Acute Limb Ischaemia

1. Clinical Overview

Summary

Acute Limb Ischaemia (ALI) is defined as a sudden decrease in limb perfusion that threatens the potential viability of the limb. [1] It presents a surgical emergency requiring recognition and intervention within hours to prevent irreversible ischemia, tissue necrosis, and amputation. The incidence is approximately 1.5 cases per 10,000 persons per year. [2] The classic clinical presentation is remembered by the "6 Ps": Pain, Pallor, Pulselessness, Paraesthesia, Paralysis, and Perishingly cold [3].

The pathophysiology involves two primary mechanisms: embolism (usually cardiac origin, e.g., atrial fibrillation) or thrombosis (in situ thrombosis of a pre-existing atherosclerotic plaque or bypass graft). Differentiating these is critical as management differs (embolectomy vs. thrombolysis/bypass). [4] Revascularisation must typically be achieved within 4-6 hours of onset of complete acute ischaemia to save the limb; beyond this, irreversible nerve and muscle damage occurs. Classification systems such as the Rutherford classification guide urgency: Rutherford I (viable), IIa (marginally threatened), IIb (immediately threatened), and III (irreversible). [5] Management involves immediate systemic anticoagulation with heparin, followed by surgical revascularisation (thromboembolectomy, bypass), endovascular techniques (catheter-directed thrombolysis, mechanical thrombectomy), or hybrid approaches. Reperfusion injury and compartment syndrome are major post-operative risks.

Key Facts

• Definition: Sudden (less than 14 days) hypoperfusion threatening limb viability.
• Time Window: "Time is Muscle". Irreversible damage begins at 4-6 hours.
• Mortality: High hospital mortality (10-15%) due to cardiac comorbidities. [6]
• Amputation Rate: 10-25% despite treatment. [6]
• Most Common Cause: Thrombosis in situ (now more common than embolism due to aging population/PAD prevalence).
• Most Common Embolic Source: Atrial Fibrillation (Cardiac).
• Key Diagnostic Tool: Hand-held Doppler (distinguishes ALI from severe claudication).
• First Line Med: IV Heparin (prevents proximal/distal clot propagation).
• Contraindication to Revascularisation: Rutherford III (fixed staining, rigor) - requires primary amputation to prevent reperfusion syndrome/death.

Clinical Pearls

Differentiation Pearl: Embolism typically presents in a patient with normal contralateral pulses, no history of claudication, and a source (e.g., AF), resulting in a "white, severe" leg. Thrombosis presents in a patient with absent contralateral pulses, history of claudication/vascular disease, resulting in a less acute presentation due to established collaterals.

Neurological Pearl: Paraesthesia (numbness) is an early sign of nerve ischaemia (small fibres). Paralysis (motor loss) is a LATE sign indicating deep muscle ischaemia and impending limb loss. Paradoxically, pain may subside as the nerve dies ("the ominous silence").

Management Pearl: Giving heparin immediately (before the CT scan) is the single most important action in the ED. It prevents the "tail" of the thrombus extending into the collateral circulation.

The "White vs Blue" Leg: An acutely ischaemic white leg ("marble white") is vasospastic and empty of blood. A blue/mottled leg implies stagnant deoxygenated blood. Fixed (non-blanching) staining implies dead tissue.

Mnemonic: The 6 Ps of Acute Ischaemia:

1. Pain (often out of proportion, requires opiates)
2. Pallor (waxy, marble-like)
3. Pulselessness (verify with Doppler)
4. Paraesthesia (light touch goes first)
5. Paralysis (foot drop, inability to wiggle toes)
6. Perishing Cold (poikilothermia)

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2. Epidemiology

Incidence & Prevalence

• Incidence: 14 per 100,000 population per year.
• Trend: The ratio of thrombotic to embolic causes is increasing due to the aging population and improved management of rheumatic heart disease (fewer emboli) but rising prevalence of atherosclerosis/diabetes (more thrombosis).
• Amputation Risk: Major amputation rates remain 15-20%.
• Mortality: 15-20% at 30 days (reflects the systemic burden of disease).

