Endovascular aneurysm repair (EVAR) allows a stent-graft to be delivered inside the aneurysm via the femoral artery, then expanded and fixed in position under fluoroscopic guidance (Fig. 13.1). The whole procedure is performed via small groin incisions, or even percutaneously in some cases. Recovery is quicker than for open repair and less fit patients can be treated. The mortality for EVAR is less than 2%, one third of that for open repair. Long term complications of EVAR include endoleaks, graft migration, iliac limb occlusion and aneurysm rupture. Long term surveillance with duplex scanning ± CT is required.

Figure 13.1 Schematic depiction of an endovascular repair of an abdominal aortic aneurysm with a bifurcated stent-graft.

Ruptured AAA (p. 96)

The presentation of a ruptured aortic aneurysm is very variable depending on the size and site of the rupture. This commonly leads to diagnostic confusion. Misdiagnoses such as ureteric colic and pancreatitis may lead to delayed diagnosis with disastrous results.

A large leak, especially one which ruptures into the peritoneal cavity, causes a swift death. Other patients have a contained retroperitoneal bleed causing pain of sudden onset which is severe and continuous, in the central abdomen and radiates to the back. The site of pain may be very variable and may be felt only in the back, or one or other flank. The signs of acute haemorrhage; tachycardia, hypotension, vasoconstriction and depressed conscious level, depend on the size of leak. In many patients the initial rupture is contained and tamponaded by the periaortic tissue and posterior peritoneum to the extent that no haemodynamic disturbance occurs, indeed the patient may even be hypertensive during this early stage. The aneurysm may be palpable as a pulsatile expansile mass in the epigastrium, but even a large aneurysm may be difficult to feel, and haematoma surrounding the aorta may mask the aortic pulsation. For these reasons, the abdominal signs of aortic aneurysm rupture are not as clear-cut as might be expected.

Immediate management of suspected ruptured AAA

The diagnosis is made on clinical grounds. Call the duty vascular surgeon and anaesthetist immediately. Give 100% oxygen, put up two large-bore IVs and take blood for FBC, U&E, amylase, clotting and cross-match. Request at least 10 units of blood and inform the haematologist that fresh frozen plasma and platelets are likely to be required urgently. Pass a urinary catheter. Do not give excessive IV fluids to patients who are conscious: a systolic pressure of 80 mmHg is more than adequate. Excessive fluid at this stage only increases bleeding into the abdomen and makes the operation more difficult. Treatment is immediate aneurysm repair and nothing should delay transfer to the operating theatre. Time spent in A&E doing X-rays, ECGs, and central lines may be lethal; these can be done in theatre.

For open repair, the anaesthetic must be induced on the operating table after preparing and draping the abdomen. As soon as the muscle relaxant is given, the abdominal muscles become paralysed and the blood pressure may collapse. It is then a race against time to get a clamp on the aorta above the leak. The rest of the operation proceeds along the same lines as for elective repair.

For emergency endovascular repair, the procedure is performed using local anaesthetic infiltration of the groins for femoral artery exposures.

In stable patients where the diagnosis is not clear, a CT scan is crucial. This confirms or excludes the presence of a ruptured aorta and may also detect pancreatitis or ureteric obstruction, the two main differential diagnoses.

An ultrasound scan is not sufficient to exclude a rupture in patients who have an AAA.

Popliteal aneurysms

The popliteal artery is usually considered aneurysmal if its diameter exceeds 1 cm. The risk factors are the same as for AAAs, indeed around 20% of individuals with a popliteal aneurysm also have an AAA, and vice versa. Rupture is rare (under 4%) but embolisation (causing chronic critical limb ischaemia) and thrombosis (causing acute limb ischaemia) are common. Mural thrombus lining the aneurysm sac leads to chronic microembolisation over many years causing severe damage to the distal small arteries. When the patient finally presents with critical limb ischaemia the situation may be difficult to salvage since successful bypass requires a patent distal vessel to accept a graft. For this reason popliteal aneurysms greater than 2–3 cm in diameter should be treated with femoropopliteal vein bypass with ligation of the proximal and distal ends of the aneurysm. Such surgery for asymptomatic popliteal aneurysms is very successful with 5-year graft patency of around 80% and limb preservation of over 95%. If treatment is delayed until the aneurysm becomes symptomatic, the outcome is poor, with nearly 20% of limbs requiring amputation.

