As lower limb arterial disease most frequently affects the SFA (Fig. 21.5), IC is usually characterized by pain on walking in the muscles of one or both calves. If the iliac arteries are affected then that pain may also be felt in the thigh and even the buttock (internal iliac disease). The pain comes on after a reasonably constant ‘claudication distance’, and usually subsides rapidly and completely on cessation of walking. Resumption of walking causes the pain to return. These and other features distinguish it from neurogenic and venous claudication (Table 21.1).

Fig. 21.5 Angiogram showing diffuse disease in both right and left superficial femoral arteries (arrows).

Table 21.1 Differential diagnosis of claudication

Typically, the superficial femoral artery (SFA) first becomes narrowed at the adductor canal (Fig. 21.6A). Ankle pulses may be palpable but are diminished, and a bruit may be heard at or below the stenosis. The ABPI is often (near) normal at rest but reduced following exercise.

Fig. 21.6 Symptoms and pathology in intermittent claudication.

A Superficial femoral artery (SFA) stenosis at adductor canal B Occlusion of the SFA and development of a collateral circulation between the deep femoral (profunda femoris) artery (PFA) and the popliteal artery C Iliac artery and PFA stenosis leading to worsening symptoms of IC and further collateralisation D Eventually CLI characterised by ischaemic rest pain and tissue loss develops due to multilevel disease affecting tibial arteries and collateral supply

Over the next few months or years, collateral vessels arising from the PFA enlarge so that they carry a higher proportion of the blood flow to the lower leg. As a result, in the majority of patients, symptoms gradually improve or even disappear. But thrombotic occlusion of the SFA (Fig. 21.6B) may lead to a sudden deterioration in walking distance. Ankle and popliteal pulses will be absent at this stage.

Continued development of the collateral circulation may lead to an improvement in symptoms and walking distance. This phase of moderate claudication may remain apparently stable for several years. However, without ‘best medical therapy’ (BMT) (see below) and a change in the patient’s lifestyle, the atherosclerosis will progress to involve other segments, such as the PFA, iliac and tibial vessels (Fig. 21.6C). The IC will progress to become severe, often forcing the patient to stop every 50–100 metres or so, and the scope for spontaneous improvement steadily diminishes. As the disease progresses further in severity and extent, symptoms are likely to worsen to a point where CLI develops due to multilevel disease (Fig. 21.6D). Such patients will often go on to develop night/rest pain and are at risk of tissue loss (see below).

An understanding of this cyclical pattern of exacerbation and resolution in IC is important as spontaneous improvement may mislead the patient into thinking all is well and that there is no longer a need to comply with medical advice (see below); and, in particular, that they can continue to smoke with impunity.

Epidemiology

IC affects up to 5% of people aged over 60 years. Provided patients comply with BMT only a small proportion (1–2%) of those affected by IC will deteriorate to a point where amputation and/or revascularization to prevent amputation is required. However, the annual mortality rate is 5–10% per year, which is 2–3 times higher than an age- and sex-matched non-claudicant population. This is because IC is a powerful marker of widespread atherosclerosis, and most of these patients succumb to MI, stroke and limb loss. The emphasis is, therefore, on the preservation of life; in most patients, measures to reduce cardiovascular mortality and morbidity (MI, stroke) will also improve the functional status of the limb.

Critical limb ischaemia

Whereas IC is usually due to single-level disease, CLI (sometimes also termed severe limb ischaemia, SLI) is caused by multiple lesions affecting different arterial segments down the leg (Fig. 21.6D). These patients usually have tissue loss (ulceration or gangrene) and/or rest (night) pain; their ankle blood pressure is often 50–70 mmHg or less. Without revascularization, such patients will often lose their limb, and sometimes their life, in a matter of months.

Night and rest pain

Ischaemic ‘night pain’ typically develops in the forefoot a few hours after going to bed. The pain is due to the accumulation of metabolites (acidosis) as a result of reduced perfusion consequent upon the loss of the beneficial effects of gravity and the reduction in blood pressure and cardiac output that usually occurs during sleep. The pain is severe and wakes the patient from sleep. At first the pain may be relieved by hanging the limb out of bed but, as the disease progresses, the patient has to get up and walk about to obtain relief. The patient then often takes to sleeping in a chair, which leads to dependent oedema. This increases interstitial tissue pressure and so further reduces arterial perfusion. The patient is then in a vicious cycle of increasing pain and sleep loss. At this point, even a trivial injury to the foot will fail to heal, and the entry of bacteria leads to infection and an increase in the metabolic demands of the foot. The result is the rapid formation of ulcers, gangrene and, without treatment, limb loss and death.

Diabetic vascular disease

Approximately 40% of patients with CLI have diabetes and such patients pose a number of unique problems for vascular specialists:

• Arteries are often calcified, which makes surgery and angioplasty technically difficult

• Calcification also leads to vessel incompressibility which results in spuriously high ankle pressures and ABPI measurements

• Reduced ability to fight infection

• Severe multisystem arterial disease (coronary, cerebral and peripheral), which increases the risks of intervention

• In the lower limbs, diabetic vascular disease has a predilection for the infrapopliteal vessels. Although vessels in the foot are often spared, the technical challenge of performing a satisfactory bypass or angioplasty to these small vessels is considerable

• Frequent coexisting neuropathy may lead to foot ulceration in its own right but may also complicate peripheral ischaemia (see below).

The diabetic foot

This refers to the combination of ischaemia, neuropathy and immunocompromise that renders the feet of diabetic patients particularly susceptible to sepsis, ulceration and gangrene. Diabetic neuropathy affects the motor, sensory and autonomic nerves.

Sensory neuropathy

This renders the patient incapable of feeling pain. Minor trauma – for example, from a stone in the shoe – remains unnoticed. Even severe ischaemia and/or tissue loss that would lead a sensate patient to seek urgent medical advice may be completely painless. For this reason, diabetic patients often present late, with extensive destruction of the foot. Sensory neuropathy also affects proprioception such that, when walking, pressure is applied at unusual sites. This leads to ulcer formation and even joint destruction (Charcot’s joint).

Motor neuropathy

The normal structure and function of the foot depends not only upon ligaments, but also upon the long and short flexors and extensors of the calf and foot. The former are affected more than the latter by motor neuropathy, leading to weakness and atrophy. The result is that the long extensors of the toes are unopposed and the toes become increasingly dorsiflexed. This exposes the metatarsal heads to abnormal pressure, and they are a frequent site of callus formation and ulceration (Fig. 21.7).

Fig. 21.7 Neuropathic ulceration of the first metatarsal head with sinus entering joint space.

Autonomic neuropathy

This leads to a dry foot deficient in the sweat that normally lubricates the skin and contains antibacterial substances. The result is scaling and fissuring of the skin, and the creation of a portal of entry for bacteria. Abnormal blood flow in the bones of the ankle and foot due to loss of autonomic control may also contribute to osteopenia and bony collapse (Charcot’s foot).

Management

If the blood supply to the foot is adequate, dead tissue can be excised in the expectation that healing will occur, provided infection is controlled and the foot is protected from pressure (so-called off-loading). If there is ischaemia as well, the priority is to revascularize the foot, if possible. Sadly, many diabetic patients present late, with extensive tissue loss and ‘unreconstructable’ disease, which accounts for the very high amputation rate.

Management of lower limb ischaemia

Medical management

All patients with atherosclerotic vascular disease should be strongly urged to comply with BMT, which comprises:

• Immediate, absolute and permanent cessation from smoking. This is by far the most important intervention and prognostic factor. In the face of continued smoking, other treatments are rendered largely ineffective and disease progression, limb loss and death (usually from cardiovascular causes) within a few years are the likely outcome.

• Control of hypertension according to current guidelines (for example, see the British Hypertension Society, www.bhsoc.org).

• Control of hypercholesterolaemia according to current guidelines (for example, see the British Heart Foundation, http://www.bhf.org.uk). All vascular patients should be prescribed lipid lowering drugs, usually a statin, so that their baseline total cholesterol is reduced by a third (ideally to below 4 mmol/l). Statins also stabilize atheromatous plaques and prevent the development and progression of aneurysmal disease through as yet incompletely understood anti-inflammatory mechanisms.

• Prescription of an antiplatelet agent (for guidance see National Institute of Clinical and Health Excellence, http://www.nice.org.uk/guidance/index.jsp?action=folder&o=51201). This is normally aspirin (75 mg daily) but clopidogrel (75 mg daily) is a more effective and safer alternative (but is also more expensive). Anticoagulation with warfarin should normally be reserved for patients with AF.

• Regular exercise as possible; it is widely accepted that supervised exercise in a health care environment is more effective than (unsupervised) simple advice to exercise.

• Control of obesity. This will help to bring down blood pressure, cholesterol and the ‘strain’ of walking; diabetes will also be easier to control. Surgical and endovascular intervention is much more difficult and morbid in obese patients.

• The identification and active treatment of patients with diabetes. This includes foot care (for further information see, for example, Diabetes UK, http://www.diabetes.co.uk).

Compliance with BMT increases not only walking distance but also affords very significant protection against cardiovascular events, improves the patient’s quality of life and life expectancy. Unfortunately, many patients fail to comply and, in particular, continue to smoke. Endovascular or open surgery for IC should not normally be considered until the patient is fully compliant with BMT and that therapy has been given adequate chance to effect symptomatic improvement. Intervention in the face of continued smoking is usually clinically and cost-ineffective and represents poor use of limited health care resources. Revascularization is in addition to, not instead of, BMT, a point that often has to be emphasized to patients anxious to return to their previous lifestyle.

