Acute peripheral arterial occlusion - Hypertension and vascular diseases

Acute peripheral arterial occlusion

Definition

Acute loss of the arterial supply to a limb.

Incidence

Commonest vascular emergency.

Age

Increases with age.

Sex

M > F

Aetiology/pathophysiology

The most common causes are emboli and thrombus.

·        Ninety per cent of emboli arise from the heart, usually due to mural thrombus (e.g. as a complication of atrial fibrillation or postinfarction) or from abnormal, infected or prosthetic heart valves. Less than 10% arise from the large vessels, e.g. aortic aneurysm or atherosclerotic vessels.

·        Thrombosis may cause acute ischaemia usually arising on a pre-existing atherosclerotic plaque or within an aneurysm, causing complete occlusion. Hypo-volaemia or hypotension often precipitates complete occlusion. Less commonly thrombosis may arise in non-atherosclerotic vessels as a result of malignancy, polycythaemia or other hypercoagulable states.

·        Other causes of acute arterial occlusion include direct trauma and dissection of an aneurysm.

Loss of arterial blood supply causes acute ischaemia and irreversible infarction occurs if the occlusion is not re-lieved within 6 hours. After the occlusion is relieved there may be secondary damage due to reperfusion injury. This is due to the production of toxic oxygen radicals, which cause further cellular damage.

Clinical features

Patients present with a cold, pale/white and acutely painful limb, which becomes weak and numb with loss of sensation and paraesthesiae, which starts distally (pain becoming painless, pallor, paraesthesia, pulseless and paralysed). Paraesthesiae or reduced muscle power are signs of severe ischaemia. As the condition progresses, the skin becomes mottled with dusky patches. Muscle tenderness is a sign of ischaemic damage. Complete loss of muscle power with tender, firm muscles is a sign of muscle infarction.

Complications

Compartment syndrome may occur (muscle swelling secondary to ischaemia and reperfusion within rigid compartments between the bones and fascial layers causes increased tissue pressure, which rises above capillary perfusion pressures, such that there is further compromise of blood supply to the affected limb). Muscle necrosis leads to the release of high quantities of creatine kinase and myoglobin, which can cause acute renal failure by a direct toxic effect (rhabdomyolysis). Volkmann’s ischaemic muscle contracture may also occur.

Investigations

Angiography may be useful but should not delay surgery in critical limb ischaemia. In cases of emboli further post-operative investigation is required to establish the source of the embolus including ECG, echocardiography and abdominal ultrasound scan.

Management

Following assessment and resuscitation treatment involves the following:

·        Heparin to minimise propagation of thrombus, in very mild cases this will be sufficient.

·        Early cases and distal arteries may be treated medically initially with thrombolytic therapy delivered directly to the vessel under radiographic guidance.

·        Acute occlusion with signs of severe ischaemia is treated with emergency surgery. Embolectomy/thrombectomy is usually performed with a Fogarty balloon catheter under local anaesthetic if possible, and complex cases may require arterial reconstruction.

·        Compartment syndrome requires urgent fasciotomy.

Prognosis

Acute upper limb ischaemia tends to have a better prognosis, as there is better collateral supply. Unfortunately, acute lower limb arterial occlusion is more common. Amputation is uncommonly necessary, but mortality is as high as 20%, depending on the degree of ischaemia at presentation and overall fitness of the patient.