Endovascular covered stenting is an alternative for patients with no suitable vein for bypass, or who are unfit for surgery.

Other peripheral aneurysms

True aneurysms of the femoral artery are much less common than the popliteal variety. Rupture is rare but symptoms result from local compression or distal ischaemia due to embolisation. Treatment is usually surgical reconstruction.

Visceral artery aneurysms

Aneurysms involving the splenic, hepatic and mesenteric arteries are rare. Splenic aneurysms are four times commoner in females and hepatic aneurysms more frequent in men. Multiple aneurysms in the same patient are usually associated with a connective tissue abnormality such as Ehlers–Danlos syndrome. Rupture is uncommon but may be fatal. Endovascular coil embolisation is the treatment of choice.

Mycotic aneurysms

This is quite different from an infected false aneurysm, where arterial damage is the primary insult and infection supervenes. Mycotic aneurysms result from infection in the vessel wall which weakens, dilates and eventually ruptures. Normal arteries are very resistant to infection so mycotic aneurysms are usually due to a particularly virulent organism or arise in immune compromised patients. The commonest cause of aortic aneurysms used to be syphilis, which affects the aortic arch. Tuberculous aneurysms are seen frequently in Africa, often in association with AIDS.

A mycotic aneurysm typically manifests as a painful, tender pulsatile mass associated with pyrexia. Mycotic aneurysms expand rapidly and rupture is often fatal. Successful treatment depends on accurate antimicrobial therapy and, where possible, avoidance of prosthetic material in any surgical reconstruction.

False aneurysms

False aneurysms occur where an artery has been damaged. Such aneurysms comprise a cavity of blood in continuity with the artery lumen surrounded by haematoma and connective tissue. Trauma, surgery or infection are the commonest causes. A frequent example is the femoral artery which has been punctured for an angiogram but fails to seal. False aneurysms may also occur at the site of an old vascular anastomosis, especially if prosthetic material was used or if it has become infected. Some splenic and gastroduodenal artery aneurysms are false aneurysms caused by erosion of the artery wall by proteolytic enzymes following pancreatitis.

Treatment depends on the site and symptoms. Duplex-guided compression is successful in inducing thrombosis in many angiogram-related femoral false aneurysms. Thrombin injection may achieve the same result, albeit with a risk of distal embolisation. More complex false aneurysms may require surgery, or endovascular treatment with a covered stent.

Lower limb ischaemia

Classification of chronic lower limb ischaemia, as described by La Fontaine, is shown in Table 13.1.

Table 13.1 The La Fontaine classification for lower limb ischaemia

Asymptomatic	I
Intermittent claudication	II
Rest pain	III
Ulceration/gangrene	IV

Causes of lower limb ischaemia

Atherosclerosis accounts for the vast majority of lower limb ischaemia in the West. Presentation of limb ischaemia in a younger adult should prompt a search for causes of accelerated atherosclerosis and consideration of less common causes of lower limb ischaemia. These include:

• aortic dissection

• aneurysms (see p. 208)

• accelerated atherosclerosis (hyperlipidaemia, hyperhomocysteinaemia, AIDS)

• Buerger’s disease (common in male smokers in the Middle/Far East)

• popliteal entrapment (artery passes medially to medial head of gastrocnemius causing compression; seen in athletes and may progress to permanent arterial damage if untreated)

• fibromuscular dysplasia (most commonly affects carotid and renal arteries but can narrow the iliac arteries in young adults)

• cystic adventitial disease (popliteal artery develops ganglion-like cysts that may connect to the knee joint)

• persistent sciatic artery (associated with atresia of the ileofemoral vessels).

Intermittent claudication

Intermittent claudication (IC) is the tight cramp-like pain felt typically in the calf muscle on walking when the blood supply to the lower limb is limited (derived from the Latin, claudere, to limp). The severity of the claudication is defined by the distance walked before onset of the pain. On resting or slowing down, the pain passes off within a few minutes. Walking uphill, carrying a heavy bag or rushing all shorten the claudication distance.

