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
• CT with i.v. contrast may show signs of bowel ischaemia
• Angiography (duplex ultrasound for the diagnosis of acute mesenteric ischaemia is highly unreliable)
• Laparotomy provides the diagnosis in most cases.

Treatment

Urgent laparotomy. Venous thrombosis (see below) without infarction requires anticoagulation. If the patient does not improve within 12 h, a ‘second look’ laparotomy may not be required to assess intestinal viability.

In the case of arterial occlusion, there is extensive irreversible ischaemia if surgical treatment may be possible. If the length of non-viable bowel is not excessive, then surgical resection with stoma and mucous fistula may be appropriate. Patients are left with a short segment of bowel and consequent metabolic problems. If no pulse is present in the superior mesenteric artery, then an embolectomy should be performed. If a tight stenosis is found to be present at the origin of the superior mesenteric artery, bypass grafting or endarterectomy should be carried out.

Chronic mesenteric ischaemia

Visceral occlusion is usually due to arteriosclerosis. In practical terms the superior mesenteric artery is most often involved.

Symptoms and signs

Cramping upper abdominal pain approximately 30 min after a meal (‘mesenteric angina’). This usually lasts 1–3 h. Patients always have weight loss because of ‘food fear’ due to the pain caused by eating. Frequently they also have diarrhoea. An upper abdominal bruit may be audible. Occlusive vascular disease is likely elsewhere.

Investigations

• Duplex scanning
• MR angiography.

Treatment

Treatment is by endovascular techniques or surgery. Endovascular treatment involved angioplasty ± stenting. Surgery involves endarterectomy with patching or bypass from aorta to distal superior mesenteric artery using either reversed vein or Dacron.

Acute mesenteric venous thrombosis

This is less catastrophic than acute arterial occlusion. Presentation may be more prolonged over several weeks; 75% of cases are due to hypercoagulability, intra-abdominal sepsis and portal hypertension.

Symptoms and signs

Abdominal pain which may get worse after eating and over time. Diarrhoea. Vomiting.

Investigations

• Duplex Doppler
• CT with contrast.

Treatment

Treatment depends on the clinical condition of the patient. If the patient has peritonitis then a laparotomy should be performed and any non-viable bowel resected and any source of intra-abdominal sepsis addressed. However, if the patient is stable then it may be managed conservatively with heparin and lifelong warfarin therapy. If CT shows no intra-abdominal cause, a thrombophilia screen should be carried out prior to commencing anticoagulation.

Aneurysms

An aneurysm is an abnormal dilatation of an artery. Aneurysms may be true or false (see below). A true aneurysm contains all layers of the vessel wall and appears as either a fusiform or a saccular dilatation. True aneurysms are commonest in the infrarenal aorta, iliac vessels, common femoral and popliteal arteries. A false aneurysm may occur anywhere and is usually the result of trauma. (For Classification of aneurysms → Table 15.2.)

Table 15.2 Aetiology of aneurysms

True  
Congenital Berry aneurysm of circle of Willis
Aneurysmal varix associated with arteriovenous fistula
Acquired Trauma: irradiation
Infection: syphilis, mycotic aneurysm
Degeneration: arteriosclerosis, cystic medical necrosis
False Trauma

Aortic aneurysms

An aorta may be aneurysmal from the ascending aorta to the aortic bifurcation. Aortic aneurysms can be divided into thoracic (→ Ch. 9), thoracoabdominal or abdominal alone. Abdominal infrarenal aortic aneurysm is the most common type.

Aetiology

Aneurysms are due to degeneration of the arterial media, particularly a reduction in elastin. The exact aetiology of aortic aneurysms is unknown but contributing factors include: (1) elastin degradation due to increased levels of metalloproteinases; (2) flow dynamics –the infrarenal aorta is a common site as pulse pressure here is maximal due to tapering calibre and reflected waves from the bifurcation; (3) hypertension – involved in formation but also rate of expansion; (4) atherosclerosis – not causally linked but often also present; (5) collagen defects, e.g. Marfan’s disease and Ehlers Danlos syndrome; (6) genetic association – 25% of first degree relatives will develop an aneurysm; (7) smoking – associated with more rapid expansion; (8) association with emphysema and inguinal hernias; this may relate to a collagen defect but the exact link is unclear.

Symptoms and signs

Often asymptomatic and picked up on abdominal examination for other conditions or ultrasound scanning for other conditions. Symptomatic ones often cause backache by pressure on the adjacent lumbar vertebral bodies or abdominal pain. Examination reveals a pulsatile abdominal mass just above the umbilicus. Look for other peripheral artery aneurysms (especially popliteal).

Investigations

• USS to assess the maximum diameter of the aneurysm, and relationship to renal arteries
• CT scan
• Investigations to assess patient’s fitness for surgery – FBC, U&E, clotting studies, ECG, chest X-ray, lung function tests, ABGs, echocardiogram.

Complications

These include:

• Rupture with retroperitoneal haemorrhage or intraperitoneal haemorrhage, or into the IVC (AV fistula)
• Distal emboli
• Severe back pain due to erosion of the lumbar vertebral bodies
• Thrombosis with distal ischaemia.

Treatment

Once diagnosed, the investigations depend upon the size of the aneurysm. If <5 cm, then the patient is kept under surveillance. Surveillance is yearly if <4.5 cm and 6-monthly if >4.5 cm. Once over 5 cm, the patient undergoes a number of investigations to assess suitability for surgery. The threshold for treatment remains a diameter of >5.5 cm. Once 6 cm the annual risk of rupture is around 10–20%. If the patient is frail with poor morbidity, no treatment may be appropriate. For those suitable for treatment, either endovascular repair (EVAR) or open repair may be undertaken. EVAR is not suitable for all aneurysms but confers a much lower earlier mortality than open repair and may be attractive for high risk cases. Open repair involves an in-lay Dacron graft or a Dacron Y graft to the iliac arteries or femoral arteries. Mortality for elective surgery should be <10%. Mortality rate is more related to MI and CVA than to direct complications of surgery to the aneurysm.

