Acute Limb Ischaemia
Sudden decrease in limb perfusion threatening tissue viability, requiring emergency revascularisation within 6 hours to prevent irreversible damage and limb loss. Causes include embolism and thrombosis in situ.
Key Facts
6 Ps: Pain, Pallor, Pulselessness, Paraesthesia, Paralysis, Perishingly cold — Paralysis and paraesthesia indicate irreversible damage is imminent Time-critical emergency: revascularisation needed within 4-6 hours to prevent irreversible ischaemia Embolism (most common cause): usually cardiac origin — AF, MI with mural thrombus, prosthetic valve; sudden onset, no claudication history Thrombosis in situ: on pre-existing atherosclerotic disease; more gradual onset, history of claudication, collateral circulation CT angiography: urgent imaging to plan intervention Treatment: emergency surgical embolectomy (Fogarty catheter) or catheter-directed thrombolysis (alteplase); systemic IV heparin immediately Compartment syndrome: risk after reperfusion (reperfusion injury); monitor for tense swollen leg, severe pain, paraesthesia — requires emergency fasciotomy Rutherford classification grades severity from viable (I) to irreversible (III)
Overview
Key Facts
Acute limb ischaemia (ALI) is a sudden decrease in limb perfusion that threatens tissue viability. It is a vascular emergency requiring immediate assessment and intervention.
Epidemiology
- Incidence: ~14 per 100,000 per year
- More common in elderly; associated with cardiovascular disease
- Embolism:thrombosis ratio ~4:1 in historical series; thrombosis now more common due to ageing population with PAD
Aetiology
Embolism (~40-50%):
- Cardiac: AF (most common source), MI with mural thrombus, prosthetic valve, endocarditis, atrial myxoma
- Non-cardiac: aortic aneurysm thrombus, paradoxical embolism (PFO/ASD)
- Atheroembolism ('trash foot'): cholesterol crystal embolisation
Thrombosis in situ (~40-50%):
- On pre-existing atherosclerotic plaque (PAD)
- Bypass graft thrombosis
- Popliteal aneurysm thrombosis
- Hypercoagulable states: antiphospholipid syndrome, malignancy
Other:
- Aortic dissection with limb malperfusion
- Trauma
- Compartment syndrome
- Popliteal entrapment
Pathophysiology
- Sudden occlusion of arterial supply → ischaemia distal to occlusion
- Skeletal muscle tolerates ~4-6 hours of complete ischaemia before irreversible necrosis
- Nerve damage occurs earliest (within 2-4 hours)
- After revascularisation: reperfusion injury — release of myoglobin, potassium, lactate → rhabdomyolysis, hyperkalaemia, metabolic acidosis, compartment syndrome
Clinical Presentation
The 6 Ps
- Pain: sudden onset, severe, in the affected limb
- Pallor: white/waxy appearance progressing to mottling
- Pulselessness: absent pulses distal to occlusion
- Paraesthesia: indicates nerve ischaemia — urgent intervention needed
- Paralysis: late sign — indicates muscle necrosis beginning; limb may be unsalvageable
- Perishingly cold: temperature difference from contralateral limb
Distinguishing Embolism vs Thrombosis
| Feature | Embolism | Thrombosis |
|---|---|---|
| Onset | Sudden | Gradual |
| History of claudication | No | Often |
| Contralateral pulses | Present | Often absent/reduced |
| Source | Cardiac (AF, MI) | Local atherosclerosis |
| Collaterals | Absent | Often present |
Red Flags
- Paralysis or anaesthesia (limb may be irreversibly damaged)
- Fixed mottling (non-blanchable — irreversible)
- Tense, tender calf after revascularisation (compartment syndrome)
Differential Diagnosis
| Diagnosis | Key Features | Investigation |
|---|---|---|
| Acute DVT (phlegmasia cerulea dolens) | Massively swollen, cyanotic limb | Duplex USS |
| Aortic dissection with limb malperfusion | Back/chest pain, BP differential | CT aortogram |
| Compartment syndrome | Tense swollen limb, pain on passive stretch | Compartment pressure measurement |
| Chronic critical limb ischaemia | Gradual worsening, rest pain, ulcers | ABPI, duplex |
| Vasospasm (Raynaud, ergotism) | Episodic, reversible | Clinical, drug history |
Diagnosis / Investigation
Bedside
- Pulse palpation: identify level of occlusion