Demographics and Risk Factors

Classification by Aetiology

1. Embolic (30-40%):

   • Cardiac (80%): AF, post-MI mural thrombus, prosthetic valves, endocarditis vegetations.
   • Arterial (20%): Aneurysm (AAA or Popliteal) shedding thrombus, "Shaggy aorta" atheroma.
   • Paradoxical: DVT passing through patent foramen ovale (PFO).

2. Thrombotic (50-60%):

   • Native Artery: Rupture of atherosclerotic plaque (commonly SFA or Popliteal).
   • Graft Occlusion: Post-bypass graft failure (intimal hyperplasia or technical).
   • Traumatic: Blunt or penetrating injury (dissection or transection).
   • Iatrogenic: Post-angiogram access site, closure device failure.
   • Hypercoagulable: Antiphospholipid syndrome, HIT (Heparin Induced Thrombocytopenia).

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3. Pathophysiology

Mechanisms of Ischaemia

Step 1: Arterial Occlusion

• Cessation of antegrade blood flow.
• Drop in perfusion pressure distally.
• Vasospasm of distal arterial tree (exacerbating the problem).

Step 2: Cellular Hypoxia (The Metabolic Clock starts)

• Aerobic metabolism ceases within seconds.
• Switch to anaerobic metabolism → production of lactate and H+ ions.
• Failure of Na+/K+ ATPase pumps → intracellular flooding (swelling) and Calcium influx.
• Nerves: Highly sensitive. Conductive failure begins within 15-30 minutes (paraesthesia). Irreversible damage > 6-12 hours.
• Muscle: Tolerates ischaemia for 4-6 hours. After this, myocyte necrosis begins. Rhabdomyolysis releases Myoglobin, Potassium, and CK.
• Skin: Most resistant tissue (can survive 24 hours). This is why a leg can be dead (muscle necrosis) even if skin looks viable.

Step 3: Stasis and Propagation

• Stagnant blood in the distal arterial tree coagulates.
• This "consecutive thrombosis" extends into the microcirculation and collateral vessels.
• Once the "run-off" vessels clot, salvage becomes technically impossible. Hence urgency of Heparin.

Reperfusion Injury: The "Second Hit"

When flow is restored to dead/dying tissue, systemic washout of toxic metabolites occurs:

1. Acidosis: Lactic acid washes into systemic circulation → myocardial depression.
2. Hyperkalaemia: Massive K+ release from dead muscle → cardiac arrhythmias/arrest.
3. Myoglobinuria: Myoglobin precipitates in renal tubules → Acute Tubular Necrosis (AKI).
4. ROS Generation: Oxygen free radicals cause extensive endothelial damage → capillary leak.

Compartment Syndrome

• Reperfusion causes capillary leak and massive muscle oedema.
• Leg muscles are bounded by fixed fascia compartments (Anterior, Lateral, Superficial/Deep Posterior).
• Pressure rises > 30 mmHg → collapses capillary bed → Secondary Ischaemia.
• Cycle: Swelling → Ischaemia → More Swelling.

The Rutherford Classification for ALI

Standardises severity and decision making.

Critical Distinction: Category IIb (Motor loss) is the tipping point where immediate surgery is usually favoured over thrombolysis because thrombolysis takes too long (12-24h).

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4. Clinical Presentation

The History

• Onset:
  • Sudden ("Strike of a dagger"): Suggests Embolism. Patient can name the exact minute.
  • Gradual (Hours/Days): Suggests Thrombosis. Often superimposed on chronic claudication history.
• Pain: Severe, relentless, unremitting. Requires opioids. Worse on elevation.
• Past Medical Hx:
  • AF / Palpitations? (Embolus)
  • MI recently? (Mural thrombus)
  • Previous claudication? (Thrombosis)
  • Aneurysm history?