By the time a patient develops CLI it is often (but not always) the case that, without surgical or endovascular revascularization, the limb will be lost. However, this does not in any way undermine the value of instituting BMT in such patients. On occasion, BMT may improve the condition of the leg such that intervention is not required or a lesser procedure becomes an option. In those undergoing intervention, BMT undoubtedly reduces the overall risks and increases the success of the procedure.

Endovascular management

Balloon angioplasty (BAP), with or without stenting, has been used successfully in the iliac, femoral, popliteal and crural arteries and is usually performed under local anaesthesia (Fig. 21.8). The arterial lesion to be treated (stenosis or occlusion) is identified and crossed with a wire. A balloon catheter is introduced over the wire and the balloon inflated. This enlarges the lumen by disrupting the atheromatous plaque. In occlusions and complex disease, metal stents may be deployed across the lesion to improve patency and reduce distal embolic complications. Sometimes these balloons and stents are coated with drugs that reduce the arterial scarring (neo-intimal hyperplasia) that follows such intervention and can lead to restenosis and reocclusion (so-called drug eluting balloons and stents). Endoluminal repair of the aortoiliac segment is the treatment of choice in most vascular units because of its high patency rates, and low morbidity compared to open surgery. Infrainguinal BAP and, less commonly, stenting is also widely used in the management of IC and CLI.

Fig. 21.8 Balloon angioplasty and stenting.

A Critical arterial stenosis. B A guidewire is used to cross the lesion. C The guidewire is used to direct a balloon angioplasty catheter across the lesion. D The balloon is inflated. E A metal stent may be mounted on a catheter. The stent may be self-expanding or require expansion with a balloon. In many cases, the first manoeuvre is to cross the lesion with a stent and in this circumstance steps C and D may be omitted. F Metal stent holding open the stenosis.

Intermittent claudication

Endoluminal treatment (BAP, stent) should be used selectively in patients with IC because it may be associated with a 1–2% morbidity rate, rarely mortality, and many patients have a pattern of disease that is unsuitable for current endovascular technologies. There is controversy with regard to its role in the femoropopliteal and infrapopliteal segments because of a perceived lack of durability of benefit. In the future, this may be improved by the use of stents. By contrast, most vascular specialists believe that endoluminal therapy should be considered in patients with IC due to aortoiliac disease (absent or reduced femoral pulses) because they:

• tend to be younger, so that their symptoms have a greater impact on their quality of life and livelihood

• often have short-segment disease that is amenable to BAP, with or without a stent

• often have (relatively) normal infrainguinal arteries, so that restoring flow in the aortoiliac segment effects a dramatic improvement in the perfusion to their leg(s)

• tend to be more symptomatic, with shorter walking distances and bilateral symptoms

• may not achieve a satisfactory increase in walking distance with BMT alone, because the ability of the body to collateralize around aortoiliac disease is not as good as it is around femoropopliteal disease.

Furthermore, the long-term patency of BAP and stenting is optimal in high-flow, large-calibre vessels, leading to a durable clinical benefit in many patients.

Critical limb ischaemia

The role of BAP and stenting in CLI remains controversial and, with present technology, many such patients remain unsuitable for endovascular therapy. The only published randomized controlled trial to compare BAP and bypass surgery (BSX) (http://basiltrial.com) indicates that although BAP is safer and less expensive than BSX in the short term (12–18 months), BSX (with vein) offers a more durable and complete revascularization in the longer term (3–5 years) (EBM 21.1). At the present time, CLI patients expected to only live 1–2 years and who do not have a suitable vein for the construction of a bypass are probably best treated by BAP where technically possible; all other CLI patients are probably best served by BSX. The role for endovascular therapy may increase in the future as technology improves.

21.1 Bypass surgery (BSX) or balloon angioplasty (BAP) for severe limb ischaemia)

‘For patients who survived for at least 2 years after randomization, a BSX-first revascularization strategy was associated with a significant increase in subsequent overall survival and a trend towards reduced amputation free survival. BAP was associated with a significantly higher early failure rate than BSX. Many BAP patients ultimately required surgery. BSX outcomes after failed BAP are significantly worse than for BSX performed as a first revascularization attempt. BSX with vein offers the best long term outcome but BAP appears superior to prosthetic BSX.’

Basil Trial Investigators and Participants. Final results of the BASIL trial (Bypass Versus Angioplasty in Severe Ischaemia of the Leg) Journal of Vascular Surgery 2010; 51(5): 5S–17S.

Indications for arterial reconstruction

Intermittent claudication

Many surgeons are reluctant to perform infrainguinal bypass surgery for IC because:

• The risk of limb loss is very low with BMT

• Those patients who fail to comply with BMT (fail to stop smoking) are those most likely to press for surgery because of on-going symptoms. However, they are also those at greatest operative risk and those least likely to gain durable benefit from their bypass

• Surgery is associated with a significant risk of mortality and major morbidity, the size of that risk depending on the procedure and the patient but probably approaching 3–5% for infrainguinal bypass and 5–10% for aorto-bifemoral bypass

• As most patients have bilateral disease, even if they have unilateral symptoms, successful infrainguinal surgery on one side often reveals limiting IC symptoms on the other, requiring a second operation (the same for endoluminal treatment)

• Grafts have a finite patency, especially in those who fail to comply with BMT and, in particular, continue to smoke (the same for endoluminal treatment)

• As soon as a bypass graft is inserted, collaterals circumventing the original lesion shrink down. For this reason, when the graft occludes, usually suddenly, the patient is normally returned to a worse level of IC than before the operation. A patient who was previously a claudicant may now have acute limb-threatening ischaemia, which then forces the surgeon or radiologist to re-intervene. Secondary interventions are technically more difficult, are associated with higher risk and enjoy a lower patency rate.

As with BAP and stenting, the balance of risks and benefits for open surgery is different in patients with aorto-iliac disease. Although the risk of surgery is higher, the long-term patency rates of such grafts are excellent, and one operation deals with both legs. Whatever the treatment being considered, patients and their families must be made fully aware of the risks and benefits so that they can give fully informed consent. These discussions must always be faithfully recorded in the notes; it is good practice to send copies of this to the patient as well as the GP. Sadly, medicolegal activity continues to grow in the UK and clear and accurate verbal and written communication between the clinician, the patient and their family affords significant protection for all parties concerned.

Principles of arterial reconstruction

Endarterectomy

This involves the direct removal of atherosclerotic plaque and thrombus and is a relatively uncommon operation in modern vascular surgical practice except at the carotid and femoral bifurcations (Fig. 21.9).

Fig. 21.9 Profundaplasty.

A Focal atherosclerotic disease of the left common femoral artery is causing severe ischaemia because it is obstructing flow down the superficial and deep femoral (profunda femoris) arteries. B Local endarterectomy and closure of the profunda femoris using a vein or prosthetic patch (profundaplasty) restores normal flow to both vessels.

Bypass grafting

For a surgical bypass operation (Fig. 21.10) to be successful in the long term, three conditions must be fulfilled:

• There must be high-flow, high-pressure blood entering the graft (inflow)

• The conduit must be suitable

• The blood must have somewhere to go when it leaves the graft (outflow or run-off).

Fig. 21.10 Femorodistal bypass graft.

A Diagram showing femoral to posterior tibial bypass graft. B On-table angiogram showing distal end of vein graft (arrow) anastomosed to the dorsalis pedis artery in the foot.

Two main types of conduit are available:

• autogenous material, most commonly the ipsilateral great saphenous vein (GSV)

• prosthetic material, most commonly expanded polytetrafluoroethylene (ePTFE) or Dacron.

The main advantage of vein is that it is lined by endothelium that is actively antithrombotic and profibrinolytic, and therefore much less liable to induce coagulation than even the most inert of man-made materials. This translates into much better long-term graft patency. Vein is also much more resistant to infection (see below) and less expensive. It is generally agreed that, wherever possible, vein from the leg or arm should be used for infrainguinal reconstruction.

Extra-anatomic bypass

In most bypass operations, the new conduit more or less follows the course of the original artery – so-called anatomic bypass (Fig. 21.11). Where this is not possible and/or desirable, a so-called extra-anatomic bypass can be inserted (Fig. 21.12).

Fig. 21.11 Anatomic aortic bypass.

Reconstruction of an occluded aortoilliac segment by means of aorto-bi-femoral bypass grafting.

Fig. 21.12 Extra-anatomic bypass.

A Unilateral iliac disease may be treated by femoro-femoral crossover graft. B Bilateral aorto-iliac disease may be treated with axillo-bifemoral bypass graft.

For example, if only one iliac artery is blocked, and the patient is unfit for abdominal surgery and unsuitable for endoluminal treatment, a femorofemoral crossover graft can be performed. If both iliac arteries are occluded, then an axillobifemoral graft can be inserted. In general, these extra-anatomic grafts do not have as good long-term patency as anatomic aortoiliac reconstructions. However, they are lesser procedures and so the preferred option in high-risk patients or those that have a limited life expectancy.

Complications of arterial reconstruction

The morbidity and mortality associated with vascular surgery is often high because vascular patients are usually elderly and unfit with widespread vascular disease, and the operations are often lengthy with significant blood loss. Meticulous perioperative care is essential for optimal results, and close liaison between the surgeon, the anaesthetist and the intensivist is essential. Longer term major complications include infection and graft occlusion for which outcome is better when identified early.

Although there is no strong evidence of benefit, many surgeons perform ultrasound scans of their grafts at regular intervals in the postoperative period, typically at 1, 3, 6, 12, 18 and 24 months. This so-called ‘graft surveillance’ is designed to pick up technical problems with the graft that are likely to increase the risk of failure. It is generally believed that it is better to correct a ‘failing’ graft before it has blocked than to try to resurrect one that has already failed.

