Vascular surgery is the surgical specialty that deals with diseases of the arterial, venous, and lymphatic systems.
Most patients on the vascular ward will have peripheral vascular disease with rest pain and/or tissue loss (ulceration, toe gangrene, etc.).
You might catch these patients in hospital having investigations (e.g. angiography) but will have to work around lots of other processes (consent, blood tests, etc.)
Ligation, sclerotherapy, and ablation usually performed as day cases so you could need to catch these patients in clinic or at day surgery unit.
Spend a day in the diabetic foot clinic if you want to see many in one place. Try to see examples of arterial, venous, and neuropathic ulcers as well as clean, healing, and infected cases.
Large palpable AAAs are likely to be fixed quickly and ruptured aneurysms are few and far between. You must use your vascular rotation to feel AAAs as students often struggle to distinguish ‘pulsatile’ from ‘expansile’.
Unpredictable and requiring swift intervention so may be missed during a short placement.
Look for the vascular lab or radiology department to observe duplex US scan of the lower limb arterial, venous, and carotid systems.
Lower limb arterial bypass, AAA repair (open and endovascular), major lower limb amputation (e.g. below-knee amputation), carotid endarterectomy, and operative management of varicose veins (e.g. sclerotherapy, laser ablation). Carotid endarterectomy provides a rare opportunity to appreciate neck anatomy.
Master the use of a hand-held Doppler and perform an ankle–brachial pressure index (ABPI).
An aneurysm is an abnormal permanent dilatation of a blood vessel by >50% of its normal diameter. The most common aneurysm is of the infrarenal (below the renal arteries) abdominal aorta. Aortas are considered aneurysmal once they reach a diameter of 3 cm and most are detected by the NHS AAA Screening Programme (single US scan for all males from age 65). They may also be found incidentally, e.g. on clinical examination or when patients are scanned for other conditions. Mortality associated with ruptured AAA is >50%. Aetiology is poorly understood but may be related to atherosclerotic disease so risk factors are cardiovascular (e.g. hypertension, diabetes, male, age, smoking). Small aneurysms (<5.5 cm) are followed up by annual US surveillance. Large aneurysms are repaired electively as the risk of operation usually outweighs rupture at 5.5 cm. Repair is by open or endovascular techniques. Associated with this are femoral and popliteal aneurysms.
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The UKSAT was a multicentre, randomized controlled trial of two management strategies for AAAs: ‘early elective open surgery’ and ‘regular US surveillance’. The study included 1100 patients and showed that small AAAs (<5.5 cm) can be monitored safely with US scanning without any 
in mortality. Indications for electively repairing AAAs are now often stated as >5.5 cm, growing >1 cm/year, or becoming tender.
Is a cramping pain in the muscle that occurs during exercise and is relieved by rest. Smoking is the biggest modifiable risk factor, claudication distance and rest period correlate with degree of arterial insufficiency and collateral supply respectively. The differential is spinal claudication (associated back pain, claudication relieved on leaning forward). Also needs distinguishing from critical limb ischaemia—arterial insufficiency with rest pain (e.g. at night when legs elevated) and/or tissue loss (e.g. ulceration) which needs prompt intervention. Most patients are managed conservatively: stop smoking, control modifiable CVD risk factors, walk through claudication distance, and primary prevention for CVD (aspirin and statin). Other interventions are to improve quality of life or for critical limb ischaemia (e.g. angioplasty, bypass, amputation).
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One traditional method for classifying PVD was proposed in 1954 by Rene Fontaine. The key thing is that PVD is a spectrum of disease severity which may be progressive, hence ‘staging’. Fontaine’s classification:
• Stage I: asymptomatic, incomplete blood vessel obstruction.
• Stage II: mild claudication pain in limb.
Are dilated and tortuous veins of the superficial venous system (e.g. great and lesser saphenous veins). Secondary varicose veins may be caused by DVT and the three Ps (pelvic mass, pregnancy, previous history). These are unsightly but symptoms include AEIOU:
Compression stockings followed by invasive options if unsuccessful: ligation/stripping, sclerotherapy, radiofrequency, or laser ablations.