The 6 Ps Explained

1. Pain:

   • Usually the first symptom.
   • Located distal to the obstruction (e.g., foot/calf pain in popliteal occlusion).
   • WARNING: Pain may diminish as nerves die (anaesthesia). A painless, paralysed leg is worse than a painful one.

2. Pallor:

   • "Cadaveric" white appearance initially.
   • Empty veins (guttering).
   • Later, it becomes mottled (purple/blue reticular pattern).
   • Test: Blanching test. If mottled skin blanches, capillaries are intact. If Fixed Staining (does not blanch), microthrombosis/necrosis has occurred (Class III).

3. Pulselessness:

   • Palpate Femoral, Popliteal, Dorsalis Pedis, Posterior Tibial.
   • Comparison with contralateral side is vital.
   • Embolus pattern: Bounding femoral pulse, absent popliteal/distal (if embolus in superficial femoral artery).

4. Paraesthesia:

   • Ask: "Does it feel numb? Like cotton wool?"
   • Test: Light touch (cotton wool) sensitivity.
   • Loss of light touch is the first sign of threatened limb (Rutherford IIa).
   • Loss of deep pressure/pain sensation implies profound ischaemia (Rutherford III).

5. Paralysis:

   • Ask: "Can you wiggle your toes?"
   • Test: Dorsiflexion (Tibialis Anterior - Deep Peroneal Nerve) and Plantarflexion.
   • Foot Drop: Sign of advanced deep peroneal nerve ischaemia.
   • Rigor: Stiff, hard calf muscles. Indicates unrecoverable muscle death (Rigor Mortis of the limb). Primary amputation indicated.

6. Perishing Cold (Poikilothermia):

   • The limb assumes room temperature.
   • Compare knee/calf/ankle on both legs with back of hand.
   • There is often a "demarcation level" where temperature changes suddenly.
     • Cold foot = Popliteal/Trifurcation block.
     • Cold mid-calf = Superficial Femoral block.
     • Cold thigh = Iliac block.

Red Flags (Immediate Escalation)

[!CAUTION] Signs of Irreversibility (Do Not Revascularise):

• Fixed mottling: Skin bruising that does not blanch.
• Muscle Rigor: Hard, woody muscles that do not move.
• Total Anaesthesia: Complete sensory loss.
• Attempting revascularisation here causes "Myonephropathic Metabolic Syndrome" (reperfusion death).

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5. Clinical Examination

Structured Vascular Exam

1. Inspection (Exposure is key)

• Expose both legs from groin to toes.
• Check Colour: Pale? Mottled? Cyanosed? Black (gangrene)?
• Check Veins: Guttering (collapsed) veins suggest severe arterial inflow block.
• Look for scars: Previous bypass surgery?

2. Palpation (Temperature & Pulses)

• Temperature slide: Run back of hand down the leg. Note the level of cooling.
• Pulses:
  • Aorta: Palpable? Aneurysmal?
  • Femoral: Site of common femoral occlusion.
  • Popliteal: difficult to feel, but check for aneurysm (wide pulse).
  • Distal (DP/PT): Often absent.

3. Neurological Assessment (VITAL for Rutherford Grading)

• Sensation: Test toes with touch. Can they feel it?
  • Yes = Class I.
  • Numb toes only = Class IIa.
  • Numbness above ankle = Class IIb/III.
• Motor: Ask patient to move toes.
  • Normal = Class I/IIa.
  • Weakness = Class IIb.
  • Paralysis = Class III.

4. Hand-Held Doppler (Bedside Gold Standard)

• Apply gel to DP/PT positions.
• Triphasic: Normal. (ALI unlikely).
• Monophasic/Damped: Collateral flow (Chronic ischaemia/PAD).
• Absent signals: Critical Ischaemia (ALI).
• Venous Signal: Listen for the "whoosh" of the vein. If arterial is silent but venous is audible, the limb is potentially salvageable. If venous signal is ALSO lost, the vascular bed is thrombosed (Class III).