Ruptured aortic aneurysm (→ Fig. 15.4)

Classically, the patient presents with severe abdominal pain radiating to the back or iliac fossa and is associated with collapse or a hypotensive episode. A pulsatile mass may be palpable. Intraperitoneal rupture is instantly fatal; retroperitoneal rupture may tamponade the bleeding allowing the patient to reach hospital. Patients with ruptured aneurysms survive to reach hospital because of vasoconstriction, abdominal tamponade, development of a prothrombotic state and the development of ‘controlled’ hypotension. The infusion of even modest amounts of crystalloid or colloid rapidly upsets that fine balance. If the patient requires significant volumes of fluids to maintain blood pressure on the way to hospital or in the emergency room, then it is very unlikely that that patient will survive surgery. A patient who is conscious and talking has an adequate blood pressure. Rarely the aneurysm may rupture to the right into the IVC causing a massive AV fistula with severe heart failure and massive lower limb oedema.

image

Figure 15.4 CT scan of the abdomen showing a large leaking abdominal aortic aneurysm. Note the areas of calcification in the wall of the aneurysm. There is evidence of leakage to the left of the aneurysm (arrow).

Investigations

If the diagnosis is clinically obvious, the patient is transferred immediately to the operating theatre for repair. If the diagnosis is in doubt and time allows, a CT scan should be performed (USS will show an aneurysm but not a rupture).

Treatment

Emergency repair should be undertaken once blood is available. Open repair is with an in-lay Dacron graft or a Dacron Y graft. Some centres are performing emergency EVAR with good results. The postoperative mortality is between 30% and 50%. Postoperative morbidity is high and results from haemorrhage, ARDS, ARF, multi-organ failure, MI, stroke, and colonic ischaemia. Late complications include graft infection, often with aorto duodenal fistula and life-threatening haemorrhage. This requires graft removal and bilateral axillofemoral grafting. However, extra-anatomical bypass is becoming less popular as they reinfect. In situ replacement with vein graft (femoral vein) or antibiotic-soaked graft (rifampicin).

Inflammatory aneurysm

Around 5% of aneurysms are described as inflammatory. This inflammation extends through all layers of the aorta. It obscures tissue planes and makes operative dissection particularly challenging. In severe cases, the inflammation may extend into the retroperitoneum to involve the IVC and ureters (ureters may require preoperative stenting).

Iliac artery aneurysm

These may involve the common iliac and internal iliac artery. The external iliac is almost never involved. They are usually present in association with aortic aneurysm. Aneurysms of the internal iliac are a particular challenge as operative access is difficult. They may rarely occur in isolation. Management options include:

• Surgical repair using a Dacron graft
• Endovascular stenting
• For internal iliac artery aneurysms, ligation if there is a patent internal iliac artery on the opposite side.

Femoral aneurysms

These usually involve the common femoral artery.

Symptoms and signs

Usually asymptomatic pulsatile mass in the groin. May be associated abdominal aortic aneurysms. Symptoms include compression of local structures, thrombosis and ischaemia, distal emboli and rupture. False aneurysms are common in the femoral artery and may result from:

• percutaneous catheterization for angiography; stab wounds
• previous surgery, especially with prosthetic grafts (infection).

Treatment

Small true aneurysms (<2.5 cm) may be treated expectantly unless symptomatic. Rapidly expanding true aneurysms require surgery. Stenting may be carried out but surgery is the preferred method of repair. Iatrogenic false aneurysms are being increasingly treated by compression therapy, usually with an ultrasound scan probe and thrombin injection.

Popliteal aneurysm

This is the commonest site for aneurysms after the aorta. Of patients with AAA, 10% have a popliteal aneurysm; 40% of patients with a popliteal aneurysm have an AAA. They are bilateral in 50% of cases.

Symptoms and signs

Pulsatile mass in the popliteal fossa. If a medical student can palpate a popliteal pulse easily, it may be aneurysmal. Complications include thrombosis with compromise of the distal circulation and distal embolism, compression of local structures, e.g. popliteal vein with DVT and rupture (rare).

Treatment

Treatment is considered when the size is >2 cm. Surgery is the preferred method of treatment but endovascular stenting may be considered for high risk patients. Stenting is carried out using a special prosthesis that allows bending at the knee. Surgical repair is either by an exclusion bypass (with ligation of the popliteal artery above and below the aneurysm) or an in-lay graft.

Visceral artery aneurysms

Aneurysms may arise from the splenic artery, hepatic artery, superior mesenteric artery or renal arteries.

Symptoms and signs

Visceral aneurysms may produce abdominal or flank pain. Renal artery aneurysms may cause haematuria or hypertension. Diagnosis is confirmed by ultrasound scanning and arteriography.

Prognosis

Splenic artery aneurysms may affect women during the child-bearing years. Rupture is an uncommon but major complication and tends to occur in the third trimester of pregnancy and is associated with a high mortality rate. If splenic artery aneurysms are picked up incidentally and are >2.5 cm, then treatment should be considered. Treatment is often possible with embolization under angiographic control. Hepatic artery aneurysms are prone to rupture. The mortality rate for surgery on visceral aneurysms is high, particularly if they rupture.

