Peripheral vascular disease

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CHAPTER 15 Peripheral vascular disease

Arterial 284
Amputations 304
Venous disorders 306
Lymphoedema 311
Vascular trauma 313

Arterial

History

Peripheral vascular disease usually affects the lower limb but may affect the upper limb, GI tract, cerebral vessels and renal vessels. Risk factors include smoking, hypercholesterolaemia (family history), hypertension, diabetes and thrombophilia.

Clinical features

Features of the history depend on the system involved.

Limbs

Intermittent claudication is the classic symptom of peripheral vascular disease involving the lower limb. It is a pain in the muscle due to ischaemia brought on by exercise and relieved by rest. It is consistently brought on by the same degree of exercise. It is typically cramping in nature and is most common in the calf (superficial femoral artery disease) or buttock (aorto-iliac disease). It can vary with temperature, e.g. it is worse in the cold and it is more severe when going uphill. The main differential diagnosis is spinal claudication (pain is present at rest and is relieved by leaning forward, i.e. it may be better going uphill) and venous claudication (the pain is ‘bursting’ and takes longer to go at rest). Any sudden deterioration in the claudication distance requires urgent assessment. More severe disease may result in the complaint of ‘rest pain’. This is a constant pain, typically in the feet and occurring at night while in bed (due to ↓ cardiac output therefore ↓ BP and peripheral vasodilation, all of which leads to decreased blood supply). It is relieved by hanging the leg out of bed or walking. Gravity increases the blood flow and hanging the leg out of bed cools it and therefore decreases metabolism and hence requires less blood flow. Eventually gangrene, i.e. tissue necrosis, may supervene. Males with aorto-iliac disease may complain of buttock claudication and impotence (Leriche’s syndrome).

Other systems

A history should be sought for symptoms involving other areas of the vascular system, e.g. cardiac (MI, angina); GI system (upper to central abdominal cramping pain coming on about 20 min after a large meal – ‘mesenteric angina’); cerebrovascular: (1) carotid (anterior circulation): stroke, TIAs, transient blindness, i.e. amaurosis fugax; (2) vertebral (posterior circulation): dizziness, drop attacks, bilateral blindness, diplopia, vertigo, problems with stance/gait; and renal (hypertension).

Examination

The patient’s limb should be examined in a warm room.

Inspection

Check the colour of the limb. An ischaemic limb may be as white as marble (acute ischaemia) or show varying degrees of pallor, purple/blue cyanosis or a red shiny appearance (chronic ischaemia). Look for scars from previous vascular procedures. In the male, the ischaemic leg is typically hairless. The vascular angle (Buerger’s angle) is the angle to which the leg must be raised before it becomes white. Normally the straightened leg can be raised to 90° and the toes will stay pink. In a severely ischaemic leg elevation to 15° may cause pallor. Following elevation, the limb is placed in the dependent position and in the presence of severe ischaemia a purple/red colour occurs as the foot is reperfused. In a normal limb, the veins should be full even when the patient is horizontal. In the ischaemic foot, veins will be collapsed and look like pale blue gutters in the subcutaneous tissue. This is the sign of guttering of the veins. Inspect the pressure areas (heel, tips of toes, ball of foot, head of fifth metatarsal) for signs of trophic changes, ulceration or gangrene; inspect between the toes.

Palpation

Check the skin temperature. Check the capillary refilling time, i.e. press the tip of the nail or pulp of the toe or finger for 2 s and observe the time taken for the blanched area to turn pink. In the normal digit this should occur immediately. Delay (>2 s) will occur in the ischaemic digit. Palpate and record all the pulses. They should be assessed for strength (assessed as normal, weak or absent). Pulses should be recorded as shown in Table 15.1 and the presence of any aneurysmal dilatation noted.

Table 15.1 Tabulation of pulses

Pulses R L
Radial ++ ++
Brachial ++ ++
Subclavian ++ ++
Carotid ++ (bruit) ++
Femoral ++ ++ (bruit)
Popliteal + −
Posterior tibial − −
Dorsalis pedis − −

++ normal volume;

+ diminished volume;

− absent.