An ulcer is a break in the skin or mucous membrane that fails to heal. The textbooks tell us these are arterial, venous, or neuropathic, although in practice most are mixed.
Caused by venous insufficiency (haemosiderin deposition 
skin breakdown and eczema chronic ulceration) and managed by elevation and four-layer compression bandages. Venous ulcers often have an arterial component in which case four-layer bandaging may be contraindicated as risks worsening arterial disease.
Caused by chronically inadequate blood supply (e.g. PVD skin breakdown without healing ulcer. Treatment to optimize blood flow (e.g. angioplasty, bypass).
Caused by loss of peripheral sensation and microtrauma. The most common type is the diabetic ulcer, which also frequently has an arterial component of poorly understood aetiology. Other causes are those of peripheral neuropathy. These are managed by a MDT (e.g. tight glycaemic control, chiropody, orthotic devices).
Is caused by atherosclerosis. The problem is plaque embolization (e.g. causing TIA and/or stroke) rather than occlusion of the vessel itself as there is usually an adequate collateral supply through the circle of Willis. Patients at high risk of CVA (e.g. significant stenosis and evidence of embolization) may benefit from carotid endarterectomy.
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Primary prevention describes measures to avoid disease in patients thought to be at risk. This is different to secondary prevention, e.g. treatment to avoid recurring coronary disease in a patient following acute MI. Patients with PVD (e.g. intermittent claudication) also probably have coronary and/or cerebrovascular disease. They may therefore be treated with strict risk factor management (smoking cessation and BP/glucose/cholesterol control). Most benefit from a statin and aspirin.
Lies on a spectrum of intermittent claudication. It is defined as inadequate arterial supply that threatens limb viability. Key red flags are rest pain, night pain, and tissue loss (e.g. ulceration, gangrene). These patients require urgent investigation and/or revascularization. It is distinct from acute limb ischaemia in that it often represents the slow deterioration of PVD rather than an acute event disrupting arterial supply (e.g. thrombosis, embolus).
Allows simultaneous visualization of tissue architecture and flow which are overlaid onto a single image. It is non-invasive, safe, and relatively cheap but operator dependent, not therapeutic and can be limited by bowel gas, calcifications, and body habitus.
Imaging technique using injected radio-opaque contrast agent (e.g. femoral artery) and X-ray imaging techniques such as fluoroscopy. The words angiogram and arteriogram are often used interchangeably, but technically refer to arterial imaging as opposed to the venous system (venogram). It can be therapeutic (e.g. angioplasty, stenting) as well as diagnostic. Disadvantages includes contrast allergy, nephrotoxicity, and complications of arterial puncture (e.g. bleeding, pseudo-aneurysm, limb loss).
Non-invasive angiograms providing detailed imaging of the arterial system, although it is not possible to intervene and risks of contrast remain.
Present as abdominal/back/loin–groin pain. Patient may be very well/stable initially. Requires high index of suspicion; often misdiagnosed as renal colic. All older (>55 years old) patients with pain should have active consideration of AAA ± US scan. The commonest presentation is collapse with hypovolaemic shock, and massive transfusion requirements. US can measure the aortic diameter (is there an aneurysm?) but bleeding is better identified by CT angiogram. CT should not delay transfer of an unstable patient to theatre, as only definitive haemorrhage control will save the patient (giving blood is supportive but ultimately need to turn off the tap). Management is as per elective aneurysms (open or endovascular aneurysm repair (EVAR)) or palliation may be appropriate.
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One approach to the bleeding and compromised patient is fluid resuscitation. This is a matter for discussion, however most leaking aneurysms cause bleeding into the retroperitoneum which tamponades the haematoma. Raising the systolic BP with excessive fluid resuscitation could rupture this haematoma and cause intra-abdominal bleeding with consequent circulatory collapse. Hence, maintain the systolic BP ≤100 mmHg but ensure the patient remains conscious—a concept known as ‘permissive hypotension’.