Although unpleasant, IC is a relatively benign condition as far as the leg is concerned. Most patients either stay the same or improve and only a small minority (5%) progress to critical limb ischaemia (Fig. 13.3). Diabetics and patients who continue to smoke have a worse prognosis.

Figure 13.3 Pie chart of intermittent claudication prognosis.

The main differential diagnosis is spinal claudication due to congestion of the spinal canal. The pain of spinal claudication resembles IC but the onset is variable; patients have good days and bad days. This is never so with vascular IC, which is very consistent. The pain of spinal claudication extends beyond the calf muscle up the back of the thigh and round onto the shin. There is often a history of back problems and straight leg raising may be limited.

A diagnosis of IC is supported by absent peripheral pulses and reduced ABPIs, typically 60–79% of normal. Non-invasive duplex imaging localises the culprit arterial flow-limiting lesions and guides treatment.

Risk factor modification

In many respects the true significance of IC is not the symptom but the risk of death from other aspects of vascular disease. Claudicants have a mortality around three times that of age-matched controls, mainly due to coronary heart disease, strokes and aneurysms. Attention to vascular risk factors including smoking, hypertension, antiplatelet and statin therapy (see p. 204) is therefore of paramount importance.

Exercise

Many patients can cure their IC by walking as much as possible. ‘Walking through the pain’, i.e. continuing to walk as long as possible after the pain starts, encourages collateral blood vessels to open up. Patients effectively do their own bypass. Simply advising patients to walk achieves limited benefit but supervised exercised programmes are highly effective.

Drugs

There is no practical drug therapy for IC though cilostazol helps some patients and may have beneficial effects after angioplasty.

Angioplasty

Angioplasty is most effective for stenoses or short occlusions in the aorto-iliac segment. Femoropopliteal disease can also be treated but the risks are higher and any benefit less durable.

Surgery

Bypass surgery for IC is becoming uncommon. The value of exercise therapy and the effectiveness of angioplasty for iliac lesions have greatly reduced the number of patients who end up requiring operations for claudication. The crucial thing to bear in mind when contemplating surgery (or even angioplasty) for claudication is that however unpleasant the IC, claudicants have a high cardiovascular mortality, and in most cases the legs will remain stable or improve if left alone. This must be weighed against the consequences of complications following intervention that could lead to loss of life or limb. In selected patients, however, surgery is highly effective and durable. This is particularly so for occlusions and stenoses of the common femoral artery which is easily accessible surgically and not readily treated with angioplasty. Here a localised endarterectomy may be the best treatment.

Critical lower limb ischaemia

Critical leg ischaemia (CLI) is ischaemia that endangers all or part of the limb and is usually defined as persistently recurring rest pain for more than 2 weeks, or ulceration or gangrene of the foot. The ankle pressure should be lower than 50 mmHg.

In the UK around 20 000 patients per year develop CLI (40 per 100 000) and this is increasing as the population becomes more elderly.

Twenty-five per cent of CLI patients are dead within a year and only half survive more than 5 years, mainly due to deaths from myocardial infarction and stroke. Unlike claudication, therefore, treatment aims are relatively short term and focus on quality of life rather than long term durability of any procedure.

The pain of CLI is felt in the toes and forefoot and is typically worse at night when cardiac output drops. Patients wake up in the early hours with severe pain, relieved by hanging the leg out of the bed allowing blood to flow down to the foot. Some patients take to sleeping in a chair. Many patients get up and walk around in the night, which stimulates flow and reduces pain. During the day the patient may suffer short distance claudication. This pattern of symptoms – calf claudication by day and rest pain in the toes at night – is strongly suggestive of CLI.

It is rare to have rest pain in the presence of palpable pedal pulses unless the problem is due to microembolisation. Pedal and usually the popliteal pulses are absent. There may be ulceration of the foot or frank gangrene of the toes. The leg may become swollen if the patient has to hang it down all the time to ease the pain. Accumulation of metabolites may make the foot look surprisingly red but it will go white if elevated for a few minutes (Buerger’s test).