Auscultation

Listen along the course of all the major arteries for bruits. Listen to the arteries in the neck, the abdomen and the groin. Measure the BP in both arms to exclude subclavian disease. The Ankle-Brachial Pressure Index (ABPI) should be measured in the lower limb.

Procedure

How to perform ABPIs

The ABPI provides a measure of the severity of peripheral vascular disease. A ratio of 0.9–>1 is considered normal; 0.5–0.9 equates to the presence of intermittent claudication and <0.5 is defined as critical ischaemia. ABPIs are measured by placing a cuff around the patient’s ankle and using a hand-held Doppler probe, the dorsalis pedis (DP) and/or posterior tibial (PT) pulses are detected. The cuff is then inflated above the systolic pressure and deflated until the signal returns. This is repeated for both DP and PT pulses. Brachial artery pressure is then measured and the ratio calculated. In diabetic patients, the arteries may be incompressible and lead to falsely elevated levels.

Arterial occlusive disease

Acute arterial occlusion

This is defined as a deterioration in the blood supply of the leg that leads to rest pain or signs of severe ischaemia of less than 2 weeks’ duration. This may range from a patient without PVD who has an embolic occlusion and presents with a dramatically ischaemic limb to a patient with chronic PVD who develops severe new onset rest pain.

Causes

Embolus

This may come from the heart (left auricular thrombus in AF, mural thrombus following MI, vegetation secondary to valvular lesions, atrial myxoma) or it may come from proximal atherosclerotic plaques or from thrombus within aneurysms.

Thrombosis

This usually occurs in an area of arteriosclerotic narrowing due to plaque rupture. There is usually a history of claudication or rest pain prior to the acute event. It may also occur with popliteal aneurysm, a blocked bypass graft and thrombotic conditions, e.g. antiphospholipid syndrome.

Trauma

This may be: penetrating trauma; a result of arterial catheterization or angioplasty; following a limb fracture, e.g. popliteal artery damage following supracondylar fracture of the femur; brachial artery damage following a supracondylar fracture of the humerus in a child; accidental intra-arterial injection, e.g. a misplaced injection in an intravenous drug abuser.

Symptoms and signs

Acute embolus in a normal limb

The classical symptoms are the six ‘Ps’: pain, pallor, paraesthesia, paralysis, pulselessness and perishing cold. Not all these symptoms are present in every case and the most reliable of these signs are paralysis and paraesthesia. In a patient with an embolic source of occlusion and with no previous PVD and thus no preformed collateral circulation, the ischaemia is sudden and profound and muscle may only survive for 6 h from the onset of symptoms. It is therefore necessary to establish the exact time of onset of symptoms.

Acute-on-chronic ischaemia in a limb with PVD

In contrast, a patient with chronic limb ischaemia may not present so acutely and the limb will certainly survive longer periods of ischaemia. In either group, the presence of sensory changes or calf tenderness on squeezing or passive dorsiflexion of the foot and toes indicates impending muscle infarction and requires immediate revascularization. After 6 h there is vasodilatation and release of deoxygenated blood as a result of tissue hypoxia. This leads to a more mottled appearance that still blanches on pressure. At this stage, the leg may be saved by prompt surgery. After 12 h, the arteries and veins thrombose, capillaries rupture and there is fixed staining that does not blanch. At this stage, the limb is unsalvageable and revascularizing the limb is inappropriate and may lead to mortality due to release of potassium, lactic acid, etc.

Investigations

• FBC
• U&Es
• Glucose
• Clotting screen
• Cross-match
• CXR
• ECG
• Duplex Doppler
• Angiography (catheter angiogram or CT/MR angiogram) – only indicated in patients who do not have an immediately threatened limb
• Echocardiogram – usually performed at a later date to identify cardiac sources of emboli.

Treatment

Initial management involves ABC – patients may be compromised secondary to arrhythmias or other cardiac events and often have significant co-morbidities. Anticoagulate with heparin. Administer analgesia. Administer oxygen via facemask.

