancy

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21
DIAGRAMMATIC REPRESENTATION OF
MANAGEMENT OF PATIENTS WITH THE CEPHALIC AND BASILIC VEINS. BOX 1

RENAL DISEASE Rule of 6’s for arteriovenous fistulas

Upper arm The rule of 6’s is a widely used informal guide to determine when an AVF will
Jing Yi Kwan, Jon De Siqueira
l
cephalic
vein support dialysis.
l It states that 6 weeks after creation, an AVF should achieve a blood flow rate of
at least 600 mL/min, a diameter of at least 6 mm, an access length of 6 cm for
cannulation, and a depth of 6 mm or less from the skin surface.

DIALYSIS ACCESS IN PATIENTS WITH END-STAGE RENAL DISEASE l It is paramount for clinicians to learn how to access for fistula thrill.

l The ideal vascular access should provide safe and effective haemodialysis by enabling the removal and
return of blood via an extracorporeal circuit.
l Routes for haemodialysis vascular access include (1) arteriovenous fistula (AVF), (2) prosthetic graft, and Peritoneal dialysis (PD)
(3) venous catheters (tunnelled and non-tunnelled). The Renal Association guidelines (UK) recommend use Indications
of AVF first, AV graft as the second option and venous catheters as the last option.
Forearm l Haemodynamically labile patients with poor cardiovascular function who may
l Peritoneal dialysis is an alternative where peritoneal catheters are placed to allow dialysate to be instilled cephalic Basilic vein tolerate haemodialysis poorly.
vein
directly into the intraperitoneal space where it remains in contact with the peritoneal membrane before Contraindications
being removed.
l Inflammatory abdominal conditions, unrepaired hernia.
Complications
Peritonitis, hernia formation, catheter migration and malposition.
Assessment of a patient for haemodialysis access creation
l PD catheters can be placed either by an open or laparoscopic surgical
History technique.
l Hand dominance, previous vascular access, upper and lower extremity venous thrombosis, symptoms of hand l The borders of the rectus muscle are preferred insertion sites to avoid the
ischaemia. superficial and inferior epigastric arteries.
Investigations l When using a Tenckhoff catheter with two cuffs, the deeper cuff should rest
l Duplex venous ultrasound – A non-phlebitic, non-calcified vein of minimum 3.0 mm diameter is preferred. The best within the pre-peritoneal space in the rectus sheath, and the superficial cuff
conduit is superficial, easily identified, straight and of large calibre. should lie 2–3 cm medial to the superficial wound. Placing the deeper cuff
outside the rectus muscle may lead to less tissue ingrowth, increasing the
likelihood of leakage and herniation. If the superficial cuff placement is too
Arteriovenous fistula creation Arteriovenous loop graft deep, serous fluid may collect in the space outside of the cuff, leading to skin
l The Society of Vascular Surgery recommends When there is no autogenous option for AV fistula creation then a irritation and infection.
placing access as distal in the upper extremity non-autogenous reconstruction is created. There are several options:
as possible to preserve future central access
while giving preference to the non-dominant
l Expanded polytetrafluoroethylene (PTFE) grafts can be
arm. cannulated 2–3 weeks after graft creation. Central venous catheters (CVCs) DIAGRAMMATIC REPRESENTATION OF SET UP FOR RENAL DIALYSIS
USING AN A-V FISTULA
l The preferred order of fistula creation is a radial
l A new PTFE-based graft known as the Accuseal graft allows for Indications
artery to cephalic vein (radiocephalic) fistula, cannulation within 24 hours by way of a mid-layer sealing l Advanced age at initiation of HD, patients
brachiocephalic fistula, and then transposed membrane.
awaiting AVF maturation.
brachiobasilic fistula. A radiocephalic fistula has Complications
Contraindications
a high rate (30–50%) of non-maturation. l Immediate complications – Pain, bleeding, haematoma, l Local infection, thrombosis or stenosis of
l When the upper arm cephalic, basilic, or oedema, loss of thrill secondary to acute thrombosis or
target vein.
brachial veins are being utilised, a two-stage intraarterial flap.
approach is advocated due to increased Complications
l Early / late complications – Failure of maturation, infection,
patency rates. The first stage is the anastomosis
stricture, venous hypertension, ischaemic steal syndrome, Bleeding, air embolism, pneumothorax,
of a primary artery to vein through a local
aneurysm formation, neuropathy. cardiac perforation, arrhythmias, central
incision. The second stage involves the
vein stenosis.
transposition of a mature vein superficially for Endovascular or surgical interventions may be warranted to
identification in cannulation. revise the existing fistula. l Central venous access is obtained via the
internal jugular vein, subclavian vein, and
femoral veins.
COMMON SITES FOR AV FISTULA FORMATION l Subcutaneously tunnelled CVCs travel
under the skin away from the point of
Brachiocephalic AV fistula Radiocephalic AV fistula venous entry and provide long-term
intravenous access for haemodialysis.
They can remain in place for weeks to
months.
l Non-tunnelled catheters should only be
placed as the last resort or in emergency
situations when more permanent access is
Brachiobasilic AV fistula with transposition not available for dialysis. They need to be
of the basilic vein (BVT) exchanged every few days to a week.