Investigation of limb ischaemia is considered on page 210. Endovascular therapy is usually first-line treatment. Many of these patients die of other problems before the benefits of angioplasty have worn off. The durability of angioplasty is not as good as surgery but the effects may be sufficient to heal the limb and convert rest pain to claudication. Moreover, occlusion of the angioplastied site frequently does NOT result in clinical deterioration and an attempt at angioplasty seems not to prejudice subsequent surgical intervention if required.

In both endovascular and surgical treatment, the strategy is to treat the most proximal flow-limiting lesions first. Thus iliac and above-knee stenoses should be treated before more distal problems.

Acute limb ischaemia

This is described on page 96.

The diabetic foot

Diabetics are prone to ulceration and infection of the foot which may progress to tissue necrosis requiring amputation. This is due to a combination of vascular disease and neuropathy. Diabetic foot ulcers are classified using the Wagner (Table 13.2) or Texas systems (Table 13.3).

Table 13.2 Wagner classification of diabetic foot ulcers

Grade 0	No ulcer on a high risk foot
Grade 1	Superficial ulcer
Grade 2	Deep ulcer penetrating to ligaments/muscle but not bone and no abscess formation
Grade 3	Deep ulcer with cellulitis or abscess, often with bone infection
Grade 4	Localised gangrene
Grade 5	Extensive gangrene

Table 13.3 Texas classification of diabetic foot ulcers

Sensory neuropathy robs the diabetic foot of the protective mechanism of pain, allowing ulceration to develop in response to minor trauma or rubbing.

Autonomic neuropathy reduces sweating and opens arteriovenous shunts in the foot. The diabetic foot is typically warm, and may have strong pedal pulses and dry, cracked skin. The skin fissuring allows entry of bacteria, causing localised infection.

Motor neuropathy causes wasting of the small intrinsic muscles of the foot with collapse of the longitudinal and transverse arches. Abnormal pressure areas then develop which progress to ulceration.

Atherosclerosis in diabetics develops at a much younger age and is more extensive and distal. It is not uncommon for a diabetic to have a critically ischaemic foot in the presence of a normal popliteal pulse due to occlusion of the crural arteries. In addition to disease of the major arteries, the capillary basement membranes thicken, impairing oxygen diffusion to the tissues of the foot.

Management

Management is aimed at prevention by careful foot care. Good diabetic control helps reduce the severity of foot complications. There is no specific treatment for neuropathy. Localised sepsis should be treated with debridement and drainage in the usual way. Plain X-rays may show evidence of osteomyelitis and MRI is an accurate way of defining the extent of sepsis in the foot. Ischaemia, if present, should be corrected.

A multidisciplinary team approach including a diabetologist, vascular surgeon, radiologist, podiatrist and infectious disease specialist improves outcomes and reduces major amputations.

Amputations

There is only one indication for a major amputation and that is to save the life of the patient. Amputation is a last resort in a patient with non-salvageable critical limb ischaemia or extensive gangrene/necrosis as a result of tissue infection. In this situation, without amputation, the gangrene/infection will progress, causing death. The most frequently performed major amputations are below-knee amputation (transtibial) and above-knee amputation (trans-femoral). The procedures have a high morbidity and mortality, not least because patients requiring such operations are very sick to start with. Surgical technique is important to obtain a well-shaped stump that heals without complication.

Rehabilitation takes several weeks but, with modern prostheses, a good proportion of patients will achieve a satisfactory degree of independence. The level of function and independence achieved depends greatly on the patient’s general health and strength, co-morbidities and social support.

Carotid artery disease

A high proportion of strokes result from embolisation from diseased carotid arteries. The origin of the internal carotid artery is prone to localised atheromatous plaque formation. Platelet thrombi form on the surface of the rough plaque then break off and embolise to the brain. This may give rise to different symptoms depending on how large the embolus is and which part of the brain it ends up in.

The goal of carotid surgery is to prevent strokes. A stroke is defined (by the WHO) as rapidly developing signs of focal (or global, i.e. coma) disturbance of cerebral function lasting more than 24 hours (unless interrupted by death), with no apparent cause other than a vascular origin. ‘Strokes’ lasting less than 24 hours are referred to as transient ischaemic attacks (TIAs).