Systemic Search for Cause

• Pulse: Irregularly Irregular? (AF).
• Heart: Murmurs? (Mitral stenosis, endocarditis).
• Abdomen: Pulsatile mass? (AAA - source of emboli).
• Popliteal fossae: Wide pulses? (Popliteal aneurysm).

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6. Investigations

Bloods

ECG

• Mandatory. Look for Atrial Fibrillation.
• Look for signs of recent MI (Q waves, ST changes).

Imaging

1. Bedside Doppler

• As detailed above. Immediate, cheap, guides urgency.

2. CT Angiogram (CTA) - The Gold Standard

• Indication: First-line imaging for almost all ALI unless limb is Class III (straight to amputation) or Class IIb in theatre (on-table angio).
• Findings:
  • Cut-off sign: Meniscus sign indicating embolus in a healthy vessel.
  • Diffuse disease: Calcification and long segment occlusion indicating thrombosis.
  • Identify targets: Is there a patent distal vessel to bypass to?
• Speed: Modern CT scanners take less than 5 mins. Do not delay if available.

3. Digital Subtraction Angiography (DSA)

• Usually therapeutic (start of thrombolysis/thrombectomy) rather than pure diagnostic.
• Performed in Angio suite/Hybrid theatre.

4. Echocardiogram

• Not for acute phase. Done later to find source (Thrombus, valve vegetation, PFO).

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7. Management

Management Algorithm

                 ACUTE LIMB ISCHAEMIA DIAGNOSED
                      (Clinical 6 Ps)
                            ↓
    ┌──────────────────────────────────────────────────┐
    │        IMMEDIATE ED MANAGEMENT (Stat)            │
    │  • IV ACCESS x 2, Bloods (Group & Save, CK)      │
    │  • ANALGESIA (Titrated IV Morphine)              │
    │  • **IV HEPARIN BOLUS** (3000-5000 IU)           │
    │    (Unless active haemorrhage)                   │
    │  • KEEP LIMB DEPENDENT (Let gravity help)        │
    │  • O2 if hypoxic, Fluid resuscitation            │
    └──────────────────────────────────────────────────┘
                            ↓
    ┌──────────────────────────────────────────────────┐
    │          RUTHERFORD CLASSIFICATION               │
    ├──────────────┬───────────────────┬───────────────┤
    │  CLASS I     │    CLASS IIa      │   CLASS IIb   │
    │  (Viable)    │   (Marginally)    │  (Immediate)  │
    │              │                   │   Threat)     │
    │ No deficits  │ Sensory loss only │ Motor deficit │
    │ Audible Dop  │ Inaudible Art Dop │ Inaudible Art │
    └──────┬───────┴─────────┬─────────┴───────┬───────┘
           │                 │                 │
           │           CT ANGIOGRAM            │
           └─────────────────┬─────────────────┘
                             │
                  ANATOMICAL / CAUSE DECISION
                             │
          ┌──────────────────┼─────────────────────────┐
    EMBOLIC (Clear target)   │     THROMBOTIC (Complex disease)
    (Healthy arteries)       │     (Calcification, no target)
          ↓                  │               ↓
    SURGICAL EMBOLECTOMY     │     ENDOVASCULAR / HYBRID
    (Fogarty Balloon)        │     • Catheter Thrombolysis (tPA)
    +/- Patch closure        │     • Mechanical Thrombectomy
                             │     • Surgical Bypass
                             │
                             │ < --- If Class IIb (bad motor loss)
                             │      Surgery often safer/faster
                             │      than 24h thrombolysis

1. Immediate Medical Management

• Heparin: UFH 5000u IV bolus stat. Followed by infusion (APTT ratio 2.0-3.0) or therapeutic LMWH depending on local unit preference.
  • Rationale: Prevents clot propagation into the "run-off" vessels. Paradoxically, the initial clot isn't the problem; the secondary clot blocking the tiny collateral vessels is what kills the leg.
• Fluids: Aggressive hydration to protect kidneys from myoglobin (if CK rising).
• Analgesia: Severe pain causes physiological stress. Opiates usually required.