False aneurysms

A false aneurysm is a pulsating haematoma, the cavity of which is in direct continuity with the lumen of an artery. It is contained by a fibrous capsule consisting of adventitia and surrounding tissues rather than the layers of the vessel wall. False aneurysms can result from trauma, occur at the site of anastomosis, maybe secondary to i.v. drug abuse or iatrogenic following insertion of percutaneous catheters, i.e. at angiography. As flow through the defect continues, the aneurysm will slowly expand and may be extremely rapid if infection is present, e.g. in intravenous drug abusers. Presentation is with a pulsatile mass, usually in the groin, or with rupture. Diagnosis is usually via duplex ultrasound. Management depends on the cause and size of the aneurysm:

• If <2 cm, they will usually spontaneously thrombose
• Compression with an ultrasound probe until thrombosed. This may be combined with an injection of thrombin
• Surgical exploration and repair of defect
• Anastomotic false aneurysm may require revision (provided no infection is present)
• In IVDUs infection is often present and this may have destroyed the femoral vessels. Here, the only option is to ligate all vessels. This is associated with a high rate of limb loss or disabling claudication.

Other vascular problems

Thromboangiitis obliterans (Buerger’s disease)

This affects small vessels of the extremities. It occurs almost exclusively in young males who are heavy cigarette smokers. It may be associated with migratory thrombophlebitis.

Symptoms and signs

Claudication in the muscles of the foot. Digital pain, cyanosis, coldness progressing to necrosis and gangrene. Ankle and wrist pulses disappear first and the proximal pulses remain normal. Progressive digital ischaemia occurs with eventual loss of feet and hands.

Investigations

Arteriography reveals discrete foci of occlusions alternating with apparently uninvolved arterial segments in the distal circulation.

Treatment

It is essential to stop smoking to avoid progression of the disease. Sympathectomy is only of temporary benefit – if the patient continues smoking, amputation is necessary for rest pain or gangrene. Reconstructive surgery is rarely possible because the disease involves the small distal vessels. Repeated prostacyclin infusions (Iloprost) may be beneficial.

Raynaud’s phenomenon

This is a vasospastic condition of diverse aetiology. The following conditions have been implicated:

• Systemic diseases or conditions, e.g. collagen diseases (scleroderma), cryoglobulinaemia, myxoedema, macroglobulinaemia
• Compression syndromes, e.g. carpal tunnel syndrome, cervical rib, thoracic outlet syndrome
• Occupational trauma, e.g. vibration-induced white finger (pneumatic drill, chainsaw, grinders), piano playing, typing, cricket.

Symptoms and signs

Sequential changes of pallor, cyanosis and rubor, particularly after exposure to cold. This represents vasoconstriction followed by reflex vasodilatation. In severe long-standing cases tissue necrosis may occur involving non-healing ulcers and gangrene of the extremities. Tissue necrosis always denotes underlying pathology, i.e. the patient has secondary Raynaud’s as opposed to primary Raynaud’s disease.

Investigations

• FBC
• Platelets
• ESR
• CXR (cervical rib)
• Cold agglutinins
• Serum protein electrophoresis
• Autoantibody screen
• Rheumatoid factor
• LE cells
• Arteriography.

Treatment

• Treatment of underlying disorder, e.g. excise cervical rib
• Avoidance of cold exposure – heated gloves and boots
• Stop smoking
• Advice from Raynaud’s and Scleroderma Association
• Drugs, e.g. calcium channel blockers (nifedipine), naftidrofuryl, i.v. prostaglandins (Iloprost)
• Plasmapheresis
• Sympathectomy (relatively ineffective)
• Very rarely amputation may be required.

Diabetic foot

Contributory factors include microangiopathy, peripheral neuropathy, impaired immunity, impaired tissue metabolism, and the glucose-rich environment, which favours bacterial overgrowth.

Symptoms and signs

The patient may present with either a neuropathic foot or an ischaemic foot with signs of both large and small vessel disease. The neuropathic and ischaemic elements frequently co-exist.

The neuropathic foot is warm, dry with palpable pulses. Calluses may be present, as may painless penetrating ulcers at pressure points and sites of minor injury. Painless necrosis of the toes may occur. Spreading infection can occur along plantar spaces. There is usually general loss of pain and thermal sensation. In severe cases, Charcot’s joints may result.

The ischaemic foot is cold with absent pulses, calluses, painful ulcers, claudication and rest pain.

Investigations

• FBC
• U&E
• Glucose
• HbA1c
• Blood culture if systemically unwell
• X-ray foot for osteomyelitis
• Duplex ultrasound
• ABPIs to assess extent of vascular disease.

Treatment

Neuropathic foot

• Control diabetes
• Stop smoking
• Lose weight
• Refer for chiropody to remove calluses
• Treat infections with antibiotics. Antiseptics and dressings may be required for ulcers
• Remove necrotic tissue
• Ray amputations with filleting out of dead tissue until healthy bleeding tissue is obtained
• Weight-bearing areas should be protected by specialized footwear.

Ischaemic foot

• Control diabetes
• Stop smoking
• Lose weight
• Chiropody
• Treat infection with antibiotics
• MRA with a view to possible arterial reconstruction or angioplasty
• Major amputations, e.g. below knee or above knee; minor amputations are rarely successful when the major element is ischaemic.

Thoracic outlet syndrome

This represents a variety of symptoms related to arterial, venous and nerve compression as they exit from the chest. Compression usually occurs in the area bounded by the clavicle, the first rib and the scalenus anterior muscle. Causes include:

• An anatomically tight thoracic outlet and compression occurs between 1st rib and clavicle
• Hypertrophy of the scalene muscles
• Cervical rib (present in <1% of population)
• Fibromuscular band (from C7)
• Clavicle or 1st rib fractures or exostoses.

Symptoms and signs

Neurological

More common cause. Presents with sensory and motor deficit in the distribution of C8/T1. Symptoms can be exacerbated by movement or arm position and tend to be worse at night.

Arterial

Less common. Claudication or rest pain. Distal arterial disease may be due to embolization from an area of dilatation or frank aneurysm just beyond subclavian artery compression. Raynaud’s phenomenon may be present.

Venous

Venous hypertension – compression of subclavian vein or axillary vein thrombosis (Paget–von Schrötter syndrome).

