Limb Embolism and Ischaemia

See related article - Peripheral Vascular Disease.

Acute ischaemia is most often due to either acute thrombotic occlusion of a previously partially occluded, thrombosed arterial segment, or due to embolus. Without surgical revascularisation, complete acute ischaemia leads to extensive tissue necrosis within six hours. The effects of sudden arterial occlusion depends on the state of collateral supply.¹

• The collateral supply in the leg is usually inadequate unless there has been pre-existing occlusive disease.
• The subclavian artery has many collateral vessels so that occlusion of a major artery does not necessarily make a limb non-viable.

Critical limb ischaemia is a condition with chronic ischaemic at-rest pain, ulcers, or gangrene in one or both legs attributable to objectively proven arterial occlusive disease. Critical limb ischaemia implies chronicity and should be distinguished from acute limb ischaemia.²

• Embolism: e.g. left atrium in patients in atrial fibrillation, mural thrombus after myocardial infarction, prosthetic and abnormal heart valves, aneurysm (aorta, femoral, or popliteal), proximal atheromatous stenosis, malignant tumour, or foreign body.
• Thrombosis: most cases of leg ischaemia result from the presence of thrombus at sites of atherosclerotic narrowing; presentation of ischaemia may be:
  • Acute, as a result of emboli from rupture of proximal atherosclerotic plaque or thrombus
  • Chronic, usually resulting from gradual extension of thrombus with development of collateral vessels
• Trauma
• Raynaud's syndrome
• Compartment syndrome: occurs when perfusion pressure falls below tissue pressure in a closed anatomical space; causes include:
  • Orthopaedic (tibial or forearm fractures)
  • Vascular: haemorrhage, phlegmasia caerulea dolens (massive thrombosis in the major veins of the limbs causing gross swelling that obstructs arterial flow)
  • Soft-tissue injury (prolonged limb compression, crush injury, burns)
• Congenital causes of early-onset leg ischaemia, e.g. aortic hypoplasia
• Ischaemia of the arm is most often embolism from the heart but may also be due to damage to the subclavian artery or thoracic outlet syndrome

• History and examination should identify the severity of ischaemia and whether it is likely to be embolic or thrombotic.
• Important features to differentiate include rapidity of onset of symptoms, features of pre-existing chronic arterial disease, potential source of embolus and the state of pulses in the contralateral limb.
• The affected part becomes pale, pulseless, painful, paralysed, paraesthetic and 'perishing with cold' ('the 6 Ps').¹
• The onset of fixed mottling of the skin implies irreversible changes.
• The limb may be red when dependent, leading to a misdiagnosis of inflammation, e.g. gout or cellulitis.

• Hand held doppler USS may help demonstrate any residual arterial flow.
• Blood tests for full blood count (ischaemia is aggravated by anaemia), ESR (inflammatory disease, e.g. giant cell arteritis, other connective tissue disorders), glucose (diabetes), lipids and thrombophilia screen.
• If diagnosis is in doubt, perform urgent arteriography.
• Identify source of embolus: ECG, echocardiogram; ultrasound of aorta, popliteal and femoral arteries.

• Admit patient - this is an emergency and often requires urgent open surgery or angioplasty. Objective sensory loss requires urgent treatment. Immediately heparinise (may double limb-salvage rate) and provide analgesia.
• Ischaemia following trauma and acute thrombosis may require urgent reconstruction.
• The limb must be checked for evidence of compartment syndrome and if necessary a fasciotomy should be performed.
• If the occlusion is embolic, the options are surgical embolectomy (Fogarty balloon embolectomy catheter) or local intra-arterial thrombolysis.
• If embolectomy with a Fogarty catheter fails, an on-table angiogram is performed and bypass graft or intraoperative thrombolysis considered. Routine intraoperative angiography for arterial thromboembolectomy has been shown to be beneficial.³
• After successful embolectomy, anticoagulation with heparin to prevent recurrence. Many surgeons postpone heparin for six hours after surgery to reduce the risk of a haematoma.⁴
• Thrombotic disease: intra-arterial thrombolysis, angioplasty or bypass surgery. If due to thrombosis of an arterial graft, initially attempt thrombolysis.
• Intra-arterial thrombolysis:⁵
  Low-dose intra-arterial thrombolytic therapy, with subsequent angioplasty and stenting, is the initial treatment of choice for many patients with acute arterial occlusions.⁶
  • For patients with acute arterial emboli or thrombosis, treatment with immediate systemic anticoagulation with unfractionated heparin has been recommended. This should be followed by long-term warfarin in patients with embolism.⁷
  • An arteriogram is performed and the catheter advanced into the thrombus. Streptokinase, urokinase or tissue plasminogen activator (tPA) is combined with heparin and thrombolysis continued for 48 hours or until clot lysis.¹
  • Fibrinolysis usually takes between 6 and 72 hours to achieve clot lysis and so patients with limb-threatening ischaemia are not candidates for local fibrinolysis, and require emergent embolectomy.⁶
  • Local thrombolytic therapy is therefore reserved for patients with non–life-threatening limb ischaemia.⁶
  • Thrombolysis can be accelerated by using pulse spray through a multiple side-hole catheter, aspiration thrombectomy (debulking thrombus aspiration) and by using a high dose over a shorter time.
  • Complications of thrombolysis are haemorrhage, pericatheter thrombosis, haemorrhagic stroke and distal embolisation.
  • The contraindications are critical ischaemia with neurological deficit, irreversible ischaemic changes.
  • Recombant tissue plasminogen activator (the preferred agent): up to 60-90% of thromboses will show clinically useful lysis. However, there is a high rate of reocclusion.¹
  • Following successful lysis, correction of the underlying problem, possibly including angioplasty or operation, may be required.
• If limb is irreversibly ischaemic, amputation will be required.

Other management

• Reduction in the rate of deterioration of underlying cardiovascular disease includes regular exercise, smoking cessation, treating hypertension and hyperlipidaemia, improving diabetes control.
• Management of associated and underlying problems: treat anaemia or polycythaemia, cardiac disease.
• Low dose aspirin or clopidogrel. Warfarin if otherwise indicated.
• ACE inhibitors have been shown to reduce morbidity and mortality due to cardiovascular disease in patients with peripheral vascular disease by 25%.
• Statin to reduce total and LDL-cholesterol.

• Reperfusion injury may cause more damage than the initial ischaemia:
  • Neutrophils migrate into the reperfused tissue causing injury.
  • Limb swelling due to increased capillary permeability may cause a compartment syndrome.
  • Leakage from damaged cells may cause acidosis and hyperkalaemia (leading to cardiac arrhythmias) and myoglobinaemia (leading to acute tubular necrosis).
• Chronic pain syndromes: acute complete ischaemia can lead to peripheral nerve injury.

• Complete acute ischaemia will lead to extensive tissue necrosis within six hours unless the limb is surgically revascularised.⁴
• The mortality associated with acute ischaemia remains high as thrombosis or embolism is not infrequently a pre-terminal event in patients dying from other causes such as heart failure.
• Surgical treatment of acute limb ischaemia, because of related complications, has a 30-day mortality rate of 15% to 25%.⁸

• Long-term anticoagulation for potential causes of thromboembolism.
• Primary prevention cardiovascular disease; secondary prevention of cardiovascular disease.