2. Surgical Options (Open)

Thromboembolectomy (Fogarty Catheter)

• Indication: Pure embolic occlusion (e.g., embolus in common femoral bifurcation).
• Technique:
  • Local or General Anaesthetic.
  • Vertical incision over femoral pulse (groin).
  • Arteriotomy (open artery).
  • Pass Fogarty catheter (balloon tip) distally and proximally.
  • Inflate balloon and withdraw, dragging clot out.
  • Check flow (on-table angio).
  • Close artery (often with patch to prevent narrowing).

Bypass Surgery

• Indication: Thrombosis on chronic disease where vessels are too narrowed for embolectomy, or embolectomy fails.
• Conduit: Vein (Long Saphenous) or Prosthetic (PTFE/Dacron).
• Examples: Fem-Pop bypass, Fem-Distal bypass.
• Risk: Higher morbidity, longer operation.

Fasciotomy

• Indication: Clinical suspicion of compartment syndrome OR prophylactic if ischaemia time > 6 hours.
• Technique: 4-compartment release of the lower leg (two incisions: lateral and medial).
• Crucial: Must be done BEFORE closing skin if limb swells on reperfusion.

3. Endovascular Options

Catheter-Directed Thrombolysis (CDT)

• Indication: Rutherford I or IIa (Viable limb, time to wait). Thrombotic occlusion of popliteal/tibial vessels where surgery is difficult.
• Agent: tPA (Alteplase) infused directly into clot via catheter.
• Protocol: Infused over 12-24 hours. Regular fibrinogen checks.
• Risks: Bleeding (10%), Stroke (1%).
• Benefit: Dissolves clot in small vessels that surgery can't reach.

Percutaneous Aspiration/Thrombectomy

• Devices (e.g., AngioJet, Indigo) that suck clot out mechanically.
• Faster than thrombolysis. Often used adjunctively.

4. Primary Amputation

• Indication: Rutherford Class III (Dead limb).
• Rationale: Revascularising dead muscle releases toxins that cause cardiac arrest (hyperkalaemia). "Life before Limb".
• Level: Below Knee (BKA) or Above Knee (AKA) depending on demarcation.

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8. Complications

Reperfusion Syndrome (Systemic)

• Occurs upon restoration of flow.
• Hyperkalaemia: Can cause VT/VF arrest. Treat with Insulin/Dextrose, Calcium Gluconate.
• Myoglobinaemia: Causes dark urine and Acute Tubular Necrosis. Treat with aggressive fluids, alkalinisation of urine.
• Metabolic Acidosis: Bicarbonate may be needed.

Compartment Syndrome (Local)

• Pathophysiology: Ischaemic endothelium leaks fluid -> tissue pressure > capillary perfusion pressure -> nerve/muscle necrosis.
• Symptoms: Pain out of proportion (especially on PASSIVE STRETCH of toes), wooden hard calf.
• Treatment: Fasciotomy. Do not wait for pressure measurements if clinical suspicion is high.
• Sequelae: If missed, leads to Volkmann's ischaemic contracture and foot drop.

Surgical Complications

• Recurrent Thrombosis: Failing graft or residual thrombus.
• False Aneurysm: At groin puncture/incision site.
• Infection: Especially with prosthetic grafts (MRSA).

Chronic Pain

• CRPS (Complex Regional Pain Syndrome): Chronic neuropathic pain post-ischaemia.
• Ischaemic Neuropathy: Permanent numbness or foot drop despite successful revascularisation.

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9. Prognosis & Outcomes

Mortality

• Acute Limb Ischaemia carries a high mortality: 15-20% at 30 days.
• This is significantly higher than elective AAA repair or CABG.
• Death is usually due to the underlying cause: Heart Failure, recurrent massive PE/Stroke, or frail physiology unable to withstand surgery/reperfusion.

Limb Salvage

• Success Rate: With timely intervention (Rutherford I/IIa), salvage rates are 80-90%.
• Delayed Presentation: Salvage drops precipitously after 6-12 hours.
• Amputation Rate: Overall 10-30% of patients will eventually lose the limb during the admission or within 1 year.