Investigations

• CXR: cervical rib (the CXR should include the thoracic inlet and the total number of ribs on a particular side counted – if there are 13, then a cervical rib is present)
• Duplex Doppler – in positions of provocation, e.g. with the arm raised above the head, will give more functional information about the impingement on the subclavian artery than will angiography
• MRA: to assess vessel compression (with stress views) – subclavian artery stenosis or constriction by fibrous band
• Venography: compression of subclavian vein or subclavian vein thrombosis
• Nerve conduction studies to distinguish from carpal tunnel syndrome.

Treatment

With minimal neurological symptoms, shoulder girdle exercises may be appropriate. For severe compression, surgical decompression of the thoracic outlet with division of fibrous bands or removal of the first rib or cervical rib if present. Aneurysms may need to be resected and repaired. For patients presenting with primary axillary vein thrombosis (Paget–von Schrötter syndrome), treatment is with a combination of thrombolysis, anticoagulation and early decompression of the thoracic outlet.

Arteriovenous fistula

Two types exist:

• Congenital – May present as multiple small lesions. Present from birth. Clinically manifest 10–20 years. May enlarge to involve most of the limb
• Acquired – Due to trauma, e.g. stabbing, arteriography, iatrogenic for dialysis. Usually history of trauma and typically single communication.

Symptoms and signs

Pain and swelling in area of fistula. Enlarged tortuous arteries and veins. Increased skin temperature. Elongation of limb. Venous hypertension distally. Ischaemia distally. Palpable thrill. Continuous machinery bruit.

Investigations

• CXR for cardiomegaly
• Limb radiograph for bone elongation
• Duplex Doppler – non-invasive
• MRI: this will show the true extent of the lesion, which is nearly always more extensive than appears to be the case clinically
• Arteriography: this should only be performed if consideration is being given to embolization.

Complications

Cosmetic, haemorrhage, thrombosis, distal ischaemia, venous hypertension in limb, high output cardiac failure (Branham’s sign – compression of the fistula results in a fall in the heart rate).

Treatment

Not all arteriovenous fistulae require treatment. Small peripheral fistulae may be observed and frequently will never cause difficulties. Indications for intervention include haemorrhage, expansion, severe venous or arterial insufficiency, cosmetic deformity and heart failure. Most fistulae are now managed by embolization under radiographic control. Simple ligation of feeding vessels should never be performed. Recurrence is inevitable and when recurrence does occur, previous ligation means that it is difficult to perform angiography and embolization. Embolization and excision may be required for very large lesions.

Vascular access for haemodialysis

Vascular access may be obtained either by a dual lumen catheter placed in a central vein (internal jugular, femoral or subclavian) or the creation of an arteriovenous fistula. Dual lumen catheters are often the first-line management for patients presenting with acute renal failure (as many as 30% of patients with renal failure present in the acute stage). Central lines may be tunnelled and used long term in some patients who have no alternative route for vascular access. Preferred long-term route for haemodialysis is via an arteriovenous fistula. This is created by anastomosing a superficial vein to a nearby artery. Flow in the vein significantly increases and over the next 4–6 weeks the veins will dilate and become suitable for needling. The most common form of fistula is the radiocephalic fistula created between cephalic vein and radial artery either at the anatomical snuff box or at the wrist. The fistula is usually created initially in the non-dominant arm (so as to be accessible for the patient to needle). In the event of failure of a radiocephalic fistula, or lack of suitable veins to create one in the first place, fistulae may be performed at the elbow (brachiocephalic fistula, brachiobasilic fistula) or ePTFE grafts may be placed in the forearm in either straight or looped configuration or as a loop in the thigh.

Complications

• Immediate – bleeding
• Early – infection and thrombosis
• Late – steal syndrome (the hand becomes ischaemic as blood is diverted into the fistula and away from the arteries supplying the hand); aneurysmal varix formation; high output cardiac failure; venous hypertension.

Amputations

Indications for amputation

• Vascular, e.g. severe rest pain with arteries unsuitable for reconstruction, gangrene
• Trauma
• Infection, e.g. gas gangrene, osteomyelitis
• Tumour, e.g. osteogenic sarcoma, soft tissue sarcomas, subungual melanoma
• Useless limb, e.g. poliomyelitis, severe brachial plexus lesions associated with vascular damage.

Principles of amputation

• Select the appropriate level. Must be adequate circulation at that level to ensure healing. Tissues must show healthy bleeding at time of surgery
• Amputation level must take into account the fitting of a prosthetic limb
• Assess joints. Contractures or arthritis may influence the amputation level.

Preparation for amputation

A major amputation is a disfiguring operation. Fully explain the operation to the patient who may take a while to accept that it is necessary. Preoperative physiotherapy and occupational therapy should be undertaken and a visit made to the Limb Fitting Centre. Ensure that the patient is pain-free. Epidural anaesthesia may be useful in this context. Give antibiotic (penicillin) with induction of anaesthesia, which is prophylactic against Clostridium perfringens (gas gangrene).

Types of amputation

Minor

This involves simple amputation at the base of the digit, or ‘ray’ amputations where, e.g. in the foot, the metatarsal head and tendons are removed. This type of amputation is useful in diabetics, Buerger’s disease and severe Raynaud’s. Occasionally for ischaemia of all toes, transmetatarsal amputation may be undertaken. This requires a long plantar flap of skin to be successful. The indications are as above.

Major

Below-knee amputation

This provides the patient with the best chance of mobilizing with a prosthesis. Healing can be expected in 80% of patients. Below knee amputation is suitable in diabetics with a palpable popliteal pulse, Buerger’s disease and in some patients with arteriosclerosis. Contraindications include ischaemia extending to involve the posterior skin flap, fixed flexion contractures and occlusion of the profunda femoris artery. The standard tibial stump is 8–12 cm long and the fibular is transected slightly higher. A long posterior flap with muscle is fashioned and this is folded over to cushion the bone end. Function is variable, less than half the patients being independently mobile at 2 years.