There are two main types of stroke: ischaemic (due to cardiac or other emboli, intracerebral thrombosis) and haemorrhagic (subarachnoid haemorrhage, intracerebral haemorrhage). In the West, 80% of strokes are ischaemic.

Carotid embolisation

Embolism from the carotid artery may manifest in several ways.

• Asymptomatic. CT and MRI scanning often reveal evidence of multiple small brain infarctions with no history of preceding symptoms.

• Amaurosis fugax. Small emboli which pass through the retinal artery cause the characteristic symptom of a greying out of the vision in the eye on the same side as the source of the embolus. Patients often describe it as a curtain coming down. The vision returns to normal within a few minutes.

• A transient ischaemic attack (TIA). These resolve within 24 hours by definition.

• Strokes result from embolisation of branches of the middle cerebral artery and cause neurological deficit on the contralateral side to the embolising artery. Strokes lasting less than 3 weeks are said to be ‘transient strokes’. Persistent deficits after 3 weeks are ‘established strokes’ and subsequent recovery may be good, moderate or poor.

These clinical distinctions are important since prognosis after carotid surgery is related to the presenting symptom.

Any patient presenting with symptoms attributable to carotid artery embolisation should have a carotid duplex scan. This identifies whether the internal carotid artery is diseased and, if so, what degree of narrowing (stenosis) is present. The percentage of stenosis is the best predictor currently available of likelihood of subsequent major (fatal or disabling) stroke.

A patient who presents with amaurosis fugax, TIA or stroke, associated with a stenosis of the relevant internal carotid artery greater than 70%, has a risk of major stroke in the following 18 months. Correcting vascular risk factors (stopping smoking, treating hypertension, instigating antiplatelet and statin therapy) go some way to reduce this risk but carotid endarterectomy is highly effective at reducing subsequent stroke risk down to normal levels.

Carotid endarterectomy

Carotid endarterectomy involves exposing the carotid bifurcation, opening the artery and carefully removing the atheromatous plaque, leaving a smooth non-thrombogenic luminal surface. The artery is usually closed with a patch to avoid narrowing. A shunt may be used during the operation to preserve cerebral blood flow while the artery is open but this is not always necessary if the circle of Willis is complete. The operation is increasingly performed under local anaesthetic so the patient remains conscious throughout. Carotid endarterectomy has a risk of death and stroke of around 2%, which is much less than the natural history of the condition left untreated. The other main complication is damage to the hypoglossal (XII) nerve, which crosses the internal carotid artery at the upper limit of the dissection.

Symptomatic carotid artery stenosis should be corrected as soon as possible after the symptom, ideally within 48 hours. This is because the risk of major stroke is greatest immediately after the TIA or transient stroke and this risk tails off gradually over the following weeks. Even though the operative risk of endarterectomy is slightly higher when operating soon after an acute symptom, more strokes are prevented by early surgery than by waiting, as many patients will stroke in the interim.

The benefits of surgery for severe (>70%) asymptomatic carotid stenosis are much more finely balanced. Improvements in medical therapy, especially use of statins, have reduced the risk of stroke caused by asymptomatic carotid artery stenosis to less than 2% per year. Successful surgery halves this risk, but only patients with a good life expectancy benefit from this modest improvement likelihood of stroke.

In summary, carotid surgery for symptomatic stenosis should be performed very promptly, and for asymptomatic stenosis very selectively.

Carotid artery stenting (CAS) is a less invasive method of correcting carotid artery stenosis. It is associated with a higher risk of stroke but a lower risk of heart attack. The results of carotid artery endarterectomy are superior to stenting for most patients in most centres.

Venous disease

Varicose veins

Varicose veins are dilated tortuous superficial veins occurring usually in the lower limb. They are common and run in families (female to male ratio 3 : 1).

Anatomy

In health there are two venous systems in the lower limb: the deep and superficial veins. The deep veins run alongside the arteries and are contained within the fascial compartments. Muscular activity compresses the deep veins, driving blood up into the abdomen (the so-called muscle pump). Reflux is prevented by valves ensuring blood flows upwards towards the heart.