Main causes are thrombosis (e.g. of a popliteal aneurysm), (embolism, e.g. commonly intracardiac due to AF), and trauma (e.g. arterial transection). Presents as 6 ‘P’s:
• Perishingly cold (poikilothermia)
Investigations include duplex US and angiography to identify the lesion site. An acutely ischaemic limb needs to be revascularized within 4–6 hours to avoid amputation. Possible interventions include thrombolysis through an indwelling arterial catheter as an infusion, embolectomy, and bypass. An insensate, paralysed limb with fixed mottling is very unlikely to be rescued and probably requires amputation. Revascularization of a necrotic limb releases a deadly concoction of metabolites into the systemic circulation (SIRS, myoglobinuric AKI, death).
The principles of operative vascular surgery are to gain proximal and distal control of the relevant vessel (e.g. using clamps or small rubber bands called ‘sloops’) before investigating the site of injury.
Most AAAs are infrarenal (70%) which means they lie entirely below the origin of the renal arteries. Supra- and juxtarenal aneurysms are more complicated. The procedure involves laparotomy, clamping the aorta proximally, excision of the diseased vessel, and suturing in a graft (usually made of a polyester called Dacron®) prior to removing the clamp. As with any laparotomy, recall layers of the abdominal wall before you are asked. You may be asked to identify a large vessel running anterior to the aorta—this is probably the renal vein, which is sometimes sacrificed to gain better access. (See Fig. 41.1 for anatomy.) Mortality rate of elective open AAA repair is 5%. Risks of cross-clamping above the renal arteries include renal and gut underperfusion so try not to disturb the surgeon once the clamp is applied as they will want to proceed swiftly with minimal interruptions. Other complications are those of any laparotomy. Open repair of a ruptured AAA is more urgent and it is best not to interrupt the surgeon at any time if you happen to encounter one of these. It is often impossible to close the abdomen without risk of abdominal compartment syndrome and the abdomen may therefore be left ‘open’. A potential long-term complication of any open AAA repair is an aorto-enteric fistula ( small ‘herald’ rectal bleed preceding massive GI haemorrhage), which is rare in practice but common in exams.
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You will hopefully notice the surgeon warning the anaesthetist before placing a cross-clamp across the aorta. This is because the clamp leads to afterload to raise arterial pressure with consequent potential for heart failure and myocardial ischaemia.
EVAR may be performed by an interventional radiologist, specially trained vascular surgeon, or both. A guide wire is passed (usually through the femoral artery) under fluoroscopic (X-ray) guidance, and placed above the aneurysm in the aorta. A stent is deployed over the guide wire to exclude the aneurysm sac from the circulation. Juxtarenal aneurysms are often repaired using a fenestrated stent, i.e. with holes to accommodate branches of the aorta. Fluoroscopic images ‘light up’ the aorta and its branches. Unsuspecting students may well be asked at this point to identify major branches so learn them (plus vertebral levels at which they emerge from the aorta) beforehand. Specific complications are related to contrast (e.g. nephrotoxicity), the stent itself (e.g. infection, migration), occlusion of aortic branches (gut, kidneys, and spinal cord at risk), and groin puncture. An endoleak describes blood refilling the aneurysm sac due to a ‘leak’ around the stent—there are multiple types (e.g. depending on whether the leak is proximal, distal, or due to back-filling from small vessels). This can be an early or a late complication. Elective mortality of EVAR is around 1%, although the scale of long-term complications (e.g. stent migration) is not yet known and these patients require regular imaging surveillance. Some patients are technically unsuitable for EVAR, e.g. small tortuous iliac artery.