Gritti–Stokes amputation

This amputation involves opening the knee joint, transecting the femur just above the femoral condyles and folding the anterior portion of the patella over the end of the femur. It is claimed to result in less blood loss than above knee amputation, to provide a better lever in bed bound patients and, in bilateral amputees, provides a more stable sitting position.

Above-knee amputation

This is a common amputation in patients with arteriosclerosis. The stump of the femur is 25 cm long measured from the greater trochanter. Equal anterior and posterior myoplastic flaps sutured over the bone end.

Less-frequently performed amputations

These include Lisfranc (tarsometatarsal disarticulation), Chopart’s (tarso-tarsal disarticulation) and Symes (ankle disarticulation). They are rarely used and are of historical significance only. Disarticulation at the hip and hindquarter amputations are usually performed for major trauma or malignancy, although they are sometimes used for vascular disease (aorto-iliac).

Postoperative care

Pain relief

The aim is to prevent breakthrough pain rather than treating pain once it occurs.

Care of the good limb

This involves physiotherapy. It is important to avoid pressure ulcers by nursing on sheepskin or air bed.

Physiotherapy

Build up muscle power and coordination. Start as soon as the patient is comfortable and continue in gymnasium. The aim is to prevent contractures and ensure rapid mobilization with prosthesis.

Prosthesis

Measure patient as soon as stump shrinks and volume of stump is stable.

Complications

Early

These include haemorrhage, haematoma, abscess, gas gangrene, wound dehiscence, ischaemic flaps and fat embolism.

Late

These include pain, sinus formation, osteomyelitis, neuroma, phantom limb and ulceration of the skin (pressure from prosthesis or continuing ischaemia).

Venous disorders

Varicose veins

These are dilated tortuous veins. They are divided into primary and secondary.

Primary varicose veins are the most common and are often familial. They are possibly due to weakness of the superficial vein wall that allows dilatation of the valve ring allowing the valve to become incompetent with retrograde flow. This then leads to increased venous pressure and further valve failure. Other contributory factors include prolonged standing, family history, hormonal factors (more common in pregnancy – progesterone has an effect on the vein wall), ageing.
Secondary varicose veins may be classified as follows:

• Obstruction to venous outflow, e.g. pregnancy, fibroids, ovarian cysts, abdominal lymphadenopathy, pelvic cancer, iliac vein thrombosis or retroperitoneal fibrosis
• Valve destruction, e.g. DVT
• High flow and pressure, e.g. AV fistulae.

Symptoms and signs

Tortuous dilated veins of the great or small saphenous system. Aching discomfort worse towards the end of the day, relieved by sitting with legs elevated. May present with complications (see below). Examine the patient standing up and assess the site and size of the veins. Palpate for defects in the fascia. Check the state of the skin and subcutaneous tissue. Carry out Trendelenburg’s test to assess the site of incompetent perforating veins. This is carried out with the patient supine, the leg being elevated and the tourniquet applied just below the saphenofemoral junction. The patient then stands erect for 30 s. If the saphenous vein fills rapidly from below with the tourniquet in place, the perforators lower down the legs are incompetent. If the long saphenous vein fills rapidly from above following removal of the tourniquet, the valve at the saphenofemoral junction is incompetent. Repeat at different levels down the leg to determine the level of incompetent perforators.

In practice, Trendelenburg’s test is rarely used nowadays and has been replaced by hand-held Doppler machine (see below). If a swelling is apparent over the saphenofemoral junction (saphena varix), the diagnosis should be confirmed by placing the hand over the swelling and tapping the varicose veins lower down the legs. A palpable thrill at the groin will confirm the presence of a saphena varix. Auscultation over the veins should be carried out to exclude arteriovenous fistulae. Perthes test may be performed to exclude deep venous obstruction (tourniquet applied below the saphenofemoral junction and the patient has to exercise on the spot. Severe ‘bursting’ pain indicates obstruction of the deep venous system.) but this is usually assessed by duplex Doppler nowadays.

Investigations

Diagnosis usually made on clinical grounds with hand-held Doppler assessment. In difficult or recurrent cases, Duplex ultrasound may be used. If a secondary cause is suspected, then abdominal ultrasound can be performed.

Procedure

How to perform hand-held Doppler assessment of varicose veins

The patient is examined with the legs exposed from the groin downwards. The leg to be examined is turned outwards with the legs slightly apart. For SFJ incompetence, the femoral artery is located and the probe moved medially, squeezing and releasing the calf until antegrade blood flow is heard in the femoral vein (a ‘whoosh’ on compression but not on releasing). Move the probe inferomedially to identify the great saphenous vein. If there is reflux, this should be heard as a ‘whoosh’ with calf compression and a further ‘whoosh’ on releasing (lasting >1 s). The small saphenous vein can also be examined and this is done about 10 cm above the knee. The probe is moved from posterior to anterior while squeezing the calf. The saphenopopliteal junction is identified by turning the patient to face away from you, the popliteal artery is identified in the knee crease and moving medially, will identify the popliteal vein and lateral to it will be the small saphenous vein. Compression of the calf again allows determination of antegrade flow and any reflux.

Complications

Superficial thrombophlebitis. Haemorrhage. Varicose eczema. Varicose pigmentation due to haemosiderin deposition. Lipodermatosclerosis. Chronic venous ulceration. Long-standing venous stasis ulcers may become malignant (Marjolin’s ulcer).