The superficial veins are just beneath the skin in the subcutaneous fat. There are two main superficial veins, the long and short saphenous veins, which drain into the deep system via the saphenofemoral and saphenopopliteal junctions. Valves in the veins and at the junctions ensure that blood flows from superficial to deep. There are also a number of perforating veins connecting the superficial and deep systems and again blood flows from superficial to deep.

The commonest cause of varicose veins is the development of incompetence of the valves at the saphenofemoral or popliteal junctions. This allows blood to reflux from the deep system into the superficial system causing dilatation and tortuosity of the saphenous tributaries.

Symptoms

Characteristic discomfort due to varicose veins is an aching sensation exacerbated by standing for long periods and eased by elevating the leg. This may be associated with a sensation or actual appearance of swelling of the leg. Varicose veins may be painless but cause considerable distress due to their appearance. Chronic venous hypertension causes skin changes including venous flares and brown pigmentation (lipodermatosclerosis) which may itch and irritate and progress to ulceration.

Signs

Varicose veins invariably crop up in clinical surgical examinations and it is worthwhile practising to become slick in examining them.

Ask the patient to stand up to allow the veins to fill. Ask about family history of varicose veins and past DVT. Inspect for:

• great or small saphenous distribution?

• associated skin changes/ulceration?

Palpate:

• groin for cough impulse or saphenovarix

• using the tap test: gently feel the lower varicosities while tapping on the proximal saphenous vein. The impulse is transmitted readily down the incompetent trunk

• using the tourniquet (Trendelenburg) test. A popular ritual in clinical examinations but rarely performed by vascular surgeons who use hand-held Doppler and duplex scanning to determine the sites of reflux.

Hand-held Doppler

Hand-held Doppler readily confirms saphenofemoral and saphenopopliteal incompetence.

Tests

Colour duplex imaging has revolutionised venous assessment, and other tests (venography, plethysmography) are rarely needed.

Treatment (see also ‘Leg ulceration’, below)

Treatment for varicose veins has changed from surgical operating-theatre based therapy to a range of minimally invasive procedures which may be performed under local anaesthetic, so-called office-based vein treatment carried out in an outpatient clinic.

Treatment options include:

• high saphenous ligation (crossectomy) and stripping (traditional treatment, usually performed under general anaesthetic)

• foam sclerotherapy

• radiofrequency ablation (RFA)

• endovenous laser therapy (EVLT)

• mechano-chemo-ablation (‘Clarivein’)

• phlebectomy

• perforator vein ablation/ligation.

Patients often require a combination of these treatments. Treatment is usually in two components. The first is to deal with the underlying incompetent vein which is causing the varicose vein. This is usually the great and small saphenous vein which may be effectively closed by an endothermal method (RFA or EVLT). The surface varicoscities are then removed by phlebectomy or sclerotherapy.

Chronic venous insufficiency

Untreated varicose veins, deep venous incompetence secondary to DVT or deep venous obstruction may cause the post-thrombotic syndrome (PTS). This unpleasant condition causes pain, limb swelling, chronic skin changes and ultimately ulceration. Treatment is usually non-surgical in the form of compression bandaging or compression stockings. Rarely the deep veins can be reconstructed but the results are limited.

Lymphoedema

Lymphoedema is limb swelling resulting from failure of the lymphatic system to transport tissue fluid via lymphatic vessels and lymph nodes. The affected limb becomes progressively more swollen, heavy and uncomfortable. As the swelling worsens, skin complications of ulceration, hyperkeratosis and fissuring develop. The limb is prone to recurrent attacks of cellulitis, which exacerbates the swelling further.

The causes of lymphoedema are shown in Table 13.4. There are three types of primary lymphoedema, determined by age of onset.

Table 13.4 Causes of lymphoedema

Primary	Congenital (symptoms appear as an infant)	Familial (Milroy’s disease) Non-familial
	Praecox (adolescence)	Familial and non-familial types
	Tarda (over 35 years)	Often associated with obesity
Secondary	Infection (commonest cause worldwide but not in the West)	Filariasis (causes elephantiasis)
	Cancer	Malignant obstruction of lymph nodes by metastases
	Surgery/Radiotherapy	Especially to axilla for treatment of breast cancer