Infection of prosthetic grafts is a serious and growing problem, largely due to the increasing prevalence of antibiotic-resistant organisms, including methicillin-resistant Staphylococcus aureus (MRSA). Once a prosthetic graft is infected, it must usually be removed to rid the patient of sepsis and/or to prevent life-threatening (anastomotic) haemorrhage. Graft removal of course renders the distal part ischaemic and, where possible, a new graft is inserted through fresh uninfected tissue. This can be extremely challenging, and on occasion is impossible. Measures to avoid graft infection include:

• Using vein wherever possible

• Peri-operative antibiotic prophylaxis

• Strict aseptic technique in the operating theatre and ward

• Always using gloves and washing hands between examining patients.

Amputation

Indications

Amputation should only be considered where arterial reconstruction is considered by a vascular surgeon to be inappropriate or impossible. In some cases, patients are admitted profoundly unwell and septic from spreading gangrene and immediate amputation may be the only means of saving the patient’s life.

Level of amputation

This is determined by local blood supply, the status of the joints, the patient’s general health and his or her age. The broad principle is to amputate at the lowest level consistent with healing (Fig. 21.13). It is important to conserve the knee joint if at all possible, as the energy required to walk on a below-knee prosthesis is much less that required to walk on an above knee prosthesis. However, if the patient has other co-morbidity or disability that would make walking with a prosthesis impossible, there is no point in attempting to conserve the knee joint at the expense of healing. A common situation is where a patient presents with a fixed flexion contracture of the knee. A below-knee amputation in such a patient is usually ill-advised because the contracture will prevent the patient from ever walking and will also result in the stump wound resting on the bed or chair, leading to poor healing and wound breakdown.

Fig. 21.13 Amputation.

A Levels of amputation and types of flap used to close the residual defect. B Below-knee amputation.

Surgical principles

A number of important principles must be observed if primary healing and satisfactory rehabilitation are to be achieved. The in-hospital mortality for major limb amputation approaches 20% and can exceed 30% in the elderly undergoing above-knee amputation. The decision to amputate, the level of amputation and the procedure itself require direct input from an experienced vascular surgeon. In some elderly patients, end of life care is more appropriate than amputation.

Rehabilitation and limb fitting

The speed of rehabilitation is variable but, typically, at about 1 week the patient should begin to bear weight on the other limb between parallel bars, and at 10 days begin to walk with a pneumatic walking aid. If healing is progressing well, a temporary prosthesis can be fitted at about 3 weeks. Final fitting of the artificial limb must await shaping and firming of the stump. Approximately 70% of below-knee amputees and 30% of above-knee amputees eventually walk although many of these do not persist with their prosthesis. It is important to appreciate that, because of the prolonged hospital admission, rehabilitation, home modifications and, in some cases, long-term care, amputation can be a much more expensive option than revascularization leading to limb salvage.

Phantom pain

Phantom limb pain can be a serious problem, especially if pain has not been well controlled before and after the amputation. With appropriate drug therapy, reassurance and time, it usually settles but can take a long time to do so. There is some evidence that if the patient goes to theatre pain-free, the risk of phantom pain can be reduced. For this reason, some surgeons request epidural anaesthesia prior to surgery. Input from a pain specialist can be invaluable.

Arterial disease of the upper limb

Overview

Occlusive arterial disease is about 10 times commoner in the leg than in the arm. Nevertheless, when the arm is affected, treatment can be difficult, and the loss of an arm (especially the dominant one) is even more devastating for the patient than loss of a leg.

The left subclavian artery just proximal to the origin of the vertebral artery is the most common site of disease. This may lead to:

• Arm claudication. This is relatively unusual, even when the subclavian artery is completely occluded, because of collateral supply, mainly from the vertebral artery

• Atheroembolism to the hand. Small emboli lodge in the vessels of the fingers and the hand and lead to symptoms that are often mistaken for Raynaud’s phenomenon, except that in this case the symptoms are unilateral (see below)

• Subclavian steal. In this circumstance, when the arm is used, blood is ‘stolen’ from the brain, with retrograde flow via the vertebral artery. This leads to vertebrobasilar ischaemia (VBI), characterized by dizziness, cortical blindness and/or collapse when the arm is used (Fig. 21.14).

Fig. 21.14 Occlusion of the left subclavian artery, causing ‘subclavian steal’.

Management

Most subclavian artery disease can be treated by means of BAP and stenting, as the results are good and surgical access to the area is difficult. If surgery is required, then the usual operation is carotid–subclavian bypass.

Cerebrovascular disease

Definitions

Stroke

Stroke may be defined as an episode of focal neurological dysfunction lasting more than 24 hours, of presumed vascular aetiology.

Transient ischaemic attack

When such symptoms last for less than 24 hours, the episode is described as a transient ischaemic attack (TIA).

Amaurosis fugax

This describes transient, usually incomplete, loss of vision in one eye owing to occlusion of a branch of the retinal artery by cholesterol emboli. The patient typically describes it as a veil or curtain coming across the eye, which remains for a few minutes and then disappears. Amaurosis fugax is never synchronously bilateral, as it is almost infinitely improbable that an embolus would enter both retinal arteries at exactly the same time. Bilateral visual loss is usually due to occipital ischaemia secondary to VBI (see below). Non-synchronous amaurosis fugax is, of course, possible in patients with bilateral carotid disease.

Carotid artery disease

Pathophysiology

Approximately 80% of strokes are ischaemic and about half of these are thought to be due to atheroembolism from the carotid bifurcation. The origin of the internal carotid artery is particularly prone to atheroma. The tighter the degree of stenosis, the more likely it is to cause symptoms. Athero-emboli entering the ophthalmic artery leads to amaurosis fugax or permanent monocular blindness on the same side (ipsilateral). If they enter the middle cerebral artery, they may cause hemiparesis and hemisensory loss on the opposite side (contralateral). If the dominant hemisphere is affected, there may also be dysphasia.

Summary Box 21.2 Carotid artery disease

• Up to 50% of all ischaemic strokes may be caused by atheroembolism from the carotid bifurcation

• Patients with carotid territory transient ischaemic attacks (TIA) and amaurosis fugax should be assessed by a vascular surgeon with a view to carotid endarterectomy (CEA)

• When compared to BMT alone, CEA in addition to BMT significantly reduces the risk of further ipsilateral ischaemic stroke in patients with high grade symptomatic internal carotid artery stenosis

• CEA for asymptomatic internal carotid artery stenosis is controversial; such patients should be discussed with a vascular surgeon

• Several large trials have shown that with current technology, carotid artery stenting (CAS) can be an effective treatment for carotid stenoses, and should be considered as an option, particularly in patients at high risk for surgery.

Assessment

The presence of a ‘carotid’ bruit bears no reliable relationship to the severity of underlying internal carotid artery disease and thus the risk of stroke. Such a bruit may arise from the external carotid artery or be transmitted from the heart. Furthermore, in the presence of a very tight internal carotid artery stenosis, flow may be so slow that no audible turbulence is present. It is important to exclude other causes of cerebral ischaemia and haemorrhage.

Colour flow Doppler (duplex) ultrasound (CDU) is the initial investigation of choice for imaging the carotid arteries (Fig. 21.15).

Fig. 21.15 Carotid ultrasound scan.

The upper image shows the narrowing (arrow). By using Doppler ultrasound to measure the peak systolic velocity (PSV) (about 300 cm/s in this case) and end-diastolic velocity (EDV) (about 120 cm/s in this case) of the blood travelling through the stenosis it is possible to quantify the degree of narrowing. In this case the stenosis is estimated at greater than 70% and so further investigation with a view to surgery is warranted.

Magnetic resonance (MRA) or computed tomographic (CTA) angiography provide excellent images and are increasingly used to plan treatment (Fig. 21.16).

Fig. 21.16 Carotid magnetic resonance angiogram (MRA).

The arterial blood to the brain from the origins of the great vessels from the aortic arch to the circle of Willis and cerebral arteries within the skull. The image confirms that there is a tight stenosis at the origin of the right internal carotid artery (arrow).

Intra-arterial digital subtraction angiography (IA-DSA) is associated with a small risk of TIA/stroke and nowadays is used rarely for diagnostic purposes.

Management

Medical therapy

All patients should receive BMT.

Carotid endarterectomy (CEA)

Patients with completed major stroke and little in the way of recovery are not candidates for carotid intervention; nor are those with an occluded internal carotid artery. However CEA combined with BMT is associated with a significant reduction in recurrent stroke, compared with BMT alone in patients with amaurosis, TIA and stroke with good recovery, provided that:

• There is a high degree of internal carotid artery stenosis (usually taken as a greater than 60–70% diameter reduction)

• The patient is expected to survive at least 2 years

• The intervention can be undertaken with a stroke and/or death rate of less than 3–5%

• The intervention can be performed soon after the index event. The exact timing remains controversial and is matter of judgment for each patient but, in general, the sooner the better.

Patients who do not fulfill these criteria should, in most cases, be treated medically. The operation can be equally well performed under general or local anaesthetic.

21.2 Carotid endarterectomy: general or local anaesthesia?

‘A definite difference in outcomes between general and local anaesthesia for carotid surgery has not been shown. The anaesthetist and surgeon, in consultation with the patient, should decide which anaesthetic technique to use on an individual basis.’

GALA Trial Collaborative Group. General anaesthesia versus local anaesthesia for carotid surgery (GALA): a multicentre, randomised controlled trial. The Lancet 2008; 372: 2132–42.

The carotid bifurcation is dissected, heparin is given and the arteries are clamped. If this may lead to cerebral ischaemia, a shunt is inserted. The plaque is shelled out (the endarterectomy) and the artery repaired with direct suture or a patch graft (patch angioplasty) (Fig. 21.17).

Fig. 21.17 Carotid endarterectomy.