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RUTHERFORD CLASSIFICATION FOR ALI GRADES THE SEVERITY OF ALI AND RISK OF LIMB LOSS
ACUTE LIMB ISCHAEMIA Category Description Capillary Motor Sensory Arterial Venous
Thomas Lyons, Julien Al Shakarchi return innervation innervation doppler doppler
I – Viable Not immediately threatened Intact Intact Intact Audible Audible

IIa – Threatened Salvageable if promptly treated Intact/slow Intact Partial loss Inaudible Audible

IIb – Threatened Salvageable if immediately treated Slow/absent Partial loss Partial loss Inaudible Audible
WHAT IS ACUTE LIMB ISCHAEMIA?
III - Irreversible Primary amputation Absent/staining Absent/fixed Complete loss/ Inaudible inaudible
l Acute limb ischaemia (ALI) is mostly synonymous with an acute arterial occlusion and is defined as a insensate
sudden reduction in limb perfusion that may threaten a limb’s viability. It can occur in any peripheral artery
of the upper and lower extremities.
Management of acute limb ischaemia
l It is a vascular emergency which needs early recognition, prompt diagnosis and intervention. Left untreated SURFACE LANDMARKS FOR WHERE TO MAKE THE
it may lead to major limb amputation. Initial management INCISIONS FOR A 4 COMPARTMENT FASCIOTOMY
l A to E assessment in accordance with CCrISP guidelines. (RED LINES).
l ALI classically presents with the 6Ps of limb ischaemia: Pain, Perishingly cold, Pallor, Pulselessness, l Initiate oxygen to optimise physiology unless concerns regarding
Paraesthesia and Paralysis CO2 retention
Bedside tests include: routine bloods including a FBC, UEs, The medial incision is
l ALI can be managed medically (intravenous heparin), endovascularly (thrombolysis or thrombectomy) or l

clotting and crossmatch. ECG to look for AF. 2cm behind the border
surgically (embolectomy). of the tibia.
l Bolus 5000 IU of IV heparin
Medical Remember to also
l Anticoagulation, initially with IV heparin bolus (check local decompress the deep
guidelines). medial compartment.