The further management depends on the clinical condition of the limb. Options include:

Embolus in a normal limb

The diagnosis is clinical (angiogram is unnecessary) and the patient should be taken to theatre immediately for embolectomy.

Thrombosis in a limb with PVD

In these patients the presentation may not be as dramatic. Angiography can provide much information about the cause of ischaemia. Treatment options include: surgical thrombectomy; bypass grafting; thrombolysis – provided that the limb will survive for at least 12 h to give time for clot dissolution.

In all patients, fasciotomy should be considered to prevent compartment syndrome after revascularization. In some patients where ischaemia is considered irreversible, a primary amputation may be performed. However, in some cases with major co-morbidities, terminal care may be more appropriate.

Prognosis

Ideally, surgery should be undertaken within 6–8 h of onset of symptoms if a good result is to be obtained. Delay in treatment increases the incidence of amputation and mortality. The mortality from embolic episodes is 20–30% irrespective of the treatment of the emboli. The mortality is more a consequence of the co-morbid conditions or the cause of the emboli.

Chronic arterial occlusion

Lower limb (aorto-ilio-femoral disease)

Causes

Invariably due to arteriosclerosis, usually consequent on smoking. Arteriosclerosis may involve the arteries of the lower limb singly or in combination. Typical patterns include aorto-iliac disease, isolated iliac stenoses and superficial femoral occlusion. Other causes include multiple recurrent small emboli, vasculitis, fibromuscular dysplasia, Buerger’s disease, cystic adventitial disease (especially in the young), popliteal entrapment (especially in the young), polycythaemia and Takayasu’s disease (rare).

Symptoms and signs

Intermittent claudication affecting the calf (block in the superficial femoral artery), the thigh (block in the external iliac artery) or buttock (block in the lower aorta or common and internal iliac arteries). Occlusion of the aortoiliac segment associated with buttock claudication and impotence is known as Leriche’s syndrome. Rest pain may develop involving an aching pain in the toes and forefoot that appears when the patient lies horizontal. It is relieved by hanging the foot over the side of the bed. Ischaemic ulcers and gangrene may supervene. Ischaemic ulcers tend to develop at pressure areas, e.g. bunion area, tips of toes, lateral aspect of head of fifth metatarsal and around the heel. The foot may be cold, pale and show venous guttering and dependent rubor. Absent or reduced pulses. Palpable thrills. Bruits.

Investigations

• Haemoglobin
• FBC
• ESR
• U&Es
• Glucose
• Lipids
• CXR
• ECG
• Treadmill test to assess claudication distance
• Duplex ultrasound – non-invasive; gives information about the degree of stenosis by visual estimation and velocity measurement
• ABPIs, i.e. ankle–brachial ratio. Normally, this is between 1 and 1.2. Pressures around 0.8 are compatible with claudication and pressures around 0.4 with rest pain. Pressures below 0.4 indicate severe ischaemia and are usually associated with ulceration and gangrene
• CT/MRI angiogram (Figs 15.1, 15.2) – non-invasive but does not allow intervention
• Angiography(by direct arterial puncture ) – invasive and thus has complications (haematoma, dissection, emboli, false aneurysm, contrast reaction and contrast nephrotoxicity) but allows therapeutic interventions to be performed (see below).
image

Figure 15.1 MRA aorta and iliac vessels. There is a tight stenosis at the origin of the left external iliac artery (large arrow) involving the origin of the internal iliac artery which is occluded. There is also a stenosis at the origin of the right external iliac artery (small arrow).

image

Figure 15.2 MRA femoral vessels. There is a block in the left (superficial) femoral artery in the adductor canal (arrow). The distal artery fills via numerous collaterals.