Treatment

Mild varicosities – compression stockings and periodic elevation of the legs. Small varicosities below the knee are suitable for injection with a sclerosing agent and compression bandaging worn for 2 weeks. This treatment can also be used for remaining varicosities after surgery. Surgery is indicated for saphenofemoral incompetence, saphenopopliteal incompetence, or thigh perforators. Mark out the varicose veins prior to surgery. Surgery includes saphenofemoral disconnection and stripping for incompetence of the great saphenous vein. Stripping is generally only performed to knee level. Saphenopopliteal disconnection can be used for varicosities involving the small saphenous system. Stripping is not performed, as this will risk damage to the sural nerve. Stab avulsions through tiny incisions at previously marked sites are used for residual veins. Compression bandaging is required postoperatively. Encourage early mobilization. Walk for 5–10 min every hour during the day. Sit with legs elevated postoperatively. Endoluminal techniques are being increasingly used, which result in quicker recovery and reduced postoperative pain. Techniques include laser and radiofrequency ablation.

Deep vein thrombosis (DVT)

This is a major cause of morbidity and mortality after surgery and trauma. It may occur spontaneously with high oestrogen contraceptive pill. HRT may be an aetiological factor. Only about 25% of DVTs cause symptoms and signs, others being silent. Pathological features (Virchow’s triad) leading to DVT include:

• Changes in the constituents of the blood
• Changes in the blood flow
• Changes in the vessel wall.

Predisposing factors include trauma and surgery, previous DVT, malignant disease, prolonged bed rest, cardiac failure, oestrogen-containing oral contraceptive pill, pregnancy, pelvic masses, obesity, dehydration, certain blood disorders, e.g. polycythaemia, thrombophilia (protein C, protein S, anti-thrombin III deficiency; factor V Leiden). In a UK study of all admissions to a district general hospital, 10% of all deaths were due to pulmonary embolism. In addition, up to 30% of patients in hospital have asymptomatic non-occlusive calf vein thrombosis.

Symptoms and signs

Swelling of the leg, tenderness of the calf muscles, increased temperature of the leg. Homans’ sign (calf pain on passive dorsiflexion of the foot) is insensitive, non-specific and potentially dangerous. Occlusion of the iliofemoral segment produces gross swelling of the whole limb, which is painful and white (phlegmasia alba dolens). Complete blockage of the iliofemoral segment with extension of thrombosis into venules and capillaries causes extreme pain with bluish discoloration and impending venous gangrene (phlegmasia caerulea dolens).

Investigations

• D-Dimer (cleavage fragment from formed thrombus – can be elevated in malignancy, infection and postoperatively)
• Duplex ultrasound
• Venography – very rarely indicated nowadays.

Treatment

The aims of treatment are to prevent propagation of the clot, minimize the risk of pulmonary embolism (PE) and to reduce the chance of developing post-thrombotic syndrome in the future.

Prevention

General measures include adequate hydration, avoiding calf pressure, and early postoperative mobilization. Some authorities recommend stopping oral contraceptives at least 6 weeks prior to surgery, while others merely recommend heparin prophylaxis. The case for stopping HRT is controversial. Patients at special risk should be treated as follows:

• Low molecular weight heparin, e.g. subcutaneous Clexane 20 mg daily
• Calf compression devices used intraoperatively
• Graded compression stockings, i.e. thromboembolic deterrent (TED) stockings. These should be worn preoperatively, intraoperatively and postoperatively until the patient is mobilizing satisfactorily.

Therapeutic

Once the diagnosis has been confirmed, then anticoagulation is commenced. This may be with i.v. unfractionated heparin or treatment dose of low molecular weight heparin. This is then converted to oral warfarin and maintained at an INR of 2–2.5 for 3–6 months. Limb elevation when resting. Calf exercises. Compression stockings. Surgery or an endovascular approach may be required. A reduction in post-thrombotic syndrome has been shown following early recanalization leading to preservation of valvular competence. However, in UK practice, it is usually only used if there is an extensive iliofemoral DVT in a young patient with a mechanical cause for the DVT or with a threatened limb with impending venous gangrene. Techniques used include:

• Catheter directed thrombolysis – catheter is directed into the thrombus for local delivery of thrombolytic agents
• Percutaneous mechanical thrombectomy – device used that actually breaks down the thrombus (may be combined with thrombolysis)
• Surgical thrombectomy – surgical removal of the thrombus.

In some cases, anticoagulation may fail, be contraindicated or result in complications. In these cases, an IVC filter may be required to prevent PE. Indications for a filter include:

• Contraindication to anticoagulation, e.g. risk of bleeding
• Thromboembolic event despite adequate anticoagulation
• Complication of anticoagulation, e.g. bleeding
• Inability to achieve adequate levels of anticoagulation
• Free-floating IVC thrombus.

Chronic venous insufficiency

This is caused by persistent and sustained ambulatory venous hypertension. Causes include:

• Muscle pump dysfunction, e.g. fused ankle in arthritis or neurological impairment after CVA
• Abnormal valve function which may be primary (affecting both the superficial and deep veins) or secondary after DVT with destruction of deep valves (known as post-phlebitic limb)
• Congenital valve absence (very rare).

Along with changes in the large veins that result in venous hypertension, there are several abnormalities at the microcirculatory level. These include:

• White blood cell trapping. WBCs become trapped in capillaries and cause endothelial activation and release of inflammatory cytokines which increase vascular permeability and contribute to the presence of a fibrin cuff together with release of proteolytic enzymes and free radicals. In addition they cause tissue ischaemia by blocking capillaries.
• Fibrin cuff. An increase in venous pressure is transmitted to the capillaries and opens endothelial pores resulting in molecules such as fibrinogen moving into the interstitial space. This polymerizes to fibrin and may act as a barrier to oxygen diffusion causing local tissue ischaemia.

