Acute Limb Ischaemia

Introduction

Acute limb ischaemia is a sudden reduction in arterial perfusion that threatens the viability of a limb, conventionally defined as developing within the preceding two weeks. It is one of the few conditions in which the delay between the first assessment and the definitive treatment translates almost linearly into tissue loss.

The relevant physiology is simply how long different tissues tolerate ischaemia. Peripheral nerve is the most sensitive and begins to fail within a few hours, which is why sensory and then motor loss are the ominous signs. Skeletal muscle tolerates roughly six hours of complete ischaemia before irreversible necrosis begins. Skin, bone and fat survive considerably longer. This hierarchy explains both the sequence of the six Ps and the classic teaching that the limb must be revascularised within six hours.

Incidence is roughly 15 per 100,000 per year.¹ Despite modern vascular services, the outcomes remain sobering: amputation rates of 10 to 15% and 30-day mortality of 15 to 20%, largely because these patients are elderly with substantial cardiac comorbidity.

Causes

Embolism

An embolus lodges where an artery narrows or bifurcates - most often at the common femoral bifurcation, then the popliteal trifurcation and the aortic bifurcation (a saddle embolus). Because the receiving artery is otherwise healthy and has no collaterals, the ischaemia is profound and the onset instantaneous.

• Atrial fibrillation - the commonest source by a considerable margin, from thrombus in the left atrial appendage
• Mural thrombus after myocardial infarction, particularly a large anterior infarct with an akinetic or aneurysmal segment
• Prosthetic heart valves and infective endocarditis vegetations
• Aneurysm - thrombus within an abdominal aortic or, particularly, a popliteal aneurysm. A popliteal aneurysm typically presents with ischaemia rather than rupture, and both popliteal fossae should be palpated in any patient with acute limb ischaemia.
• Atrial myxoma, and cholesterol embolisation from an ulcerated proximal plaque
• Paradoxical embolus through a patent foramen ovale, from a venous thrombosis
• Iatrogenic - dislodged thrombus during catheterisation or intervention

Thrombosis in situ

Thrombosis occurs on a pre-existing atherosclerotic plaque. Because the artery was already stenosed, collaterals have developed, so the ischaemia is often less severe and comes on over hours to days rather than instantly.

• Rupture or progression of an atherosclerotic plaque in a patient with known peripheral arterial disease
• Bypass graft occlusion, which is a common and often forgotten cause in a patient with previous vascular surgery
• Thrombosis of a popliteal aneurysm
• Low-flow states - hypovolaemia, sepsis, heart failure, dehydration - precipitating thrombosis in an already stenosed vessel
• Hypercoagulable states - malignancy, antiphospholipid syndrome, polycythaemia, thrombocythaemia, heparin-induced thrombocytopenia
• Aortic dissection extending into an iliac artery, and arterial trauma or dissection from injury or intervention
• Compartment syndrome and external compression

Clinical features

The six Ps, in the order in which they appear:

1. Pain - sudden, severe, constant, distal, and worse on passive movement of the muscles. It may paradoxically diminish as sensory nerves die, which is a bad sign and not an improvement.
2. Pallor - initially white, later mottled. Mottling that blanches on pressure indicates a salvageable limb; fixed, non-blanching mottling means the skin capillaries have thrombosed and the limb is not salvageable.
3. Pulselessness - confirm with a hand-held Doppler, since pulses can be impalpable in a cold or oedematous limb
4. Perishing cold (poikilothermia) - compare with the other leg and note the level at which the temperature changes, which is usually one joint below the occlusion
5. Paraesthesia - loss of light touch first, then proprioception and pinprick. This is a late sign and marks a threatened limb.
6. Paralysis - inability to move the toes or foot, with tenderness of the calf muscles. This is the latest sign and indicates an immediately threatened limb requiring surgery without delay.

The last two Ps are the ones that convert a limb from marginally to immediately threatened, and they are the reason that a careful sensory and motor examination is not optional.¹ Ask the patient to wiggle their toes, and test light touch between the toes on the dorsum of the foot.

Investigations

Acute limb ischaemia is a clinical diagnosis. In a Rutherford IIb limb, investigations must not delay theatre.

• Hand-held continuous wave Doppler at the bedside - the single most important investigation. Assess for arterial and venous signals at the ankle, and measure the ABPI if a signal is present.
• ECG - to identify atrial fibrillation or a recent myocardial infarction as an embolic source
• Bloods - FBC, U&Es, clotting screen, group and save, and a venous or arterial gas for lactate and potassium
• Creatine kinase - a baseline, and to monitor for rhabdomyolysis after reperfusion
• CT angiography - defines the level and nature of the occlusion and plans intervention. Appropriate in Rutherford I and IIa, and in IIb only if it can be obtained without delaying surgery.
• Echocardiography - after the acute event, to look for an embolic source
• Thrombophilia screen in a young patient with no obvious cause, taken before anticoagulation where possible

Management

Immediate measures

1. Telephone the vascular team immediately. This call precedes imaging and precedes writing the referral.
2. High-flow oxygen and continuous monitoring
3. Intravenous access and adequate analgesia with titrated opioid
4. Intravenous unfractionated heparin - a bolus followed by an infusion, titrated to APTT ratio. This does not dissolve the existing clot but prevents propagation and protects the collateral circulation and distal run-off. Confirm there is no contraindication and no likelihood of imminent surgery precluding it, and follow local protocol.
5. Nil by mouth, and intravenous fluid to optimise perfusion
6. Position the limb dependent to maximise perfusion pressure, and keep it in a warm room but do not apply direct heat, which raises the metabolic demand of already ischaemic tissue and can cause burns in an anaesthetic limb
7. Protect the heel and pressure areas, and avoid tight dressings or compression stockings
8. Correct any precipitating factor - rate control atrial fibrillation, correct hypovolaemia, treat sepsis

Revascularisation

After successful revascularisation, the underlying cause must be treated: lifelong anticoagulation for a cardiac embolic source, and antiplatelet therapy with a statin and risk factor modification for atherosclerotic thrombosis, together with repair of any popliteal or aortic aneurysm identified.²

Complications

• Limb loss - major amputation in 10 to 15%, with the consequent loss of mobility and independence
• Death - 30-day mortality of 15 to 20%, driven by the cardiac comorbidity of the population and by reperfusion injury
• Compartment syndrome requiring fasciotomy, with subsequent wound problems and the need for skin grafting
• Acute kidney injury from rhabdomyolysis and contrast
• Hyperkalaemic cardiac arrest on reperfusion
• Reocclusion and recurrent ischaemia, particularly where the underlying cause has not been treated
• Bleeding complications of heparin and thrombolysis, including intracranial haemorrhage
• Chronic pain, contracture and functional loss in a salvaged but damaged limb

Red flags

Prognosis

Outcome is determined almost entirely by two things: the Rutherford category at presentation, and the time to revascularisation. A category I or IIa limb treated within hours has a high chance of full functional recovery. A category IIb limb revascularised beyond six to eight hours frequently develops compartment syndrome, permanent nerve damage or muscle contracture even when the arterial supply is restored.

Overall figures remain poor: amputation in roughly 10 to 15% and 30-day mortality of 15 to 20%. The mortality is not principally from the limb but from the patient - this is an elderly population with atrial fibrillation, heart failure and coronary disease, in whom a major physiological insult is often the final event.

The practical implication for a junior clinician is that the diagnostic and organisational steps matter more than any technical detail. Recognising the six Ps, examining the other leg, checking a hand-held Doppler, giving heparin and telephoning a vascular surgeon can all be done within ten minutes of meeting the patient, and they are what determine whether the limb is still there a week later.