Treatment

Medical

Mild to moderate claudication that is not disabling does not require surgical treatment. Advice is given to patients to lose weight, stop smoking, exercise regularly within their claudication distance. Advice is also given on foot care, particularly chiropody. Antiplatelet agents should be given, usually aspirin, but in patients who will not tolerate aspirin, an alternative antiplatelet agent should be prescribed, e.g. clopidogrel. Correct any cholesterol or triglyceride abnormality with a statin. There is clear evidence that cardiac events can be reduced by up to one-third by reducing low density lipoproteins/cholesterol by one-third, regardless of the baseline cholesterol, down to a total cholesterol of 3.5 mmol/L by use of a statin. Control hypertension. Nicotine patches to help stop smoking. Drugs such as naftidrofuryl and cilostazol have been used and may increase pain-free walking distance. Infusions of Iloprost (a prostacyclin analogue) are occasionally used in critical ischaemia with no hope of reconstruction but are rarely helpful. Regular patient follow-up is required. Patients should be encouraged to seek medical advice if claudication suddenly deteriorates or rest pain develops.

• Endovascular. Intervention consists of angioplasty ± stenting. Intervention may be divided into supra-inguinal and infra-inguinal:

— Supra-inguinal. Angioplasty of aorto-iliac disease is relatively straightforward and results in good patency rates. The use of stents is generally reserved for sub-optimal angioplasty (i.e. residual pressure gradient across the stenosis) or a technical complication such as dissection.
— Infra-inguinal. Endovascular intervention is not as successful for infra-inguinal disease. For femoro-popliteal disease, the long term patency rates are lower. However, lesions in the superficial femoral and popliteal artery are often suitable for intervention. Stents are not generally used unless due to procedural complications. In critical ischaemia sub-intimal angioplasty can be used to recanalize occluded vessels with good rates of limb salvage.

Chemical lumbar sympathectomy with injection of phenol under radiological guidance can occasionally be used in patients with unreconstructable disease in an attempt to control pain.

Surgical

Surgical options include endarterectomy, bypass (supra-inguinal and infra-inguinal) and primary amputation.

• Endarterectomy. Performed for flow limiting common-femoral/profunda femoris origin disease. This essentially involves dissecting out the occluding plaque and closing the vessel with or without a patch to allow increased blood flow.
• Bypass:

— Supra-inguinal. Surgical methods of treating aorto-iliac disease include aorto-bifemoral bypass, ilio-femoral bypass or femoro-femoral cross over grafts (for unilateral iliac occlusion).
— Infra-inguinal. There are numerous options. These include femoro-popliteal bypass (above or below knee) and femoro-distal bypass (to posterior tibial, anterior tibial, dorsalis pedis or peroneal arteries). Ideally reversed vein should be used, usually the great saphenous vein, as is offers better patency rates and lower risk of infection. If vein is unavailable then prosthetic material such as ePTFE may be used. They may be used with a collar/cuff of vein at the anastomosis to improve patency, i.e. Miller cuff, Taylor patch or St Mary’s boot.

• Amputation. Areas of tissue loss may be amputated after arterial reconstruction has been performed and the tissues have demarcated. However, in some cases of critical ischaemia where reconstruction is not an option and pain is uncontrolled or the leg is not viable, the only option is primary amputation.

Prognosis

The majority of patients with intermittent claudication are managed conservatively with <7% progressing to critical ischaemia. Patients with critical ischaemia have a poor prognosis, 50% dying within 5 years.

Upper limb

Causes

The upper limb is significantly less affected by peripheral disease with most episodes of acute ischaemia being secondary to emboli. Thoracic outlet syndrome (see below) may be responsible for claudication or rest pain. Distal arterial disease may be due to embolization from an area of dilatation or frank aneurysm just beyond the subclavian artery compression.

Symptoms and signs

Emboli usually lodge in one of three sites in the brachial artery: (1) proximally at the origin of the profunda brachii; (2) at the mid-arm level at the origin of the superior ulnar collateral artery and (3) distally at the brachial bifurcation. It is rare for emboli to lodge in the subclavian or axillary arteries. Symptoms and signs are similar to those in the lower limb, as are the initial investigations.

Treatment

Analgesia. Oxygen. Intravenous heparin 5000 units. Embolectomy in the acutely ischaemic limb. Thrombolysis. Conservative management with an i.v. heparin (the rich collateral circulation in the upper limb means that the limb is not always acutely threatened).