- Handheld Doppler: assess for arterial signals distally
- ABPI: <0.4 in affected limb
- Temperature assessment: compare both limbs
Bloods
- FBC, U&Es, coagulation: baseline and surgical preparation
- CK (creatine kinase): muscle damage marker; massively elevated in rhabdomyolysis
- Lactate: elevated in severe ischaemia
- Blood gas: metabolic acidosis
- Group and save/crossmatch
- Myoglobin (urine): dark brown urine suggests rhabdomyolysis
Imaging
- CT angiography: urgent; identifies site and extent of occlusion, guides intervention
- Duplex ultrasound: may be used initially; less detailed than CTA
- Digital subtraction angiography: at time of intervention
- Echocardiography: identify cardiac embolic source
Rutherford Classification
| Category | Prognosis | Sensory | Motor | Doppler |
|---|---|---|---|---|
| I — Viable | Not immediately threatened | Normal | Normal | Audible |
| IIa — Marginally threatened | Salvageable if promptly treated | Minimal loss | Normal | Often inaudible |
| IIb — Immediately threatened | Salvageable with immediate revascularisation | Sensory loss | Mild-moderate weakness | Usually inaudible |
| III — Irreversible | Major tissue loss/amputation inevitable | Profound anaesthesia | Paralysis (rigor) | Inaudible |
Management
Non-pharmacological
- Emergency: do not delay treatment
- Keep limb in dependent position (gravity-assisted perfusion)
- Protect from trauma; avoid excessive warming
Pharmacological
- IV unfractionated heparin: bolus 5,000 IU then infusion 1,000 IU/hour (prevent clot propagation)
- Analgesia: IV opioids (morphine) for severe pain
- IV fluids: prevent renal injury from rhabdomyolysis post-revascularisation
- Sodium bicarbonate: consider if severe acidosis or rhabdomyolysis
Surgical/Interventional
Category I (viable):
- Anticoagulation with heparin, further investigation
Category IIa/IIb (threatened — salvageable):
- Surgical embolectomy (Fogarty balloon catheter): first-line for embolic occlusion
- Usually via femoral arteriotomy under local anaesthesia
- Catheter-directed thrombolysis: for thrombosis in situ or distal occlusion
- Alteplase (tPA) infused directly into thrombus via catheter
- Takes 6-24 hours; patient monitored in HDU
- Follow with angiography and angioplasty/stenting if underlying stenosis
- Surgical bypass: for extensive thrombosis in situ
- Fasciotomy: if compartment syndrome develops post-revascularisation
Category III (irreversible):
- Amputation: limb is non-viable; revascularisation would cause lethal reperfusion injury (myoglobin, K⁺)
- Palliation if patient not surgical candidate
Referral Criteria
- All acute limb ischaemia: emergency vascular surgery referral
- Do not delay for imaging if limb is immediately threatened
- Post-revascularisation: monitor for compartment syndrome
Prognosis
- Overall 30-day mortality: ~15-20% (reflects significant comorbidity burden)
- Amputation rate: ~10-15% (higher in thrombosis than embolism)
- Embolectomy: limb salvage rate ~75-90%
- Thrombolysis: effective in ~70-80% of cases
- Post-revascularisation complications: compartment syndrome (~5-10%), reperfusion injury (rhabdomyolysis, AKI, hyperkalaemia)
- Category IIb: revascularisation within 6 hours = good outcomes; >6 hours = increasing tissue loss
- Category III: amputation required; revascularisation may be lethal
- Long-term: address underlying cause (anticoagulation for AF, PAD management)
Other Relevant Information
Embolism vs Thrombosis Summary
| Feature | Embolism | Thrombosis |
|---|---|---|
| Onset | Sudden (seconds-minutes) | Hours |
| Claudication history | Absent | Present |
| Contralateral pulses | Normal | Reduced |
| Severity | Often severe (no collaterals) | May be milder (collaterals) |
| Source | Cardiac (AF, MI) | Local atherosclerosis |
| Treatment | Embolectomy | Thrombolysis ± revascularisation |
Reperfusion Injury Complications
| Complication | Mechanism |
|---|---|
| Compartment syndrome | Tissue oedema within fascial compartments |
| Rhabdomyolysis | Myoglobin release → AKI |
| Hyperkalaemia | Potassium release from damaged cells |
| Metabolic acidosis | Lactate washout |
| ARDS | Systemic inflammatory response |