Symptoms and signs

• Peripheral oedema. This gets worse towards the end of the day and tends to settle with elevation
• Varicose veins
• Venous eczema and brawny induration of the skin
• Venous pigmentation associated with haemosiderin deposits in the tissues
• Venous stasis ulceration, which is common in the area of the medial malleolus
• There is often severe pain associated with the swelling and ulceration
• Venous claudication. This indicates obstruction of the deep venous system. It is described as a ‘bursting’ pain which comes on with exercise and takes 10–20 min to settle.

Investigations

• Hand-held Doppler – to assess superficial venous incompetence and can allow assessment of arterial system (via ABPIs)
• Duplex Doppler – allows assessment of both superficial and venous systems
• Venography (rarely used).

Treatment

Difficult to treat and patient rarely gets complete relief.

Medical

Advise patient to avoid long periods of standing and to sit with legs elevated. Graduated compression stockings or 4-layer bandaging (ensure ABPI >0.8 before using compression). Treat venous stasis ulcers by reducing swelling of the leg by bandaging, excision of necrotic tissue and control of any cellulitis with antibiotics. Clean ulcers with normal saline, osmotic preparations, or enzymatic preparations. Emollients for venous eczema.

Surgery

Options for surgical intervention include:

• Superficial venous surgery. As for management of varicose veins and includes ligation of the SFJ and stripping of the GSV. Useful in isolated superficial reflux or combined deep and superficial reflux. Has been shown to aid healing of ulcers
• Perforator vein surgery. Involves use of an endoscope to locate and ligate venous perforators. Has been shown to achieve good rates of ulcer healing
• Deep vein surgery. Rarely indicated. Options include veno-venous bypass, vein transposition and vein valve transplantation
• Ulcer debridement and skin grafting
• Amputation. Carried out if ulceration becomes complicated or is intractable.

Superficial thrombophlebitis

This is characterized by a local inflammation of a segment of superficial vein. The vein is tender, red and feels like a ‘cord’. The causes are shown in Table 15.3. Treatment is usually symptomatic and depends on the underlying cause. However, when it involves the great saphenous vein at the saphenofemoral junction, this has a risk of thromboembolism and is treated as for a DVT with anticoagulation or urgent ligation.

Table 15.3 Causes of superficial thrombophlebitis

Varicose veins
Occult carcinoma:

• bronchus
• pancreas
• stomach
• breast

Mondor’s disease – superficial thrombophlebitis on chest wall Buerger’s disease Polycythaemia Local bacterial infection Polyarteritis Iatrogenic – intravenous infusions Drug abuse Idiopathic

Lymphoedema

This is a condition of localized fluid retention and tissue swelling due to hypoplasia or obstruction of lymphatics. It may be primary or secondary.

Primary

Primary lymphoedema can be classified into two subsets: isolated, where the condition is not inherited and familial where there is a definite inherited trait. Further sub-divisions can then be made according to the age of onset. Congenital hereditary lymphoedema presents at birth or within the first 2 years of life. Milroy’s disease is an autosomal dominant familial form of congenital lymphoedema. Lymphoedema praecox occurs at puberty or shortly afterwards. Lymphoedema tarda occurs after the age of 30. However, lymphoedema presenting for the first time in later life should prompt a search for underlying malignancy, especially pelvic.

Secondary

Lymphatic obstruction may occur secondary to other disease processes, e.g. secondary neoplasms in lymph nodes, infection in lymph nodes, e.g. filariasis (common worldwide, rare in UK) or may occur following surgical removal of lymph glands, i.e. block dissection or radiotherapy.

Symptoms and signs

There is progressive swelling of one or both extremities, usually beginning around the ankle but often involving the whole extremity. The scrotum may be involved. Oedema is non-pitting and does not settle with elevation. Often the leg aches and feels tight but there is no pain. Minor trauma will cause cellulitis. Need to differentiate from other causes of leg swelling (→ Table 15.4).

Table 15.4 Causes of swelling of the leg

Local  
Acute swelling Trauma
DVT
Cellulitis
Allergy
Rheumatoid
Ruptured Baker’s cyst
Chronic swelling Venous:
•varicose veins (uncomplicated varicose veins rarely cause leg swelling)
•obstruction to venous return, e.g. pregnancy, pelvic tumours, IVC
•obstruction, post-phlebitic limb
Lymphoedema
Congenital malformations, e.g. arteriovenous fistulae
Paralysis (failure of muscle pump)
Dependency
General Congestive cardiac failure
Hypoproteinaemia, e.g. liver failure
Nephrotic syndrome, malnutrition
Renal failure
Fluid overload
Myxoedema

Investigations

Lymphoedema is essentially a clinical diagnosis and no further investigations are required in the great majority of patients. Where investigations are necessary, the following may be used:

• Lymphoscintigraphy
• Lymphangiography (used rarely). Isotope lymphoscintigraphy is easy to perform and less traumatic for patients than lymphangiography
• CT scan to exclude pelvic malignancy.

Treatment

It is important that lymphoedema is differentiated from other causes of lower limb swelling. Treatment is either medical or surgical. The aim of treatment is to control the oedema and to prevent infection. Compression stockings or compression devices (Flowtron therapy) are the mainstay of treatment. Check ABPIs before applying compression. Compliance is essential. Diuretics are contraindicated in lymphoedema. Avoid prolonged standing. Massage. Exercise. If any breaks in the skin occur, e.g. insect bites or minor trauma, antibiotics should be prescribed. Cellulitis and fungal infections should be treated promptly. Occasionally, surgical treatment is helpful but does very little to improve the cosmetic appearance. Surgery is only suitable for a minority of patients. The choices include reduction procedures (excess tissue is removed and the defect either closed directly or skin grafted) or bypass (via omental pedicles, anastomosing lymph nodes to veins or direct lymphovenous anastomosis). Complications include recurrent cellulitis and lymphangitis usually caused by Streptococci, which respond to penicillin. Lymphangiosarcoma may occur. The tendency is for steady progression of the swelling and recurrent infections.