Cerebrovascular disease

Some 80% of strokes are ischaemic and 20% are haemorrhagic. Atherosclerosis is the commonest cause and usually affects the internal carotid artery just distal to the common carotid bifurcation. Disruption of a plaque at this point can lead to thrombus formation and secondary embolism, leading to a stroke or TIA. A stroke is defined as a focal neurological deficit of >24 h of presumed vascular origin. A TIA has a similar definition but lasts <24 h. In practice, TIAs often last <30 min.

Symptoms and signs

These may be classed as carotid (anterior circulation) or vertebrobasilar (posterior circulation).

• Carotid. Paralysis or numbness of the contralateral arm or leg or temporary loss of vision of ipsilateral eye (amaurosis fugax). Dysphasia
• Vertebrobasilar. Bilateral motor/sensory signs, dysarthria, bilateral visual loss, balance problems, nystagmus and homonymous hemianopia. The presence of a carotid bruit has no real clinical relevance as it can be present with a non-significant stenosis and absent with a severe stenosis. Examination may reveal reduced carotid pulses or bruits over the carotid artery.

Investigations

• FBC
• U&E
• Cholesterol
• Clotting screen
• Glucose
• Thrombophilia screen (younger patient)
• Autoimmune screen (younger patient)
• ECG. Arrhythmias may cause embolic strokes.
• Echocardiogram – if embolic source is suspected
• CT scan – identify cerebral infarcts or haemorrhage or rare causes of CVA, i.e. cerebral tumour or abscess
• Duplex. Identification of significant stenosis of the internal carotid artery on the affected side (remember right-sided symptoms would be from a left carotid stenosis and vice versa). If an internal carotid artery is occluded, then surgery is pointless
• Carotid angiography – rarely performed nowadays as small risk of stroke associated with the procedure
• MR angiogram (Fig. 15.3) – largely replaced carotid angiography in the assessment of internal carotid disease.
image

Figure 15.3 MRA carotid artery. (A) Common carotid artery. (B) Internal carotid artery. (C) External carotid artery. (D) Vertebral artery. There is a tight stenosis (arrow) of the internal carotid artery.

Treatment

Management depends on two factors, i.e. degree of stenosis and whether it is symptomatic or asymptomatic. Patients with a carotid stenosis of <50%, whether symptomatic or not, should be managed medically. Patients with a symptomatic stenosis >50% are generally best treated by carotid endarterectomy. Asymptomatic patients with stenosis >60% are best treated by carotid endarterectomy. Another group of asymptomatic patients that often require intervention are patients undergoing coronary artery bypass grafting. In these patients, a high grade stenosis (i.e. >90%) or a combined stenosis (right and left carotid) >150% are indications for treatment.

Medical

Medical management of internal carotid artery stenosis consists of:

• Risk factor modification – control BP, control diabetes, stop smoking, treat high cholesterol.
• Statins are used to treat high cholesterol but also reduce the number of strokes and major cardiovascular events even with normal cholesterol.
• Anti-platelet drugs – treatment with aspirin alone, in combination with dipyridamole or clopidogrel alone are acceptable treatment.

Endovascular

Recent trials have suggested higher rates of stroke with internal carotid stenting. As such, most centres would reserve its use for patients unfit for carotid endarterectomy or with contraindications to carotid endarterectomy such as previous neck radiotherapy or neck scarring around the operative site.

Surgical

Operative treatment of carotid artery stenosis is carotid endarterectomy. This involves opening the artery longitudinally and creating a subadventitial plane to remove the arteriosclerotic plaque. The operation may be performed under GA or with a local anaesthetic regional cervical block. A carotid shunt (taking blood from common carotid to internal carotid) may be used. Generally, all GA cases will use a shunt while cases performed under LA will use a shunt selectively depending on the patient’s neurological condition after the application of clamps. A Dacron patch is used to close the arteriotomy after endarterectomy to prevent later stenosis.