A Diagram showing carotid endarterectomy using a shunt in the internal carotid artery to maintain cerebral blood flow while the occluding plaque is removed and the artery repaired either by direct primary closure as shown here or, more usually, with a patch of vein or prosthetic material. B Operative photograph of plaque (arrow) being removed at carotid endarterectomy (no shunt being used in this case).

Carotid stenting

The role of carotid artery stenting (CAS) remains uncertain and controversial. While CAS avoids a neck wound and the risks of cranial nerve injury, and possibly reduces the risk of perioperative myocardial infarction, there is a growing body of evidence to show that the short-term risks of clinical and subclinical brain injury are greater than with CEA. For these reasons, most UK vascular specialists believe that CAS should be reserved for patients where CEA is either not possible or desirable because of anatomic and clinical factors (for example, recurrent stenosis after previous

21.3 Carotid stenting

‘Completion of long-term follow-up is needed to establish the efficacy of carotid artery stenting compared with endarterectomy. In the meantime, carotid endarterectomy should remain the treatment of choice for patients suitable for surgery.’

International Carotid Stenting Study Investigators. Carotid artery stenting compared with endarterectomy in patients with symptomatic carotid stenosis: an interim analysis of a randomised controlled trial. The Lancet 2010; 375: 985–997.

surgery or radiation arteritis) optimal in the common carotid and inominate arteries.

Asymptomatic carotid disease

The evidence that undertaking CEA (or CAS) in addition to BMT confers clinical benefit in patients with asymptomatic ICA disease is weak. The risks of such people developing TIA/stroke are low (probably less than 10% at 5 years). So, even if one could halve that risk with intervention (relative risk reduction of 50%) the absolute risk reduction would be only 1% per year. This means the number of interventions needed to prevent one TIA or stroke is potentially quite large (perhaps 20–30 or more). By contrast, the number needed to treat for symptomatic disease is less than 10. CEA for asymptomatic carotid artery disease is, therefore, a highly cost-ineffective means of stroke reduction and a poor use of finite health care resources. Nevertheless, in many fee-for-service health care environments such as in the US, large number of CEA and CAS are still performed for asymptomatic carotid disease.

Vertebrobasilar disease

The vertebrobasilar system feeds the occipital cortex, cerebellum and brain stem. Patients with vertebrobasilar insufficiency (VBI) may complain of (bilateral) cortical blindness, vertigo and loss of balance. Few patients have focal, discrete disease amenable to vascular or endovascular intervention, and the great majority receive BMT only.

Renal artery disease

Pathophysiology

Atherosclerosis is by far the commonest cause of renal artery stenosis and usually affects the origin of the artery as part of aortic wall disease. Underperfusion of the juxtaglomerular apparatus leads to an increase in renin and angiotensin and the development of hypertension. The disease may also lead to ischaemic necrosis of the renal parenchyma and progressive renal failure. Fibromuscular hyperplasia is an uncommon condition that mostly affects young and middle-aged women. It may cause hypertension, but rarely renal failure.

Management

The indications for intervention remain controversial and, especially since the ASTRAL trial results were published (EBM 21.4), most patients with renovascular disease are treated medically in the UK. Although the evidence for benefit is weak, primary stenting for atherosclerotic renal artery disease may be considered in selected patients to:

• control hypertension that is refractory to medical therapy

• preserve renal function.

21.4 Intervention for renal artery disease

‘Substantial risks but no evidence of a worthwhile clinical benefit from revascularization in patients with atherosclerotic renovascular disease was found.’

The ASTRAL Investigators. Revascularization versus Medical Therapy for renal-artery stenosis. New England Journal of Medicine 2009; 361: 1953–62.

Major complications (1–2%) include acute arterial occlusion, embolization and rupture. Surgical reconstruction is a major undertaking with significant associated morbidity and mortality that nowadays is rarely, if ever, performed. BAP alone is effective for fibromuscular hyperplasia.

Mesenteric artery disease

Owing to rich collaterals between them, it is usually necessary for two of the three visceral vessels (coeliac axis, superior and inferior mesenteric arteries) to be occluded or critically stenosed before patients develop symptoms and signs. Typically, the patient develops severe central abdominal pain (mesenteric angina), sometimes with diarrhoea, 15–30 minutes after eating. Food avoidance and intolerance always leads to significant weight loss. The condition can mimic many much more common intra-abdominal pathologies. Surgery is associated with significant morbidity and mortality (5–10%). but the long-term symptom relief is usually excellent. BAP and stenting are increasingly used, particularly in patients with high operative risk and in those who have limited life expectancy.

Acute mesenteric ischaemia is usually caused by occlusion of the superior mesenteric artery (SMA) by embolus (usually from the heart in patients with AF) or acute thrombosis on top of pre-existing atherosclerosis. There is usually sudden onset of excruciating abdominal pain, collapse, bloody diarrhoea and peritonitis. Treatment comprises emergency SMA embolectomy (embolus) or SMA bypass (thrombosis) and resection of non-viable bowel. Unfortunately, extensive bowel necrosis is often already present at the time of surgery and mortality exceeds 50%. Endovascular techniques have little to offer, as the exclusion of bowel infarction requires a laparotomy.

Summary Box 21.3 Acute limb ischaemia

• Acute limb ischaemia is the most common vascular emergency

• The most common causes are embolus from the left atrium in association with atrial fibrillation and acute thrombosis at a site of long-standing atherosclerotic narrowing

• It is often but not always possible to distinguish these two conditions on clinical grounds alone

• The treatment of embolism is urgent embolectomy, usually without prior angiography

• Patients with thrombosis in situ should undergo angiography if possible; treatment comprises a combination of medical therapy, thrombolysis, angioplasty and bypass

• Paralysis, paraesthesia and muscle tenderness are the cardinal signs of complete acute ischaemia; when they are present, the limb must be revascularized within 4-6 hours if it is to be saved and full function restored. Fasciotomy should always be considered upon successful reperfusion to avoid compartment syndrome.

Acute limb ischaemia

Aetiology

Acute limb ischaemia is caused most frequently by acute thrombotic occlusion of a pre-existing stenotic arterial segment (60%), thromboembolism (30%) and trauma, which may be iatrogenic. Distinguishing between thrombosis and embolism is important because investigation, treatment and prognosis are different (Table 21.2).

Table 21.2 Embolus vs. thrombosis in situ

Clinical features	Embolus	Thrombosis
Severity	Complete ischaemia (no collaterals)	Incomplete ischaemia (collaterals)
Onset	Seconds or minutes	Hours or days
Limb	Leg 3:1 arm	Leg 10:1 arm
Multiple sites	Up to 15%	Rare
Embolic source	Present (usually AF)	Absent
Previous claudication	Absent	Present
Palpation of artery	Soft; tender	Hard/calcified
Bruits	Absent	Present
Contralateral leg pulses	Present	Absent
Diagnosis	Clinical	Angiography
Management	Embolectomy, warfarin	Medical, bypass, thrombolysis
Prognosis	Loss of life > loss of limb	Loss of limb > loss of life

More than 70% of peripheral emboli are due to AF. Thrombosis in situ may arise from acute plaque rupture, hypovolaemia, increased blood coagulability (for example in association with sepsis) or ‘pump failure’ (for example heart attack) (see below).

Classification

Limb ischaemia is classified on the basis of onset and severity (Table 21.3). Incomplete acute ischaemia (usually due to thrombosis in situ) can often be treated medically, at least in the first instance. Complete ischaemia (usually due to embolus) will normally result in extensive irreversible tissue injury within 6 hours unless the limb is revascularized. Irreversible ischaemia mandates early amputation or, if the patient is elderly and unfit, end-of-life care.

Table 21.3 Classification of limb ischaemia

Terminology	Definition/comment
Onset
Acute	Ischaemia < 14 days
Acute-on-chronic	Worsening symptoms and signs (< 14 days)
Chronic	Ischaemia stable for > 14 days
Severity (acute, acute- on-chronic)
Incomplete	Limb not threatened
Complete	Limb threatened
Irreversible	Limb non-viable
Severity (chronic)
Non-critical	Intermittent claudication
Subcritical	Night/rest pain
Critical	Tissue loss (ulceration ± gangrene)

Clinical features

Apart from those that indicate ‘loss of function’, namely paralysis (inability to wiggle toes/fingers) and paraesthesia (loss of light touch over the dorsum of the foot/hand), the so-called Ps of acute ischaemia are non-specific and/or inconsistently related to its severity and should not be relied upon (Table 21.4).

Table 21.4 Symptoms and signs of acute limb ischaemia

Symptoms/signs	Comment
Pain	May be absent in complete acute ischaemia; severe pain is also a feature of chronic ischaemia
Pallor	Also a feature of chronic ischaemia
Pulseless	Also a feature of chronic ischaemia
Perishing cold	Unreliable, as the ischaemic limb takes on the ambient temperature
Paraesthesia and paralysis	Loss of function is the most important feature of acute limb ischaemia and denotes a threatened limb that is likely to be lost unless it is revascularized within a few hours

Acute loss of limb function, of which vascular insufficiency is only one cause, must always be taken very seriously indeed; the patient should never be discharged until a diagnosis has been made. In the presence of ischaemia, pain on squeezing the calf indicates muscle infarction and impending irreversible ischaemia.

At first, acute complete ischaemia is associated with intense distal arterial spasm and the limb is ‘marble’ white. As the spasm relaxes over the next few hours and the skin fills with deoxygenated blood, mottling appears. This is light blue or purple, has a fine reticular pattern and blanches on pressure: so-called ‘non-fixed mottling’. At this stage, the limb is still salvageable. As ischaemia progresses, blood coagulates in the skin, leading to mottling that is darker in colour, coarser in pattern and does not blanch. Finally, large patches of fixed staining progress to blistering and liquefaction (Fig. 21.18). Attempts at revascularization at this late stage are futile and will lead to life-threatening reperfusion injury (see below).