Long Term

• Survivors have a high risk of cardiovascular events (MI/Stroke).
• Functional outcome depends on nerve recovery (foot drop usually permanent if present at admission).
• Management of AF (anticoagulation compliance) helps prevent recurrence.

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10. Evidence & Guidelines

Key Guidelines

1. ESVS Guidelines (2020): European Society for Vascular Surgery - Management of Acute Limb Ischaemia.

   • The definition of ALI includes a 14-day window.
   • Strong recommendation for Heparin immediately (Class I, Level C).
   • Strong recommendation for Fasciotomy if ischaemia > 4-6h (Class I).

2. AHA/ACC Guidelines (2016): Management of Patients With Lower Extremity Peripheral Artery Disease.

   • Emphasises catheter-directed thrombolysis for Category I/IIa.

Landmark Trials

1. STILE Trial (1994) - "Surgery vs Thrombolysis for Ischemia of the Lower Extremity"

• Design: RCT comparing Catheter Thrombolysis (rt-PA/Urokinase) vs Surgery.
• Findings:
  • For ischaemia less than 14 days: Thrombolysis had lower amputation rates and better amputation-free survival than surgery.
  • For ischaemia > 14 days: Surgery was superior.
• Impact: Established Thrombolysis as first line for sub-acute or viable ALI (Thrombotic), while surgery remains key for Embolic/Late ALI.
• [PMID: 8092895]

2. TOPAS Trial (1996) - "Thrombolysis or Peripheral Arterial Surgery"

• Design: Urokinase vs Surgery for ALI.
• Findings: Amputation-free survival was equal at 1 year. Thrombolysis group had fewer open procedures but more bleeding complications.
• Impact: Confirmed Thrombolysis is a safe alternative to surgery in selected patients, sparing them major operations.
• [PMID: 8526101]

3. Mr CLEAN / Stroke Trials (extrapolated)

• While stroke trials, the evolution of mechanical thrombectomy (removing clot with stent-retrievers) has heavily influenced vascular surgery. Devices like AngioJet and Indigo Penumbra are increasingly used as "Endo-first" options for ALI, decreasing the use of lytics (bleeding risk).

Clinical Consensus

• Embolism: Surgery (Embolectomy) is best (clean clot, healthy artery, quick fix).
• Thrombosis: Thrombolysis is best (dissolves clot in diseased microvasculature, avoiding complex bypass in acute setting).
• Prophylaxis: All patients with AF and ALI should be anticoagulated for life.

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11. Patient/Layperson Explanation

What is Acute Limb Ischaemia?

It is a "leg attack" — similar to a heart attack, but in the leg. A blood clot suddenly blocks the main artery supplying fresh blood to the limb.

Why does it happen?

Usually one of two reasons:

1. Embolism: A blood clot travels from the heart (often due to an irregular heartbeat called Atrial Fibrillation) and gets stuck in the leg artery.
2. Thrombosis: A "furring up" of the arteries (hardening of arteries) suddenly clots off completely.

The Warning Signs (6 Ps)

• Pain: Severe, sudden pain.
• Pale: The leg goes white.
• Pulseless: You can't feel a beat in the foot.
• Paralysed: You can't move your toes properly.
• Pins and Needles: The foot feels numb.
• Perishing Cold: The leg feels like ice.

Is it an emergency?

Yes. It is a limb-threatening emergency.

• less than 4-6 hours: The limb can usually be saved.
• > 6-12 hours: The muscles and nerves start to die permanently. Amputation becomes likely.

Treatment

1. Blood Thinners: Rapid injection of Heparin to stop the clot growing.
2. Surgery: "Embolectomy"

• A cut in the groin to pass a small balloon down the artery and fish the clot out.

3. Thrombolysis: "Clot-busting" drugs injected directly into the clot via a tube (used for less severe cases).
4. Amputation: Sadly necessary if the leg is already dead, to save the patient's life from toxins released by dead muscle.