Vascular trauma

This includes penetrating trauma (90%), blunt trauma and iatrogenic trauma. In penetrating trauma, the vessel may be partially or completely transected. High velocity gun shot wounds cause massive tissue loss and extensive vascular damage. With blunt trauma, vessels can be injured directly, e.g. crush injury or indirectly by distraction, e.g. fractures and dislocations. Iatrogenic trauma may occur during surgery, angiography, angioplasty, or while obtaining access to the circulation, e.g. arterial lines and CVP lines. It may also occur with accidental intra-arterial injection, e.g. intravenous drug abusers. Prompt diagnosis and treatment are essential to save life and limb. Complete transection of an artery because of penetrating trauma may stop bleeding, owing to vessel retraction. Partial transection is more serious as the remaining intact wall holds the vessel open, resulting in torrential haemorrhage. Blunt injury usually leads to an intimal tear with a resulting intimal dissection flap, which may compromise the distal circulation. Arteriovenous fistula may occur when an artery and a vein close to each other are injured. Venous injuries are usually due to penetrating trauma. Haemorrhage and/or thrombosis may result.

Symptoms and signs

Mechanism of injury, degree of violence, type of weapon, time of incident. Hypotension. Hypovolaemic shock. Clinical signs can be divided into HARD signs (pulseless cold limb, expanding and/or pulsatile haematoma, palpable thrill or audible bruit and active bleeding) and SOFT signs (history of bleeding from wound, injury close to the course of a major vessel, haematoma, neurological injury). Associated injuries, e.g. nerve injuries, fractures, head injury.

Investigations

There may be no time for investigations, as urgent transfer to theatre may be required.

• Plain radiographs if time permits, e.g. fractures, position of bullets or foreign bodies
• Pulse oximetry can assess oxygen saturation in both limbs – a decrease may indicate injury
• ABPIs – compare injured to uninjured limb – a ratio of <1 in a healthy limb indicates vascular compromise
• Duplex ultrasound
• CT angiogram
• Angiography – this is both diagnostic and therapeutic (placement of covered stents for bleeding and stents for intimal flaps).

Treatment

Principles of treatment include:

• Arrest of haemorrhage
• Management of airway
• Correction of hypovolaemia
• Diagnosis of type and degree of injury
• Repair of vessels
• Management of associated injuries
• Rehabilitation.

Emergency measures

Initial management should be guided by ATLS principles with attention to airway and breathing first. Circulation is addressed with insertion of two large-bore i.v. lines and compression of any external haemorrhage (tourniquet should not be used). Major thoracic penetrating injuries – emergency thoracotomy is occasionally necessary to control bleeding. In exsanguinating penetrating abdominal trauma, it may be necessary to perform a thoracotomy or laparotomy to cross clamp the aorta. Fracture/dislocations with obvious deformity and distal ischaemia need reduction and splinting. If no vascular injuries are obvious (i.e. no hard signs) then any investigations are carried out after the primary survey is completed and the patient is stable.

Principles of surgical management include:

• Fractures should be stabilized before vascular repair. A shunt can be inserted during orthopaedic repairs if necessary (suitable for large and medium sized arteries).
• Simple lacerations may be closed by direct suture.
• Lacerations in smaller arteries can be closed by a vein patch.
• In vessels that are transected, end-to-end anastomosis can be performed. If the ends are far apart, then an interposition graft using either reversed autologous vein or PTFE may be used.
• In complex injuries, bypass procedures may be required after ligation of major arteries. These may need to be extra-anatomic (i.e. running in a different course to the bypassed artery), to provide tissue coverage in major injuries.
• In some cases, the patient may be too unstable for complex vascular reconstruction. In these cases, vessels may be simply ligated (external carotid, subclavian artery, internal iliac artery may be ligated with little sequelae and virtually all veins other than the suprarenal IVC and portal vein can be ligated).
• Packing can be used for venous bleeding but it is unlikely to stop arterial bleeding.
• Fasciotomy should be performed in prolonged ischaemia to prevent compartment syndrome. Rarely, amputation may be required for the unsalvageable limb.

Complications

Thrombosis. Secondary haemorrhage. False aneurysm. AV fistulae. Compartment syndrome. Lymphatic leaks or lymphocele due to damage of lymphatic vessels. Distal vascular insufficiency. Ischaemic muscular contractures.

Procedure

Femoral embolectomy

The stages of a femoral embolectomy are as follows:

• A longitudinal incision is made in the groin over the femoral artery at the mid-inguinal point, i.e. halfway between the anterior superior iliac spine and the pubic symphysis. This is the surface marking of the femoral artery which will not be palpable due to the embolism.
• The incision is extended through the subcutaneous fat to the femoral vessels. The common femoral, superficial femoral and the profunda femoris arteries are dissected free and controlled with vascular slings.
• An arteriotomy is made in the artery directly over the origin of the profunda femoris artery. This may be a transverse incision which is less likely to lead to subsequent stenosis or longitudinal, which is easier to extend if a bypass operation becomes necessary.
• A 5F embolectomy catheter is passed up the common femoral into the iliac vessels. The balloon is inflated and gently withdrawn.
• Once the clot is retrieved, an assistant will need to control the inflow with the vascular sling and a vascular clamp (return of inflow with clot withdrawal will lead to a sudden gush of blood). This is repeated until no further clot is retrieved and the surgeon is happy with the inflow. The common femoral artery is then flushed with heparinized saline and clamped.
• A 4F embolectomy catheter is now passed down the profunda femoris artery and the superficial femoral artery. Once no more clot is retrieved and the surgeon is happy with the degree of back bleeding the vessels are flushed with heparinized saline and clamped.
• The arteriotomy is closed with interrupted 6/0 Prolene sutures.
• Fascia and subcutaneous fat is closed with 3/0 Vicryl and clips are used for skin closure.

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