Fig. 21.18 Mottled right foot due to advanced acute limb ischaemia.

Management

All suspected acutely ischaemic limbs must be discussed immediately with a vascular surgeon; a few hours can make the difference between amputation or death, and complete recovery of limb function. If there are no contraindications, such as trauma (especially head injury) or suspected aortic dissection, an intravenous bolus of heparin (typically 3000–5000U) is administered to limit propagation of thrombus and protect the collateral circulation. If ischaemia is complete, the patient proceeds directly to the operating theatre for attempted embolectomy (preferably under local anaesthesia). If ischaemia is incomplete, preoperative imaging is obtained wherever possible, as simple embolectomy or thrombectomy is unlikely to be successful; a ‘road-map’ for distal bypass is helpful; and it is often possible, at least initially, to manage the patient medically depending on the results of imaging.

Acute embolus

Embolic occlusion of the brachial artery is not usually limb-threatening and, in an elderly patient, non-operative treatment is reasonable. Younger patients should undergo embolectomy to prevent subsequent claudication, especially where the dominant arm is affected.

A leg affected by embolus is nearly always threatened and requires immediate surgical revascularization. Femoral embolus is usually associated with profound ischaemia to the level of the upper thigh because the deep femoral artery is also affected. Acute embolic occlusion of the aortic bifurcation (saddle embolus) leads to absent femoral pulses and a patient who is ‘marble’ white or mottled to the waist. Such patients may also present with paraplegia due to ischaemia of the cauda equina, which may be irreversible. Embolectomy can be performed under local/regional or general anaesthetic (Fig. 21.19).

Fig. 21.19 Embolectomy.

A Diagram showing removal of an embolus with a balloon catheter. The balloon is inflated once it is beyond the thrombus and then withdrawn. B Embolectomy catheter. C Tip of embolectomy catheter with balloon inflated.

Postoperatively, the patient should continue on heparin. Warfarin reduces the risk of recurrent embolism but is associated with an annual risk of significant bleeding of 1–2% in the long term. The in-hospital mortality from cardiac death and/or recurrent embolism, particularly stroke, is 10–20%.

Thrombosis in situ

There is usually a reason why the limb affected by stable chronic ischaemia suddenly deteriorates due to thrombosis in situ on top of atherosclerosis. These include ‘silent’ or overt MI (drop in blood pressure); underlying, perhaps hitherto asymptomatic, malignancy (increase in thrombogenicity of the blood); septicaemia, particularly pneumococcal and meningococcal; and dehydration from any cause, which may be associated with widespread thrombosis. Many patients can be managed medically. If the limb remains threatened then it may be possible to clear the thrombus by open surgical or endoluminal means; to dissolve the clot by means of thrombolysis or bypass the affected segment. If urgent surgery is required the in-hospital limb loss rate may approach 30%; in hospital mortality is 10–20%

Popliteal aneurysm

Popliteal aneurysm can undergo thrombosis or act as a source of emboli. Bypass (or stent-grafting) should be performed to exclude the aneurysm (see below) and thrombolysis may be required to re-establish the distal run off. Acute thrombosis of popliteal aneurysm is associated with an in-hospital limb loss rate that can approach 50%.

Trauma

In the UK, acute traumatic limb ischaemia is frequently iatrogenic. The most common causes of non-iatrogenic injury are limb fractures and dislocations, blunt injuries occurring in the course of road traffic accidents, and stab wounds (gun shot wounds are mercifully rare in the UK but common in many other parts of the world). The presence of distal pulses emphatically does not exclude significant arterial injury, especially in otherwise young and fit trauma patients. Where there is any suspicion at all of major vascular injury, vascular imaging (e.g. MR or CT angiography) should be performed immediately; operating ‘blind’ is to be avoided if at all possible.

Intra-arterial drug administration

This leads to intense spasm and microvascular thrombosis. The leg is mottled and digital gangrene is common, but pedal pulses are often palpable. The mainstay of treatment is supportive care, hydration to minimize renal failure secondary to rhabdomyolysis, and full heparinization. Vascular reconstruction is almost never indicated, but fasciotomy may be required to prevent compartment syndrome (see below). Limb loss rates are high.

Thoracic outlet syndrome

Pressure on the subclavian artery from a cervical rib or abnormal soft tissue band may lead to a poststenotic dilatation lined with thrombosis, predisposing to occlusion or embolization. The distal circulation may be chronically obliterated and digital ischaemia advanced before the diagnosis is made. The diagnosis is confirmed on duplex scan and/or MRA. Treatment options include thrombolysis, thrombectomy/embolectomy, excision of the cervical rib and repair (replacement) of the aneurysmal segment.

Postischaemic syndromes

Reperfusion injury

Activated neutrophils, free radicals, enzymes, hydrogen ions, carbon dioxide, potassium and myoglobin released from reperfused tissue can lead to acute respiratory distress syndrome (ARDS), myocardial stunning, endotoxaemia and acute tubular necrosis, and in turn, to multiple organ failure and death.

Compartment syndrome

Endothelial cell injury during ischaemia leads to increased capillary permeability and oedema on reperfusion. In the calf, where muscles are confined within tight fascial boundaries, the increase in interstitial tissue pressure can lead to continuing muscle necrosis despite apparently adequate arterial inflow: the so-called compartment syndrome. There is swelling and pain on squeezing the calf muscle or moving the ankle or toes. It is very important to remember that palpable pedal pulses do not exclude compartment syndrome. The key to management is prevention through expeditious revascularization and a low threshold for fasciotomy to relieve the pressure (Fig. 21.20).

Fig. 21.20 Medial and lateral fasciotomy to decompress compartment syndrome in a patient who presented with bilateral acute limb ischaemia due to saddle embolus (the crosses marked on the skin indicate the position of palpable pulses) and underwent successful embolectomy.

Aneurysmal disease

Classification

An aneurysm may be defined as an abnormal focal dilatation of an endothelial-lined vascular structure (artery, vein, heart chamber). Arterial aneurysms are by far the most common. Aneurysms may be classified according to their site, underlying aetiology and morphology.

Site

Any artery can be affected. The most common site for aneurysmal disease requiring treatment is the infrarenal aorta; others include the popliteal, femoral and subclavian arteries.

Aetiology

Atherosclerotic

Most aneurysms are ‘non-specific’ in aetiology; in the past they were termed ‘atherosclerotic’. However, it is now widely believed that aneurysmal disease is a distinct pathological process from occlusive arterial disease, although they share some of the same risk factors (smoking and hypertension) and may coexist in the same patient.

Mycotic

The term mycotic, meaning fungal, is a misnomer because fungi do not cause aneurysms. The term is used nowadays to include all aneurysms that are believed to be infectious in origin. The infection can be primary or secondary to other pathology. Arteries are generally resistant to infection, but two organisms, Treponema pallidum (syphilis) and salmonella, have a particular ability to produce primary mycotic aneurysms. Septic emboli from heart valves affected by subacute bacterial endocarditis may also lodge in the distal vasculature and produce secondary mycotic aneurysms. ‘Non-specific’ aneurysms and the layers of laminated thrombus within them may become infected in the course of a bacteraemia from another site. Lastly, infection of prosthetic grafts can lead to infected anastomotic aneurysms.

True aneurysms

All three layers of the arterial wall enclose a true aneurysm, which may be saccular or fusiform (Fig. 21.21).

Fig. 21.21 True and false aneurysms.

False aneurysms

If the wall of an artery is damaged, the resulting surrounding haematoma can remain in continuity with the lumen leading to a pulsatile swelling whose wall comprises compacted thrombus and surrounding connective tissue. Small aneurysms (1–2 cm in diameter) often thrombose spontaneously but larger aneurysms tend to expand (especially if the patient is on aspirin, heparin or warfarin) and compress surrounding tissues. The most common site is the groin after common femoral artery instrumentation, and this may cause femoral vein compression and deep venous thrombosis (DVT). Surgery is increasingly being replaced by ultrasound-guided thrombin injection. Where such aneurysms develop in less accessible sites, such as the aorto-iliac segment, then the hole can be sealed using a covered stent introduced percutaneously or by blocking the artery (embolization) usually via the femoral artery.

Abdominal aortic aneurysm (AAA)

Summary Box 21.4 Abdominal aortic aneurysm (AAA)

• AAAs are present in up to 5% of men aged over 70 years; more than half are asymptomatic and go undetected until they rupture

• Ruptured AAA is the 10th most common cause of death in men. Only a third of patients with ruptured AAA reach hospital alive and, of these, only about half survive surgery. The overall mortality for the condition therefore exceeds 80%. Population screening of men over the age of 65 years with ultrasound may reduce the number of ruptured AAAs by up to 50%

• Patients with asymptomatic AAA should be considered for repair if the maximum diameter reaches 5.5 cm and the surgeon believes the operation will be associated with a mortality of less than 5%

• An increasingly large number of AAAs are being treated by endovascular aneurysm repair (EVAR), which is associated with a significant reduction in peri-operative morbidity and mortality although questions still remain around long-term durability and protection from rupture.

Epidemiology

AAA is present in up to 5% of men aged over 70 years and is 2–3 times commoner in men than in women of the same age. In about 70% of cases, only the infrarenal aortic segment is involved. In the remainder, the rest of the abdominal aorta, the thoracic aorta or a combination of both is involved.

Clinical features

An AAA may present in the following ways:

• Asymptomatic (60%). The AAA may be detected incidentally on routine physical examination, plain X-ray or, most commonly, abdominal ultrasound scan conducted for another reason. Even a large AAA can be difficult to feel. Patients in whom an incidental finding of an AAA is made should be considered for treatment or surveillance.