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12. References

Guidelines

1. Björck M et al. European Society for Vascular Surgery (ESVS) 2020 Clinical Practice Guidelines on the Management of Acute Limb Ischaemia. Eur J Vasc Endovasc Surg. 2020 Feb;59(2):173-218. PMID: 31899099

2. Gerhard-Herman MD et al. 2016 AHA/ACC Guideline on the Management of Patients With Lower Extremity Peripheral Artery Disease. Circulation. 2017 Mar 21;135(12):e726-e779. PMID: 27840333

3. NICE UK. Peripheral arterial disease: diagnosis and management (CG147). 2012 (Updated 2020).

Key Trials

4. The STILE Investigators. Results of a prospective randomized trial evaluating surgery versus thrombolysis for ischemia of the lower extremity. The STILE trial. Ann Surg. 1994 Sep;220(3):251-66. PMID: 8092895

5. Ouriel K et al. (TOPAS). A comparison of thrombolytic therapy with operative revascularization in the initial treatment of acute peripheral arterial ischemia. J Vasc Surg. 1994 Jun;19(6):1021-30. PMID: 8201702

6. Weaver FA et al. Surgical revascularization versus thrombolysis for nonembolic lower extremity native artery occlusions: results of a prospective randomized trial. The STILE Investigators. J Vasc Surg. 1996 Oct;24(4):513-21. PMID: 8911400

Review Articles

7. Creager MA et al. Acute Limb Ischemia. N Engl J Med. 2012 Jun 7;366(23):2198-206. PMID: 22670905

8. Obara H et al. Acute Limb Ischemia: Clinical Practice Guidelines. Ann Vasc Dis. 2018 Dec 25;11(4):443-448. PMID: 30636997

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13. Examination Focus

Common Exam Questions

1. MRCS / Medical Finals: "What is the management of a patient with Rutherford Class III ischaemia (rigor/fixed staining)?"

   • Answer: Primary Amputation. Revascularisation is contraindicated due to life-threatening reperfusion injury.

2. ED / Acute Med: "A patient presents with a cold, painful white leg and atrial fibrillation. What is the single most important immediate action?"

   • Answer: IV Heparin Bolus (5000 units). Do this before imaging (unless stroke/trauma contraindications).

3. Vascular Viva: "Differentiate Embolic from Thrombotic ALI clinically."

   • Embolic: Sudden onset, normal contralateral pulses, embolic source (AF), severe "white" ischaemia (no collaterals).
   • Thrombotic: Gradual onset, history of claudication, absent contralateral pulses, "mottled" ischaemia (collaterals present).

4. Pathophysiology: "Explain Reperfusion Injury."

   • Answer: Washout of Potassium (arrhythmia), Myoglobin (renal failure), and Acidosis (myocardial depression) when flow is restored to dead tissue.

Viva Points

• The "White Leg" vs "Blue Leg": White is arterial spasm/empty (early/severe). Blue is venous congestion/stagnant blood (late/thrombotic).
• Compartment Syndrome: The most common cause of litigation after embolectomy. Always consider prophylactic fasciotomy if ischaemia time > 6 hours.
• TOPAS/STILE Trials: Know that Thrombolysis is a valid alternative for Category I/IIa thrombotic occlusions (non-inferior to surgery).

Common Mistakes

• ❌ Sending patient to CT Angio without giving Heparin first.
• ❌ Diagnosing "Sprained Ankle" or "Sciatica" in an elderly patient with leg pain (Always feel pulses!).
• ❌ Elevating the leg (makes ischaemia worse - keep dependent).
• ❌ Attempting revascularisation on a dead leg (Rigor/Fixed staining).

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Last Reviewed: 2026-01-04 | MedVellum Editorial Team

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Medical Disclaimer: MedVellum content is for educational purposes and clinical reference. Clinical decisions should account for individual patient circumstances. Always consult appropriate specialists and current guidelines.