6 signs of acute limb ischaemia l Following the bolus, an infusion is started initially at a rate The anterior incision is
BOX 1 determined by weight followed by the APTT ratio thereafter. half way between the
Aetiology Endovascular tibia and the fibula.
l Thrombolysis
Thrombosis n Use of a thrombolytic agent (t-PA or urokinase) to
l Atherosclerotic – plaque rupture !"#$ !"#"$%&'$%(" dissolve a thrombus.
l Graft / stent occlusion n The thrombolytic agent is given directly to the site of the
l Popliteal aneurysm thrombus (intra-arterial), with percutaneous access to
place a catheter within the thrombus to deliver the BOX 2
Embolism !"##$% thrombolytic agent locally. Contraindications:
o Active internal bleeding
Popliteal artery aneurysms
l Cardiac (e.g. atrial fibrillation
o Risks associated with bleeding Popliteal aneurysms are the most common peripheral aneurysm
(AF), myocardial infarction (MI),
o Pregnancy (>80% of peripheral aneurysms) and 50% of popliteal aneurysms are
infective endocarditis) !"#$%&$'()*+
l Non-cardiac (e.g. atherosclerotic ,-).
!"#"$%&'& o Stroke/TIA within 2 months associated with abdominal aortic aneurysms. Risk factors include
o Vascular or abdominal surgery within 2 weeks smoking, atherosclerosis, connective tissue disorder, age, male
disease, aneurysm)
l The embolism classically lodges l Thrombectomy gender and history of abdominal aortic aneurysm.
at an arterial bifurcation n Percutaneous thrombectomy
o Aspiration Asymptomatic aneurysm of less than 2 cm can be safely monitored
!"#$%#%$$ with regular duplex imaging. Popliteal aneurysm repair should be
Trauma o Mechanical
considered once the maximal diameter reaches 2.0–2.5 cm.
Arterial dissection Surgical
Embolectomy – most commonly performed procedure is a femoral Acute thrombosis of a popliteal
embolectomy with less commonly performed brachial and popliteal aneurysm poses the highest risk to a
embolectomy. limb. Due to the amount of movement
l Expose artery and control inflow and outflow at the knee joint, there is increased
risk of disintegration of the thrombus
l Transverse arteriotomy
leading to microembolism (trash)
How to diagnose acute limb ischaemia l Check inflow distally. This can often occur silently
n If poor inflow, proceed to proximal embolectomy, imaging hence why there is approximately a
History Examination will also inform as to whether any up stream clot 50% limb loss.
l The classical clinical presentation of l Look for obvious signs of ALI – pallor, mottling, fixed-mottling
n If still poor inflow after embolectomy, then may need to consider
acute limb ischaemia are the 6Ps of limb some alternative vascular surgical reconstruction In an acutely thrombosed popliteal
l Assessment of lower limb pulses (also comparison with pulses of n If there is good inflow, proceed to distal embolectomy aneurysm, it is important to ensure
ischaemia: Pain (severe and resistant to the non-affected limb)
analgesia), Perishingly cold, Pallor, with appropriately sized Fogarty balloon catheter there is viable distal run-off. This can
l Palpation (temperature and muscle compartments) n If no improvement after embolectomy, can consider be managed with embolectomy +/-
Pulselessness, Paraesthesia and
Paralysis. l Assess the neurological status of the limb (sensory and motor) operative thrombolysis, more distal embolectomy or thrombolysis to the distal vessels
distal bypass. On-table angiography is useful to assess followed by an exclusion bypass of the
l Risk factors for vascular disease: history Imaging the distal outflow in such circumstances. thrombosed popliteal aneurysm.
of intermittent claudication, cardiac l First line imaging is commonly CT angiography which provides Fasciotomies
history (atrial fibrillation, ischaemic heart
cross sectional imaging and is fast and usually the most readily Patients who undergo revascularisation for acute limb ischaemia should
disease including recent myocardial MRA showing a left
available imaging modality. be considered for 4 compartment fasciotomies. Two long incisions are
infarction), diabetes, smoking history and popliteal artery aneurysm
any previous intervention. l Prompt imaging is required to allow planning for intervention, made along the lower leg (medial and lateral) to allow access to the
however imaging should not delay referral with the vascular compartments where the fascias are incised to release them. It is
l Recent cessation of anticoagulation. on-call team and clinical findings should trigger urgent review. important to decompress the deep medial compartment.

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23
progressing in later Chronic mesenteric ischaemia
MESENTERIC AND OTHER VISCERAL stages to loss of l Chronic mesenteric ischaemia occurs due to reduced blood supply to the bowel, which occurs gradually commonly due to
enhancement in the
DISEASE bowel wall and
pneumatosis, with
progressive atherosclerosis to the coeliac, SMA and/or IMA. This condition is more common in females. Other risk factors
include smoking, diabetes mellitus, hypertension and hypercholesterolaemia.
Mary Weisters, Tom Baker or without evidence l Due to the collateral nature of the mesenteric blood supply, at least two of the three mesenteric arteries need to be affected for
of perforation. the patient to become symptomatic. Most often, at least one of these vessels is occluded.
Thrombus in one How to diagnose chronic mesenteric ischaemia?
or more mesenteric
WHAT IS MESENTERIC ISCHAEMIA? arteries. History l OGD
l Mesenteric ischaemia is a condition characterised by reduced or obstructed blood flow to the large and/or l Post-prandial abdominal pain – l Ultrasound of biliary tree
Management
small intestine. It can present as an emergency acutely or as a chronic progressive condition. classically occurs within 4 hours +/- MRCP if deranged
l Initial management of eating – ‘mesenteric angina’ LFT or dilated biliary
l The mesenteric arteries supply the gastrointestinal organs focuses on patient l Fear of eating tree
A-E resuscitation,
These include the coeliac trunk, superior mesenteric artery (SMA) and inferior mesenteric artery (IMA), all Significant unintentional weight l CT Angiogram
alongside l