• Symptomatic (10%). AAA may cause pain in the central abdomen, back, loin, iliac fossa or groin. Thrombus within the aneurysm sac may be a source of emboli to the lower limbs. Much less commonly, the aneurysm may undergo thrombotic occlusion. AAA may also become inflamed and then compress surrounding structures such as the duodenum, ureter and the inferior vena cava.

• Rupture (30%). AAA may rupture, usually into the retroperitoneum, but sometimes into the peritoneal cavity or rarely into surrounding structures, most commonly the inferior vena cava, leading to an aorto–caval fistula.

Studies have shown that screening for AAA by means of ultrasound results in a reduction in the number of deaths from rupture (EBM 21.5). The UK has begun introducing a national screening programme for AAA (http://aaa.screening.nhs.uk).

21.5 Screening for AAA

‘The mortality benefit of screening for AAA in men aged 64–73 years was maintained in the longer term and screening was cost effective.’

Lindholt, J S. Long-term benefit and cost-effectiveness analysis of screening for abdominal aortic aneurysms from a randomized controlled trial British Journal of Surgery 2010; 97: 826–34.

Investigations

Ultrasound is the best way of establishing the diagnosis, of obtaining an approximate size, and of following up patients with asymptomatic AAAs that are not yet large enough to warrant surgical repair (Fig. 21.22). CT angiography (CTA) will provide much more accurate information about the size and extent of the aneurysm, involvement of visceral arteries and the surrounding structures, and whether there is any other intra-abdominal pathology. It is the standard preintervention investigation but is not suitable for surveillance because of the ionizing radiation and cost (Fig. 21.23).

Fig. 21.22 Abdominal ultrasound showing a transverse section through a large abdominal aortic aneurysm.

Measurement 1 shows the front to back (AP) diameter of the AAA from wall to wall while measurement 2 shows the diameter of the lumen through the thrombus lining the aneurysmal sac

Fig. 21.23 Computed tomography (CT) in abdominal aortic aneurysm.

A Transverse section (L = lumen, T = thrombus). B CT angiography (CTA): 3-D reconstruction.

Asymptomatic AAA

Trials have shown that the risks of open surgery generally outweigh the risks of rupture until an asymptomatic AAA has reached 5.5 cm in anteroposterior maximum diameter. It is, therefore, unusual in the UK for an AAA smaller than this to be operated upon in the absence of symptoms. Once a small AAA has been detected, the best way of following up the affected patient is by repeated ultrasound scans at regular intervals (depending on the size). Patients are encouraged strongly to comply with BMT, which affords the same benefits as it does in patients with occlusive disease (which often coexists). Ultrasound is only accurate to about 0.5 cm and tends to underestimate AAA size. Thus, many specialists will arrange for a CT when the AAA reaches 5.0 cm, along with other tests designed to assess fitness for surgery. Once the AAA reaches 5.5 cm and assuming the clinical assessment and investigations indicate that the patient is fit for surgery, the surgeon will normally begin discussions with the patient with a view to open repair (OR) or endovascular aneurysm repair (EVAR).

Symptomatic AAA

All symptomatic AAAs should be considered for repair, not only to rid the patient of their symptoms, but also because pain often predates rupture. Distal embolization is a definite indication for repair, even if the AAA is small, as limb loss is common if the AAA is left untreated.

Ruptured AAA

This is the most common emergency presentation of AAA. Patients survive rupture for the following reasons:

• The rupture is usually into the retroperitoneum, which tamponades (restricts the extent of) the leak

• There is intense vasoconstriction of non-essential circulatory beds

• The patient develops an intensely prothrombotic state

• The patient’s blood pressure drops, which helps to limit the blood loss.

Any medical intervention that upsets this delicate balance will convert a relatively stable, potentially salvageable patient into one unlikely to reach the operating theatre or to survive intervention. Specifically, large volumes of intravenous fluid (saline or plasma expander) increase the patient’s blood pressure, impair haemostasis and abolish vasoconstriction, and must therefore not be given. The only way of saving the patient is to either clamp and graft the aorta or insert a stent graft (EVAR) (if necessary having controlled the bleeding through angioplasty balloon occlusion of the thoracic aorta); there must be absolutely no delay in getting the patient to a hospital where this can be done (Fig. 21.24).

Fig. 21.24 Intraoperative photograph of repair of a ruptured abdominal aortic aneurysm.

Open AAA repair (OR)

This entails replacing the aneurysmal segment with a prosthetic graft (Fig. 21.25). The 30-day major morbidity and mortality for this procedure is approximately 5–10% for elective asymptomatic AAA, 10–20% for emergency symptomatic AAA and up to 50% for ruptured AAA.

Fig. 21.25 Open repair of an abdominal aortic aneurysm.

Diagram showing insertion of a ‘trouser’ bifurcation graft within the opened aneurysmal sac.

Endovascular aneurysm repair (EVAR)

EVAR involves placing a covered stent graft inside the aneurysm via a femoral arteriotomy, or percutaneously, under radiological guidance (Figs 21.26 and 21.27). The procedure can be performed under regional (epidural) or even local anaesthesia. Laparotomy and cross-clamping of the aorta are avoided. The patient is often fit to go home within 48 hours, as opposed to the 7–10 days that are typical following OR. Patients also usually make a rapid return (4–6 weeks) to their preoperative functional status, whereas those who have undergone OR often take 4–6 months to feel as well as they did before their operation. Not surprisingly therefore, several trials have shown that EVAR is associated with a marked reduction in hospital mortality and morbidity, reduced hospital stay and improved early postoperative quality of life (EBM 21.6). There are, however, downsides; specifically, the devices are expensive (£5000 or more); a significant proportion of AAAs are unsuitable for the procedure with present technology; and there are still questions over durability in that the secondary intervention rate following EVAR is much higher than it is following OR, and EVAR appears to afford less protection from rupture than OR in the long term. In patients unfit for open surgery, the addition of EVAR to BMT is of no benefit when compared to BMT alone (EBM 21.6).

Fig. 21.26 Endovascular stent-graft repair of an abdominal aortic aneurysm.

A A guidewire is passed through the aneurysm via an incision in the right common femoral artery. B A catheter containing the main body of the stent graft is passed over the guidewire and into position within the aneurysm. C The outer cover of the catheter is removed, allowing the upper part of the stent graft to spring open and become attached by hooks to the wall of the aorta just below the renal arteries. D The rest of the catheter is removed, allowing deployment of the main body of the graft and the right (long) limb within the common iliac artery. Note the short (left) limb of the graft. E Via an incision in the left common femoral artery a second guidewire is passed up through the short limb of the stent graft. A second catheter containing the rest of the stent graft is passed over the guidewire and into the main body of the stent graft. As before, retraction of the outer cover allows the top of the second limb of the stent graft to open within the short limb of the main body. F Deployment is complete and the aneurysm sac completely excluded from the circulation. The femoral arteries are closed.

Fig. 21.27 3-D CT reconstruction of a stent graft deployed inside an abdominal aortic aneurysm.

(Courtesy of Mr Donald Adam.)

Over the coming years, the technology is likely to continue to improve, such that the morbidity and mortality associated with EVAR will fall even further; the secondary intervention rates will also fall; and most patients can be treated by EVAR, which is likely to become the standard treatment. The technique also has applicability in patients with thoracic and thoraco-abdominal aneurysms and dissection. Several groups have published encouraging results of EVAR for ruptured aneurysms.

Peripheral aneurysms

Any peripheral artery, and very rarely vein, can be affected by aneurysmal dilatation. The aetiology, clinical features and treatment vary depending upon the site of disease.

Iliac aneurysms

In approximately 20% of patients, AAAs extend into one or both common iliac arteries and about a third of these extend into the internal iliac artery; the external iliac artery is rarely

21.6 Endovascular aneurysm repair (EVAR)

‘Six years after randomization, endovascular and open repair of abdominal aortic aneurysm resulted in similar rates of survival. The rate of secondary interventions was significantly higher for endovascular repair.’

DREAM Study Group. Long-term outcome of open or endovascular repair of abdominal aortic aneurysm. New England Journal of Medicine 2010; 362(20): 1881–9

‘In this large, randomized trial, endovascular repair of abdominal aortic aneurysm was associated with a significantly lower operative mortality than open surgical repair. However, no differences were seen in total mortality or aneurysm-related mortality in the long term. Endovascular repair was associated with increased rates of graft-related complications and re-interventions and was more costly.’

UK EVAR Trial Investigators. Endovascular versus open repair of abdominal aortic aneurysm. New England Journal of Medicine 2010; 362(20): 1863–71

‘In this randomized trial involving patients who were physically ineligible for open repair, endovascular repair of abdominal aortic aneurysm was associated with a significantly lower rate of aneurysm-related mortality than no repair. However, endovascular repair was not associated with a reduction in the rate of death from any cause. The rates of graft-related complications and re-interventions were higher with endovascular repair, and it was more costly.’

UK EVAR Trial Investigators. Endovascular repair of aortic aneurysm in patients physically ineligible for open repair. New England Journal of Medicine 2010; 362(20): 1872–80

affected. Isolated iliac aneurysms can also occur. The bifurcation of the aorta is at the level of the umbilicus, so that a pulsatile mass felt below that level is likely to be iliac in origin. Iliac aneurysms are most often treated in the course of AAA repair. Isolated iliac aneurysms should be considered for EVAR or surgical repair if they are causing symptoms or have reached twice the normal diameter of the native artery.