The neck is dissected (you might be asked about platysma—a large superficial subcutaneous muscle) and the arteries exposed. Know the contents of the carotid sheath (common carotid, internal jugular, vagus) and relative location of key structures before getting too close to a surgeon performing this operation. The external carotid is identified by its first branch (superior thyroid artery), the internal carotid having no branches outside the skull. The artery is controlled proximally and distally (e.g. with clamps or sloops), opened, and the intimal layer with associated atherosclerotic plaque removed. The artery is then repaired, e.g. with a vein patch which prevents stricture formation if the artery was closed primarily. Sometimes a shunt (temporary tube) is used to temporarily bypass the operative site. Complications include cranial nerve damage (VII, XII, and X at risk), stroke, haematoma, and hyper-perfusion syndrome.
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Carotid endarterectomy (surgical excision of plaque from the carotid artery) is performed to prevent embolization cranially which can cause disabling stroke. There is a <5% risk of death or disabling stroke perioperatively and so the procedure must be balanced carefully against its potential benefits. Commonly accepted indications include:
• symptomatic patients with >70% stenosis
• symptomatic patients with 50–69% stenosis—marginal benefit
• asymptomatic patients with >60% stenosis—marginal benefit.
Fig. 41.1 Abdominal aorta anatomy. Reproduced from Anatomy & Physiology, Connexions Web site. http://cnx.org/content/col11496/1.6/, Jun 19, 2013. under the Creative Commons Attribution 3.0 Unported license.
‘Bypass’ is a method of re-plumbing vessels so blood proceeds past an obstruction. Every bypass requires an inflow, conduit, and an outflow. Inflow describes adequate blood supply proximally, the conduit may be vein (e.g. great saphenous vein) or synthetic (e.g. PTFE), and the outflow describes distal ‘run-off’: vessel patency distal to the occlusion. Bypasses are described by their origin (anatomical vs extra-anatomical) and insertion (e.g. femoral–popliteal, axillary–femoral). Complications are of the graft (e.g. thrombosis, infection) and ‘steal’ phenomenon in which a limb is deprived of blood which has been diverted elsewhere (e.g. to the other leg).
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Possible factors might include the presence of a suitable vein, projected bypass length, infection risk, and likelihood of thrombosis/reocclusion). In some patients, the decision might be obvious (e.g. great saphenous vein previously harvested for CABG) but in others less so.
The artery (e.g. brachial or femoral) is dissected, the surgeon gains proximal and distal control, a small cut is made in the artery, and a Fogarty catheter is passed along the vessel. A small balloon at the end of the catheter is inflated with water and withdrawn to remove the embolus. Complications include intimal lesions (causing thrombosis), cholesterol emboli, and those related to arterial puncture.
Trivia
Dr Thomas J. Fogarty (b. 1934) watched lots of operations before going to medical school and was concerned that the amputation rate for patients with acutely ischaemic limbs due to embolus was >50%. At this time, a large part of the artery had to be cut out and the embolus removed with forceps. Fogarty tied a piece of glove to the end of a urethral catheter and proposed that it could be used to scoop out the embolus. No one accepted this idea until he went to medical school, trained as a cardiovascular surgeon, and proved the concept on his own patients. The Fogarty catheter is now used worldwide 300,000 times per year and is thought to have saved 15 million patients from death and/or amputation.
Amputation describes removal of a body extremity. Its indications are sometimes described as either:
• ‘dead limb’ (e.g. ischaemic necrosis)
• ‘deadly limb’ (e.g. malignancy, life-threatening infection)
• ‘dead loss’ (e.g. paralysed limb hampering function).
Major lower limb amputations are described anatomically (e.g. below knee, through knee, above knee, hindquarter). The knee is preserved if possible as it functions as a useful lever even when little is left distally. Prosthetic fitting is also something to consider. However, this must be balanced against the need for adequate stump healing (significant proximal vascular lesion unlikely adequate supply to heal below-knee amputation stump).