direct branches of the abdominal aorta. loss abdominal aorta

administration of CT scan showing
broad-spectrum l Nausea and vomiting sometimes Differential diagnosis advanced
antibiotics. occur l Peptic ulceration/GORD atherosclerosis of
MDT care with Loose stools sometimes occur the SMA.
l l l Chronic pancreatitis
Primitive Gut Portion Adult Derivatives Supplying artery involvement of Examination l Biliary colic
general surgery,
1. Foregut Oesophagus, stomach, proximal half of the duodenum, liver Coeliac trunk
vascular surgery
l Often non-specific, such as mild l UGI malignancy
and biliary tree general tenderness.
and interventional Management
2. Midgut Distal half of the duodenum, jejunum, ileum, caecum, SMA radiology l Cachexia / evidence of major
l Management of risk factors for atherosclerosis, to minimise
appendix, ascending colon and most of the transverse colon weight loss e.g. baggy clothes
l Early consideration disease progression.
for involvement of Investigations
3. Hindgut Remainder of the transverse colon, descending colon, IMA Lifestyle changes (smoking cessation).
ITU Comprehensive and often best guided
sigmoid colon, rectum, superior portion of the anal canal Medical management with anti-platelet and high-dose statin
Surgical by gastroenterologist. Chronic
l
therapy.
management is mesenteric ischaemia is often a
the definitive diagnosis of exclusion. l Revascularisation usually endovascular or occasionally
Acute mesenteric ischaemia How to diagnose acute mesenteric ischaemia? surgical. Intervention is HIGH RISK.
management for l Routine blood tests: FBC, U+Es,
l Acute mesenteric ischaemia occurs History acute mesenteric LFTs may be normal. Electrolytes Endovascular: options are for mesenteric angioplasty and/or
due to a sudden reduction in blood l Sudden onset severe abdominal pain – diffuse and constant in nature ischaemia, and such as magnesium and stenting.
supply to the bowel, resulting in will focus on two phosphate should be checked in
+/- Nausea and vomiting Surgical: options are endarterectomy or bypass
bowel ischaemia, bowel necrosis and l
aspects: presence of malnutrition.
subsequent death if not treated promptly. l Often occurs in a setting of an acutely unwell patient e.g. pneumonia,
Overall mortality from the condition is Resection of
recent myocardial infarction
estimated at 60–80%. The most common non-viable / necrotic
cause is an embolic event but there are
l May be a history of atrial fibrillation or palpitations/chest pain/shortness bowel. Post- Mesenteric aneurysms
of breath or recent cessation of anticoagulation operatively this may
other rarer causes. True mesenteric aneurysms are rare. The detection of asymptomatic atherosclerotic mesenteric aneurysms has grown in recent years
Examination involve the patient
Aetiology due to increased use of axial imaging (CT scans). They appear as small calcified slow growing aneurysms.
l
undergoing a re-
l Initially abdomen may be soft with generalised tenderness throughout. look laparotomy in They may occur after a dissection that weakens the artery wall. Occasionally mesenteric aneurysms rupture leading to haemorrhage and
Embolism Atrial fibrillation, LV l In later stages, where risk of perforation is higher, patients may have 24–48 hours and death.
thrombus e.g. after signs of generalised peritonism. may require the Aneurysms of the pancreaticoduodenal and gastroduodenal arcades have a higher risk of rupture and History
myocardial infarct, abdomen to “remain should be treated irrespective of size.
Investigations Asymptomatic
aneurysms open” l

l Blood gas: metabolic acidosis and raised lactate levels. NB In late after the initial Pseudoaneurysms can occur after severe acute pancreatitis or trauma. They have a high risk of bleeding l Occasionally
Unstable plaque phase with dead bowel lactate can be normal laparotomy. and also should be treated. abdominal pain
Thrombus
in situ rupture from l Routine blood tests: FBC, U+Es, coagulation, LFTs. Revascularisation Splenic artery aneurysms should be considered for repair at any size in a woman of childbearing age as the Investigations
underlying of the bowel. aneurysm can undergo rapid growth and rupture during pregnancy with a risk of maternal and foetal death. CT angiogram
atherosclerosis Note that if there is coeliac trunk involvement, this may result in hepatic Embolism is rare. Thrombosis and thromboembolism often go unnoticed due to the collateral circulation
l