Femoral aneurysms

There are three main types of femoral aneurysm: iatrogenic false aneurysm (see above), non-specific aneurysm and anastomotic aneurysm. ‘Non-specific’ aneurysms of the common femoral artery are found in 10% of patients with AAA and also as an isolated occurrence. Patients presenting with a femoral aneurysm should have an AAA excluded by ultrasound scan. In 50% of cases they are bilateral. They are frequently asymptomatic but may cause pain and compression of surrounding structures (femoral vein and nerve); rupture is uncommon. If large (>3 cm) or symptomatic, they should be considered for surgical repair. Anastomotic false aneurysms are increasingly being seen in patients who have previously undergone bypass grafting for occlusive or aneurysmal disease. They may not present until many years after the original surgery, but once present, they usually grow inexorably and require repair. They are usually due to mechanical disruption of the anastomosis as a result of late suture failure or progressive disease of the femoral artery; less commonly, they are due to late graft infection.

Popliteal aneurysms

These are present in 20% of patients with AAA and their presence must be sought, if necessary with ultrasound, in all such patients. Around 50% are bilateral. If a patient presents with a popliteal aneurysm, there is a 50% chance that he or she also has an AAA, which again must be sought by ultrasound. The main complications of popliteal aneurysm are distal embolization and acute thrombosis; the latter is associated with limb loss in up to 50% of cases because the calf vessels are often chronically occluded, which makes surgical bypass difficult. The best treatment is by surgical bypass using the long saphenous vein. Sometimes, in severely ischaemic limbs, it is necessary to instill a thrombolytic agent at the same time as, or before, operative exclusion and bypass. Rupture of popliteal aneurysms is extremely rare. Occasionally, they can compress the popliteal vein and present as a DVT.

Buerger’s disease (thromboangiitis obliterans)

This is an inflammatory obliterative arterial disease that is quite distinct from atherosclerosis. It is rare in Caucasians but more common in people from the Mediterranean, Asia and North Africa. It usually presents in young (20–30 years) male smokers and characteristically affects the peripheral arteries, giving rise to claudication in the feet or rest pain in the fingers or toes. Such pain in the feet on walking is often misdiagnosed as musculoskeletal in nature, whereas pain in the fingers or toes is often misdiagnosed as primary Raynaud’s phenomenon. The condition also affects the veins, and superficial thrombophlebitis is common. Wrist and ankle pulses are usually absent, but brachial and popliteal pulses are palpable. Arteriography shows narrowing or occlusion of arteries below the diseased segment, but relatively healthy vessels above that level.

The condition often remits if the patient stops smoking; sympathectomy and prostaglandin infusions may be helpful. If amputation is required, it can often be limited to the digits at first. However, if the patient continues to smoke, then bilateral below-knee amputation is a frequent outcome. Although the disease is uncommon in the UK, it is very important to consider and exclude it in patients presenting with vascular symptoms in their legs and arms, especially if the symptoms are atypical and the patient is young (under 50 years of age). Failure to make the diagnosis often leads to avoidable limb loss and is a source of medicolegal activity.

Raynaud’s phenomenon

Raynaud’s phenomenon describes digital pallor due to vasospasm of the digital arteries, followed by cyanosis owing to the presence of deoxygenated blood, then rubor due to reactive hyperaemia upon restoration of flow, in response to cold and emotional stimuli.

Primary Raynaud’s phenomenon

Raynaud’s disease affects 5–10% of young women in temperate climates, and usually appears between the ages of 15 and 30 years; a family history is common. It does not progress to ulceration or infarction. No investigation is necessary and the patient is given reassurance, advised to avoid exposure to cold, and treated in the first instance with nifedipine (a calcium channel blocker). The underlying cause is unclear.

Secondary Raynaud’s phenomenon

This is also known as Raynaud’s syndrome and tends to occur in older people in association with:

• connective tissue disease, most commonly systemic sclerosis

• vibration-induced injury, from the use of power tools (vibration white finger, hand-arm vibration syndrome)

• atherosclerosis, most commonly thoracic outlet obstruction from the cervical rib (see above).

Unlike primary disease that is due to reversible spasm, secondary disease is usually associated with fixed obstruction of the digital arteries. Fingertip ulceration and necrosis are often present. The fingers must be protected from cold and trauma, infection is treated with antibiotics, and surgery is avoided if possible. Vasoactive drugs have no clear benefit. Sympathectomy helps for a year or two. Prostacyclin infusions are sometimes beneficial. In the UK, hand arm vibration syndrome (HAVS) is a compensatable industrial occupational disease.

Pathophysiology of venous disease

Anatomy

The great (GSV) and lesser (LSV) (somewhat confusingly previously known respectively as the long and short) saphenous veins and their tributaries lie outside the deep fascia and in health carry about 10% of the venous return from the limb. The GSV begins at the medial end of the dorsal venous arch, crosses in front of the medial malleolus and ascends the medial side of the leg. It penetrates the deep (cribriform) fascia 2.5 cm below and lateral to the pubic tubercle to enter the common femoral vein at the saphenofemoral junction (SFJ). The LSV starts at the lateral end of the dorsal venous arch, passes posterior to the lateral malleolus, then ascends the median posterior line of the calf to join the popliteal vein at the saphenopopliteal junction (SPJ), usually just above the knee. Anatomical variations are very common.

The deep venous system comprises intramuscular veins and axial veins that accompany the main arteries; they are usually paired in the calf. Communicating veins perforate the deep fascia to connect the superficial and deep systems (Fig. 21.28).

Fig. 21.28 Diagrammatic representation of the venous drainage of the lower limb.

Physiology

Weight-bearing compresses the veins in the sole of the foot, which propels blood into the calf (‘foot pump’). Pushing off when walking is associated with calf muscle contraction and the compression of venous blood in the muscular sinuses and axial veins; this propels blood further up the leg (‘calf pump’). When the leg is lifted off the floor and the muscles relax, blood is prevented from refluxing back down the leg by the closure of valves. During this relaxation phase, blood passes from the superficial to the deep veins via perforators, ready to be expelled during the next step. In motionless standing, the venous pressure at the ankle is approximately 100 mmHg: that is, the hydrostatic pressure exerted by the column of venous blood stretching from the ankle to the right atrium. However, upon walking, the mechanisms described above reduce the ankle pressure to less than 25 mmHg (ambulatory venous pressure, AVP). The symptoms and signs of lower limb venous disease are largely due to failure of these protective mechanisms and the presence of a high AVP.

Summary Box 21.5 Venous disease

• Varicose veins are present in over 50% of the adult population; approximately 10% have skin changes of chronic venous insufficiency; and the life time risk of chronic venous ulceration is about 1%

• Compression therapy is the mainstay of treatment for chronic venous insufficiency, but should never be implemented unless the arterial status of the leg is known to be satisfactory (palpable pedal pulses and/or an ABPI > 0.8)

• If patients with lower limb venous disease are being considered for surgical or endovenous treatment, they should undergo duplex ultrasonography to delineate the pattern of superficial and deep venous reflux and obstruction

• DVT in postoperative patients is often asymptomatic. Most postoperative patients developing (fatal) PE have normal legs on clinical examination. Duplex ultrasound or venography should be used to confirm the diagnosis of DVT; V/Q scan or CT pulmonary angiography can be used to diagnose PE

• All hospital patients, medical and surgical, should have their thromboembolic risk assessed and receive prophylaxis accordingly. PE remains the most common cause of potentially preventable death in hospital

Varicose veins

Classification

Trunk varices

These involve the main stem and/or major tributaries of the GSV and LSV, are usually > 4 mm in diameter (and may be much larger); lie subcutaneously; are palpable; do not usually discolour the overlying skin; and are present in about a third of the adult population (Fig. 21.29).

Fig. 21.29 Great saphenous varicose veins and saphena varix (arrow).

Although 2–3 times more women than men present for treatment, the prevalence is roughly equal between the sexes. There appears to be a familial tendency; obesity, pregnancy, constipation and (occupational) prolonged standing may be aggravating factors.

Reticular varices

These lie deep in the dermis, are < 4 mm in diameter, are impalpable, and render the overlying skin dark blue. They are present in about 80% of the adult population, and may or may not be associated with trunk varices.

Telangiectasia

These are also called spider and thread veins. They lie superficially in the dermis, are usually 1 mm or less in diameter, are impalpable, and render the overlying skin purple or bright red. Again, they may be associated with trunk and reticular varices, and are present in 90% of adults. Like reticular veins, they appear to be more common in women, possibly because of poorly understood hormonal reasons.

Epidemiology

Varicose veins (VV) are so prevalent that they could almost be considered a variant of normal for a creature that spends its life on two as opposed to four legs. Their prevalence increases markedly with age and they are an almost universal finding in individuals over the age of 60.

Clinical features

The great majority of individuals with VV are asymptomatic, or at least they do not seek treatment. Those that attend the surgical clinic do so because they are unhappy about the appearance of their leg(s), and/or they associate lower limb symptoms with their VV, and/or they are concerned about developing complications.

Cosmetic issues

Many patients, especially young women, seek treatment because they consider their veins to be unsightly. Possibly because they are unwilling to admit that cosmesis is the main issue, they frequently complain of various lower limb symptoms as well.

Symptoms

A wide variety of lower limb symptoms have been attributed to VV. Lower limb symptoms are present in about half of the adult population, and there is an inconsistent relationship between these symptoms and the size and extent of VV on clinical examination and duplex ultrasound examination.

Complications

Only a proportion of patients with VV go on to develop the complications of chronic venous insufficiency (CVI): for example, leg ulcers, haemorrhage and thrombophlebitis. There is on-going controversy as to whether VV are a risk factor for DVT but in young, otherwise healthy individuals, they are probably not. However, in the elderly, in whom VV are more likely to be associated with skin changes of chronic venous insufficiency and in whom they may be a marker for coexistent deep venous disease, they probably are. At present, it is difficult to predict which patients will develop these complications and to know whether early VV surgery would prevent them, because the necessary longitudinal studies have never been done.