Significant complications include those related to the wound (e.g. infection, dehiscence) and stump (e.g. phantom pain, need for revision). Most patients require prolonged rehabilitation and are assessed for suitability to receive a prosthetic limb. Try to see a major amputation if possible—it is an important operation and a great opportunity to revise lower limb anatomy. Although they may be performed by other specialties (e.g. orthopaedic surgery), the vascular surgeons do more than anyone else. You are likely to be asked about the four compartments of the lower limb (anterior, lateral, posterior superficial, posterior deep) and their contents so look these up beforehand. When asked to identify structures, start by recalling the level of the amputation (e.g. no popliteal artery in a below-knee amputation).
This term describes injection of dye into an artery (e.g. coronary angiography). In the vascular setting, angiography is often of arteries in the lower limb. A radio-opaque dye is injected through a catheter in the femoral artery and X-ray technology used to visualize arterial flow. It can be diagnostic (e.g. showing occlusions) and/or therapeutic (e.g. stent insertion) in which case it may be called angioplasty. Complications are due to the dye (e.g. nephrotoxicity, anaphylaxis), arterial puncture (e.g. arterial rupture, pseudoaneurysm), and distal embolization of thrombus.
Angiography is usually performed in a specialist angiography suite, possibly signposted as ‘fluoroscopy’, rather than in theatres. It is usually performed by an interventional radiologist rather than a surgeon. Interventional radiologists are usually approachable and enthusiastic about teaching as they are rarely assigned their own medical students. The best place to find them is at the end of the vascular MDT meeting—going direct to fluoroscopy risks catching them mid procedure.
During your vascular placement, ensure that you can perform and elicit the procedures and signs in this section.
The most common vascular history will be intermittent claudication because this beautifully tests all elements of the standard history structure. A patient or actor will give a history of leg pain on exercise and you will doubtless draw out the following features within a few minutes of effective history taking. Practise this history on real patients before the exam—vascular wards are full of cheerful older men awaiting angioplasty/bypass/amputation who are otherwise bored and keen to aid learning.
SOCRATES pain history. In ‘site’, which leg is worst? In ‘onset’, ask about claudication distance (short distance claudicants, e.g. 10 m, have worse arterial disease). In ‘symptoms’, ask about vascular red flags: rest pain, night pain, and tissue loss. Although tissue loss is usually something you would find on examination, play safe in a history station and ask ‘Have you noticed any breaks in the skin of your feet?’ Do not leave the exam room without asking explicitly about these features.
Ask generally, ‘Do you have any medical conditions?’, then demonstrate your understanding of PVD by asking specifically about risk factors (hypertension, high cholesterol), consequences (MI, stroke), and complicating factors (diabetes).
Assessment of risk so specifically MI and stroke with ages (first-degree relative MI at 40 years is a greater risk than at 90 years).
Ask generally, ‘Do you take any medications, and have any allergies?’, then ask specifically: statin, aspirin, clopidogrel?
Smoking (including pack-years and ‘Have you ever smoked?’), alcohol, and impact on life (‘How do you get around normally? What stops you from walking further? What do these symptoms stop you doing?’). These last questions are not tick-box exercises in PVD: revascularization will not cure chronic heart failure or if SOB on exertion/painful knees are the main restrictions to mobility. Disabling PVD warrants aggressive intervention. One other possibility (although less likely) is a history of TIAs in a patient with carotid disease. Ask about amaurosis fugax, limb weakness, and time to resolution of symptoms. Ask about AF (and any associated treatment) in PMHx.
Vascular cases are common in surgical exams because they are chronic, often stable, and effectively test your ability to elicit clinical signs. The most common cases are:
Many patients with PVD will have a full constellation of vascular signs (e.g. cool foot with prolonged capillary refill and absent pulses) so the best students will trot out a full list (assuming all signs are present!) when summarizing their findings.
There are many patients with chronic venous disease and they can be recognized by their legs which are said to be shaped like an ‘inverted champagne bottle’. Create a script for describing these characteristic legs as above for chronic arterial disease, e.g. ‘both legs exhibit thickened shiny skin with brown discoloration which is consistent with long-standing chronic venous insufficiency. There is no evidence of cellulitis, ulceration, or varicose eczema’. If asked to examine such a patient, do not be fooled into thinking that there is a separate venous disease exam. Carefully inspect and assess the arterial system (including sensation etc.) as well as noting features of chronic venous disease.