ischaemia and derangement of LFTs and/or INR. The white cell count is This may involve or MRA
endovascular of the gut.
Non- Prolonged usually elevated.
techniques or
occlusive hypotension Imaging:
l
open surgical Type of aneurysm Management
mesenteric (e.g., hypovolaemic
CT scan showing evidence of CT abdomen and embolectomy.
ischaemia shock / cardiogenic True mesenteric aneurysm, Surveillance
thrombus within the SMA. pelvis with arterial, Often this is a
“NOMI” shock), l
symptomatic <2.5 cm
vasoconstriction venous and portal ‘preterminal event’
venous phase and management is True mesenteric aneurysm Consider endovascular treatment with stent
contrast. >2.5 cm, asymptomatic placement or coil embolisation
Venous Mesenteric palliative
occlusion venous Bowel ischaemia Symptomatic true mesenteric Endovascular treatment with stent placement or
thrombosis will initially show on aneurysm coil embolisation
CT as oedematous Mesenteric pseudoaneurysm Endovascular treatment with stent placement or
bowel loops. coil embolisation
CT scan showing evidence of
thrombus within the SMA. Splenic artery aneurysms in a Consider endovascular treatment with stent
woman of childbearing age placement or coil embolisation

56 MESENTERIC VASCULAR DISEASE 57

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ACKNOWLEDGEMENTS OF FIGURES

We would like to acknowledge Smartservier (smart.servier.com) as the source of the following images:

Page 4. The Circle of Willis: https://smart.servier.com/smart_image/circle-of-willis/

Page 4. The extracranial carotid artery: https://smart.servier.com/page/2/?s=Arteries

Page 5. The arterial supply of the upper limb: https://smart.servier.com/page/2/?s=arteries

Page 6. The aorta and the veins of the abdomen: https://smart.servier.com/smart_image/abdominal-aorta/

Page 7. The lower limb arterial and venous suppl: https://smart.servier.com/smart_image/venous-disease-spider-veins/

Page 8. Atherosclerosis (all images): https://smart.servier.com/page/5/?s=atherosclerosis

Page 9. The damaged venous valve: https://smart.servier.com/smart_image/venous-circulation-leg/

Page 9. The layers of the arterial wall: https://smart.servier.com/page/5/?s=atherosclerosis

Page 20. Arterial supply of the groin and foot: https://smart.servier.com/?s=Arteries

Page 23. Monofilament test for diabetic neuropathy (all images): ttps://smart.servier.com/?s=Diabetic+foot

Page 26. The bones of the lower limb and pelvis: https://smart.servier.com/page/4/?s=Bones

Page 34. Aortic dissection diagrams: https://smart.servier.com/page/3/?s=Cardiovascular+system

Page 36. The arch of the aorta: https://smart.servier.com/page/3/?s=Cardiovascular+system

Page 37. The use of open surgical (surgical grafts) in the management of aortic pathology:
https://smart.servier.com/page/3/?s=Cardiovascular+system

Page 52. The upper limb: https://smart.servier.com/?s=Arm

Page 53. The venous supply of the upper limb: https://smart.servier.com/?s=veins

Page 53. Diagrammatic representation of renal dialysis: https://smart.servier.com/smart_image/dialysis/

The diagram from chapter 7 is referenced in the text and as follows:

https://www.nice.org.uk/guidance/ng136/resources/visual-summary- pdf-6899919517

We would also like to thank Mid Yorkshire Teaching NHS Trust for the use of the following images:

Page 9. palpation of the doralis pedis pulse

Page 20. palpation of the posterior tibial and dorsalis pedis pulse

Page 21. performing an ABPI

Page 42. Legs that show skin changes due to venous hypertension (2 images)

Page 43. Various methods of applying compression (3 images)

Page 55. Surface markings for the incisions for a 4 compartment fasciotomy

The authors from chapter 20 provided the thorax image from page 5.

The rest of the images have been provided by authors from the book.

NOTE: Links to the images taken from the Servier website are found within the powerpoint presentation

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Vascular Society of Great Britain & Ireland

c/o Executive Business Support Limited, City Wharf, Davidson Road,
Lichfield, Staffordshire, WS14 9DZ
Email: admin@vascularsociety.org.uk

www.vascularsociety.org.uk