Indications for treatment

In correctly selected patients, it is clear that interventions for VV are associated with a marked improvement in health related quality of life (HRQL) and symptom relief. In patients with uncomplicated VV, surgeons must use their own judgment and experience to determine whether the patient truly does have symptoms, whether those symptoms are of venous aetiology, and, if so, whether they are likely to be relieved by intervention. Many VV interventions are performed in the private sector for purely cosmetic indications.

Aetiology

The true aetiology of VV remains unclear. The favoured hypothesis is that there is a structural defect in the vein wall, that may at least in part be inherited, which causes progressive dilatation in response to increased venous pressure consequent upon our bipedal posture and other factors. This leads to secondary incompetence of the valves (reflux), which in turn leads to more stress on the wall and more dilatation. These are sometimes termed primary VV. As in the deep venous system, thrombosis in the superficial veins (superficial thrombophlebitis) can destroy the valves leading to reflux. And lastly, deep venous obstruction, usually due to DVT, can lead to the appearance of superficial varices which act as collateral pathways around that obstruction. These are sometimes termed secondary VV. Such secondary VV should not be removed as that will result in a further reduction in the venous outflow of the leg leading to worsening post-thrombotic syndrome characterized by pain and swelling, especially on walking (venous claudication).

Examination and investigation

The patient should be examined standing in a warm room; the whole leg is visualized from toes to groin with the lower abdomen also exposed. The distribution of VV may indicate whether they are great or lesser saphenous or both. Various percussion and tourniquet based tests, such as the famous Trendelenburg test, are highly inaccurate and should not be performed these days. Some surgeons use hand-held Doppler probes to help delineate patterns of reflux but even in the best of hands the method lacks precision and accuracy. In reality, as duplex ultrasound machines become smaller, more portable, easier to use and cheaper, there is a move towards performing duplex examinations in the clinic on all patients being considered for intervention.

Severe VV, especially in children, of atypical distribution or associated with skin discoloration, soft-tissue hypertrophy or limb overgrowth, should raise the suspicion of congenital vascular malformations. Such patients should undergo MRI to assess the extent of the lesion and the arterial component.

Management

Conservative treatment

Many patients with uncomplicated VV can be managed conservatively in primary care. Elastic support hose, weight reduction, regular exercise and the avoidance of constricting garments and prolonged standing all help to relieve tiredness and reduce swelling. However, many patients, especially those seeking treatment for cosmetic indications, will refuse to wear unfashionable compression garments and seek surgical or endovenous treatment.

Surgery

VV surgery aims to remove varices and intercept incompetent connections between deep and superficial veins so that further varices do not form. In patients with GSV disease, the SFJ is ligated flush with the femoral vein (Fig. 21.30). Recurrence is very much less likely if the LSV is stripped out from knee to groin. Care must be taken not to damage the saphenous nerve, which joins and runs with the GSV below the knee. In patients with LSV disease, the SPJ is dealt with in a similar fashion. However, the LSV is not normally stripped for fear of injuring the sural nerve with which it runs. Remaining varices are avulsed through multiple tiny incisions.

Fig. 21.30 Saphenofemoral disconnection.

A Diagram showing ligation of the tributaries of the great saphenous vein. B Operative photograph showing proximal great saphenous vein (arrow) and major tributaries.

Although such surgery has been the mainstay of VV treatment for many decades, even in the best of hands, the outcomes can be suboptimal with a significant incidence of minor but nevertheless undesirable complications and disappointing cosmetic results. It is salutary to note that VV surgery remains the commonest cause of litigation against vascular surgeons in the UK.

For these reasons, there has been a significant investment in time and money to try to find more satisfactory, non-surgical (endovenous) solutions.

Endovenous treatment

Surgery is being increasingly replaced by a range of minimally invasive endovenous treatments that can be performed under local anaesthesia as a day case or even as an outpatient procedure. The techniques include:

• Radiofrequency ablation (RFA)

• Endovenous LASER ablation (EVLA)

• Ultrasound guided foam sclerotherapy (UGFS) (Fig. 21.31).

Fig. 21.31 Ultrasound guided foam sclerotherapy.

A Cannula (arrow) inserted into great saphenous vein under duplex ultrasound control (longitudinal view). B Tip of cannula in varicose vein (longitudinal view). C Multiple cannulae inserted under local anaesthetic into a patient with recurrent great saphenous varicose veins that have previously been mapped using duplex ultrasound. D Foam made from 3% sodium tetradecyl sulphate (STS) sclerosant and a mixture of oxygen and carbon dioxide. E Injection of foam into great saphenous vein. The duplex ultrasound probe is used to check when foam reaches the saphenofemoral junction and that it does not enter the deep veins. F As soon as foam enters the great saphenous vein it goes into spasm. The foam destroys the endothelium leading to permanent occlusion. The bubbles in the foam make it extremely echogenic so it can be seen easily on ultrasound (arrow). G Once the varicose veins to be treated are full of foam compression bandaging and stocking is applied and worn for 5 days to keep the varicose veins closed.

Each of these techniques has pros and cons. However, performed correctly by appropriately trained clinicians, they appear to work at least as well as (often better than) surgery in many patients, and offer significant advantages in terms of less pain and a speedier return to normal activities. The catheter based techniques (RFA, EVLA) can deal with most truncal reflux but many patients require adjuvant treatment, such a stab avulsions or sclerotherapy, to deal with the varices themselves. UGFS has the advantage of being extremely versatile offering a complete treatment of truncal reflux and varices usually in one setting; foam is also much less expensive than RFA and EVLA and so more cost-effective.

Superficial thrombophlebitis

Inflammation and thrombosis of a previously normal superficial vein may result from trauma, from irritation due to an intravenous infusion or from the injection of noxious agents. Except when it arises from a septic puncture sites, superficial thrombophlebitis is usually non-bacterial. When it arises spontaneously, it almost invariably occurs in a VV. Redness and tenderness follow the line of the vein. Thrombosis may spread through communicating channels into the deep veins and give rise to DVT and pulmonary embolism (PE).

Treatment comprises analgesia, anti-inflammatory drugs, support stockings and active exercise. Once the inflammation has settled down, it is usually wise to remove the underlying VV, as recurrence is common. Propagation towards the deep veins usually requires heparin therapy, and rarely thrombectomy or vein ligation. Recurrent migrating superficial phlebitis is occasionally seen in malignant disease.

Chronic venous insufficiency

Pathophysiology

Chronic venous insufficiency (CVI) may be defined as the presence of (usually irreversible) skin damage (such as eczema, lipodermatosclerosis) in the lower leg as a result of sustained ambulatory venous hypertension. This hypertension is due to failure of the mechanisms (see above) that normally lower venous pressure upon ambulation, namely:

• Venous reflux due to valvular incompetence (90%). This may affect the superficial veins, the deep veins or both, and may be due to primary valvular insufficiency (as in VV) or to post-thrombotic damage.

• Venous obstruction (10–20%). This is usually post-thrombotic in nature and coexists with reflux.

CVI affects about 10% of the adult population and the lifetime risk of chronic venous ulceration (CVU) is around 1%.

Most patients with CVI and CVU (Fig. 21.32) are over 50 years of age and the incidence increases exponentially with advancing years. In 1992 it was estimated that the treatment of lower limb venous disease accounted for about 1–2% of health-care spending in the UK (£400–600 million per annum at the time). The female to male ratio is about 3:1. Approximately 70% of all leg ulcers are venous in aetiology and 20% are due to mixed arterial and venous disease. In many cases, the situation is aggravated by old age, poor social circumstances, obesity, trauma, immobility, osteoarthritis, rheumatoid arthritis, diabetes and neurological problems. It is usually possible to differentiate venous from arterial ulceration on clinical examination alone (Table 21.5).

Fig. 21.32 Chronic venous ulcer.

Table 21.5 Differential diagnosis of leg ulceration

Clinical features	Arterial ulcer	Venous ulcer
Gender	Men > women	Women > men
Age	Usually presents > 60 years	Typically develops at 40–60 years but patient may not present for medical attention until much older; multiple recurrences are the norm
Risk factors	Smoking, diabetes, hyperlipidaemia and hypertension	Previous DVT, thrombophilia, varicose veins
Past medical history	Most have a clear history of peripheral, coronary and cerebrovascular disease	More than 20% have a clear history of DVT; many more have a history suggestive of occult DVT, i.e. leg swelling after childbirth, hip/knee replacement or long bone fracture
Symptoms	Severe pain is present unless there is (diabetic) neuropathy; pain may be relieved by dependency	About a third have pain, but it is not usually severe and may be relieved on elevation
Site	Normal and abnormal (diabetics) pressure areas (malleoli, heel, metatarsal heads, 5th metatarsal base)	Medial (70%), lateral (20%) or both malleoli and gaiter area
Edge	Regular, ‘punched-out’, indolent	Irregular, with neo-epithelium (whiter than mature skin)
Base	Deep, green (sloughy) or black (necrotic) with no granulation tissue; may involve tendon, bone and joint	Pink and granulating but may be covered in yellow-green slough
Surrounding skin	Features of severe limb ischaemia	Lipodermatosclerosis, varicose eczema, atrophe, blanche
Veins	Empty, ‘guttering’ on elevation	Full, usually varicose
Swelling	Usually absent	Often present

The assessment and management of CVI and CVU should commence as follows: the patient first, then the leg, and then the ulcer.

Assessment

History

This should include the history of the present and previous episodes of ulceration; previous thrombotic episodes; previous venous and non-venous surgery to the leg, pelvis and abdomen; arterial symptoms; diabetes; autoimmune disease; other medical conditions; locomotor problems; current medications; and allergies.

Examination

This should include a description of the ulcer, concentrating on the features outlined in Table 21.5. Pulse status and ABPI should be recorded. Gait, particularly ankle mobility which is vital for the proper functioning of the calf muscle pump, should be assessed.