Complications of carotid endarterectomy include bleeding, infection (very rare but catastrophic given the presence of a prosthetic patch), MI, stroke (in the region of 2–4% risk and may occur via embolism caused by dissection technique or postoperative thrombosis secondary to an intimal flap), nerve damage (marginal mandibular nerve, hypoglossal, vagus, superior laryngeal and recurrent laryngeal).

Renovascular disease

Hypertension may be caused be renal hypoperfusion with release of renin from juxtaglomerular cells with activation of angiotensin. The most common causes are arteriosclerosis and fibromuscular dysplasia of the renal arteries. Arteriosclerosis usually involves the origin of the artery and occurs in the older patient. Fibromuscular dysplasia affects the middle to distal part of the artery and usually occurs in the younger patient. Renal artery stenosis has been shown to increase 5-year mortality in patients with peripheral vascular disease and in coronary artery disease it has been shown to double the risk of death, despite coronary revascularization.

Renal artery stenosis is an important, and potentially correctable, cause of renal failure in the older patient. The diagnosis of renal artery stenosis is frequently made following a deterioration of renal function in patients commenced on angiotensin-converting enzyme (ACE) inhibitors or angiotensin II receptor (AR) blockers.

Symptoms and signs

Hypertension – either symptomatic or picked up on routine examination, e.g. insurance medical. Rapid onset or accelerated hypertension. Hypertension in a young adult or child. Hypertension refractory to treatment. Sudden deterioration in renal function. Deterioration in renal function after ACE inhibitors or AR blockers. Occasionally it may be picked up on an IVU when a non-functioning or poorly functioning kidney is noted. It may be picked up when there is a small kidney on CT or the presence of a bruit in the flank. Flash pulmonary oedema.

Investigations

• Duplex scanning
• CT/MR angiography
• MAG3 scan with and without captopril – this can demonstrate any difference between the two kidneys and if this is exacerbated by an ACE inhibitor.

Treatment

A stenosis of >50% is considered significant and critical if >70%. Treating the stenosis is no guarantee that either hypertension or renal failure will improve. Current indications for intervention include: ↓ renal function or ↑ BP despite maximum medical treatment; flash pulmonary oedema; rapid onset renal failure; renal failure in patients with cardiac disease while taking ACEI or AR blockers; loss of renal mass on conservative treatment; progression of stenosis.

Treatment options include medical, radiological and surgical.

Medical

Control BP. Antiplatelet drugs. Statins. Good diabetic control. Lifestyle changes, i.e. stop smoking. Diet.

Endovascular

Options include angioplasty alone or with stenting. Offers good results, particularly with fibromuscular dysplasia.

Surgery

Occasionally indicated. Options include bypass, endarterectomy and patch, nephrectomy + bench surgery and auto-transplantation. Nephrectomy (if kidney unsalvageable).

Visceral ischaemic disease

Visceral ischaemic disease covers a number of conditions including acute mesenteric ischaemia, chronic mesenteric ischaemia and acute mesenteric venous thrombosis.

Acute mesenteric ischaemia

This carries a very high mortality rate as a result of late diagnosis and due to its relative rarity. Causes are generally embolic or as a result of in situ thrombosis on an underlying stenosis. Less common causes include non-occlusive infarction (due to low flow states, i.e. hypotension and inotropes), vasculitis, fibromuscular dysplasia, aortic dissection and thrombosis of visceral arterial aneurysm.

Symptoms and signs

Embolus classically presents as acute severe abdominal pain with few clinical signs. Vomiting or diarrhoea, which may be bloody. There may be a history of atrial fibrillation, sepsis, oral contraceptive, ‘mesenteric claudication’ (chronic mesenteric ischaemia), portal hypertension. The pain experienced is usually out of proportion to the early physical findings. Subsequently, the patient will develop fever, abdominal tenderness, distension and ultimately peritonitis and shock.

Investigations

• FBC
• WCC ↑
• HCO3 ↓
• Serum lactate ↑
• Serum amylase may be raised with infarcted bowel (confusion with acute pancreatitis)
• AXR – may not be helpful or show air/fluid levels
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