This case tends to make students uncomfortable as there is a huge ‘inspection’ element which students often race through so they have time for the complex (but probably less important) clinical tests. It is nothing more than gambling to go into a surgical exam without having performed the tourniquet test on a real patient with varicose veins. Although this is not commonly used in practice, ask a doctor in the veins clinic to show you if textbook descriptions are unhelpful. YouTube and online videos may also be instructive.
These are palpable when a good arterial supply crosses an underlying non-compressible structure, e.g. pressing the radial artery against the radius. It should not take >20 sec to grip both hands (temperature), inspect them carefully (colour, ulceration), then palpate the distal pulses:
• Radial: lateral aspect of the distal wrist on the volar aspect.
• Ulnar: medial aspect of the distal wrist on the volar aspect.
• Brachial: medial to the biceps tendon in the antecubital fossa. Ask the patient to flex their elbow while feeling in the antecubital fossa for the biceps tendon which becomes taut.
• Carotid pulse: is palpated between the trachea and sternocleidomastoid. It is a vital landmark in cardiac arrests and you will need to be fairly confident about its presence (to certify death).
• Abdominal aorta: ends at L4 which is identified by palpating the iliac crests and is approximately at the umbilicus in slim people. An aneurysm should feel like an expansile mass on the abdomen.
• Femoral: mid-inguinal point—halfway between ASIS and pubic symphysis (not to be confused with midpoint of the inguinal ligament).
• Popliteal: flex knee to 90° and feel behind deeply with your finger pulps. It is often impalpable so do not be surprised if it is absent.
• Posterior tibial: Pimenta’s point—halfway between medial malleolus and insertion of Achilles tendon. Alternatively 2 cm ‘below and behind’ the medial malleolus.
• Dorsalis pedis: lateral to extensor hallucis longus (EHL). Ask the patient to point their toe towards their head in dorsiflexion to bowstring the tendon. Follow on the lateral side of EHL until you find bone where the pulse should be present. Absent in 2–3%!
Common pitfalls include insufficient gel but there is a definite technique to angling the probe appropriately to detect flow. Three waveforms (triphasic) relate to arterial wall expansion/contraction: three ‘whooshes’ = normal, two = stenosed, and monophasic = severe stenosis. You are more likely to have to use this as part of measuring ABPI.
ABPI is a ratio calculated by systolic BP leg/systolic BP in arm. A BP cuff is applied to the arm, Doppler probe applied to the brachial artery, and the cuff inflated until the signal disappears, which signifies the systolic BP. The same process is repeated at the ankle with the cuff around the calf, measuring both the anterior tibial and posterior tibial. The best score at the leg is used. Beware diabetics with calcified arteries who may have abnormally high ABPIs.
This is a test/sign seen in patients with severe lower limb arterial disease. The patient lies supine and one leg is raised. In the presence of arterial insufficiency, the leg may become white at an angle known as ‘Berger’s angle’. The white leg is then swung over the side of the bed in which case it may become dark red/purple (anaerobic metabolites vasodilatation hyperperfusion)—a positive ‘Berger’s sign’.
These are two very similar tests, both of which are used to determine the level of venous incompetence. With the patient supine, lift the leg and milk the varicose vein proximally—back hand along the path of the vein. Once the leg is raised and the vein ‘milked’, place two fingers over the saphenofemoral junction (SFJ) in the Trendelenburg test or apply a tourniquet at this level in the tourniquet test. The SFJ lies 4 cm lateral and inferior to the pubic tubercle. Once the SFJ is occluded, ask the patient to stand and observe for refilling of the varicose vein. If the incompetence is limited to the SFJ, varicosities will not reappear. If they return, then repositioning the tourniquet sequentially along the lower limb (mid thigh, above knee, and below knee) will help identify the level of the incompetence.