Classification of limb ischaemia
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ischaemic syndromes
Classification of limb ischaemia
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Apart from paralysis (inability to wiggle toes or fingers) and anaesthesia (loss of light touch over the dorsum of the foot or hand), the symptoms and signs of acute ischaemia are non-specific or inconsistently related to its completeness. Pain on squeezing the calf indicates muscle infarction and impending irreversible ischaemia.
Symptoms and signs of acute limb ischaemia
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Acute arterial occlusion is associated with intense spasm in the distal arterial tree, and initially the limb will appear “marble” white. Over the next few hours, the spasm relaxes and the skin fills with deoxygenated blood leading to mottling that is light blue or purple, has a fine reticular pattern, and blanches on pressure. At this stage the limb is still salvageable. However, as ischaemia progresses, stagnant blood coagulates leading to mottling that is darker in colour, coarser in pattern, and does not blanch. Finally, large patches of fixed staining progress to blistering and liquefaction. Attempts to revascularise such a limb are futile and will lead to life threatening reperfusion injury. In cases of real doubt the muscle can be examined at surgery through a small fasciotomy incision. It is usually obvious when the muscle is dead.
Differentiation of embolus and acute arterial thrombosis (thrombosis in situ)
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Acute limb ischaemia is most commonly caused by acute thrombotic occlusion of a pre-existing stenotic arterial segment (60% of cases) or by embolus (30%). Distinguishing these two conditions is important because treatment and prognosis are different. Other causes are trauma, iatrogenic injury, popliteal aneurysm, and aortic dissection.
More than 80% of peripheral emboli arise from the left atrial appendage in association with atrial fibrillation. They may also arise from the left ventricle, heart valves, prosthetic bypass grafts, aneurysmal disease, paradoxical embolism, and atrial myxoma (rare). In 15% of cases the source of embolus is obscure. Thrombosis in situ may arise from acute plaque rupture, hypovolaemia, or pump failure (see below).
Factors predisposing to acute thrombosis
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A leg affected by embolus is nearly always threatened and requires immediate surgical revascularisation. Emboli usually lodge at the common femoral bifurcation or, less commonly, the popliteal trifurcation. Femoral embolus is associated with profound ischaemia to the level of the upper thigh because the deep femoral artery is also affected. A femoral pulse does not exclude the diagnosis. Embolectomy can be done under local, regional, or general anaesthetic.
The adequacy of embolectomy should be confirmed by angiography while the patient is on the operating table. On-table thrombolysis should be considered if mechanical clearance has been unsuccessful. If the embolus has occurred in an area of longstanding atherosclerotic disease, surgical bypass may be necessary.
Postoperatively the patient should continue to receive heparin to prevent formation of further emboli. Many surgeons postpone heparin for six hours after surgery to reduce the risk of a haematoma forming. Warfarin reduces the risk of recurrent embolism, and unless contraindicated, should be prescribed to all patients long term. Patients should not be given warfarin without first being on heparin for 48 hours since warfarin can produce a transient procoagulant state due to inhibition of the vitamin K dependent anticoagulant proteins C and S.
Opinions differ about how thorough you should be in establishing the source of emboli. Transthoracic echocardiography is poor at detecting a thrombus in patients with atrial fibrillation, and a negative result does not exclude the diagnosis. Transoesophageal echocardiography provides excellent views of the left atrium but is moderately invasive and not universally available. In patients with suspected paroxysmal tachyarrhythmias, 24 hour electrocardiographic monitoring should be considered. Even if no source of embolism is found, anticoagulation should continue long term.
Although immediate loss of a limb after correctly managed acute embolus is unusual, many series report a 10-20% in-hospital mortality from heart failure or recurrent embolism, particularly stroke.
Initial management of acute limb ischaemia Sensation and movement absent
Sensation and movement present
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The presence of distal pulses does not exclude serious arterial injury. Pulse oximetry, Doppler signals, and measurement of the ankle brachial pressure index may be helpful, but in cases of doubt, proceed to angiography.
General—Acidosis and hyperkalaemia occur due to leakage from the damaged cells, causing cardiac arrhythmias and myoglobinaemia, which can result in acute tubular necrosis. Acute respiratory distress syndrome may also develop, and gastrointestinal endothelial oedema may lead to increased gastrointestinal vascular permeability and endotoxic shock.