Acute limb ischaemia

Surgical approach

  • Time-critical limb salvage: decision based on viability (Rutherford classification) and imaging availability
    • Viable / marginally threatened: urgent imaging (often CTA) then revascularisation
    • Immediately threatened: proceed to theatre without delay (imaging only if it will not delay)
    • Irreversible: primary amputation; avoid reperfusion of necrotic limb
  • Typical operative options (depend on cause and level)
    • Embolectomy (Fogarty balloon) for embolus; may include on-table angiography
    • Catheter-directed thrombolysis (e.g. alteplase) for thrombosis in selected stable cases (often in IR suite)
    • Bypass grafting (e.g. fem-pop) or endarterectomy/stenting for in-situ thrombosis/critical stenosis
    • Fasciotomy if prolonged ischaemia/reperfusion risk or compartment syndrome
    • Amputation if non-viable limb or life-threatening sepsis/metabolic derangement
  • Perioperative anticoagulation
    • IV unfractionated heparin as soon as diagnosis suspected unless contraindicated (e.g. active bleeding, intracranial haemorrhage)
    • Intraoperative heparinisation often used for open revascularisation; coordinate with anaesthesia (neuraxial implications)

Anaesthetic management (overview)

  • Type of anaesthesia: GA commonly; regional may be appropriate in selected cases (but consider anticoagulation, urgency, ability to tolerate lying flat, and need for fasciotomy)
    • Neuraxial (spinal/epidural): useful for infra-inguinal surgery and analgesia but often limited by urgent heparin and antiplatelets; follow ASRA/RA-UK timing guidance
    • Peripheral blocks (e.g. femoral + sciatic): may be an option for distal procedures; beware masking compartment syndrome pain post-op
  • Airway: ETT usually (full stomach, sepsis/physiological derangement, long/variable duration); SGA only if low aspiration risk and short stable case
    • RSI often appropriate: opioids/induction titrated to haemodynamics; consider ketamine/etomidate in shock
  • Duration: highly variable (≈1–4+ h); can extend with bypass, fasciotomy, complex endovascular work
    • Expect unpredictability; plan for invasive monitoring and temperature control
  • How painful: moderate–severe (ischaemic pain pre-op; significant post-op pain especially with fasciotomy/amputation)
    • Multimodal analgesia; consider catheter techniques if anticoagulation permits; avoid hypotension compromising perfusion
  • Monitoring/lines: arterial line early; 2 large-bore IV; consider CVC if vasoactive infusions/poor access; urinary catheter
    • Point-of-care: ABG/VBG, lactate, K+, glucose; consider TEG/ROTEM if bleeding/major surgery
  • Key intra-op risks: reperfusion syndrome (acidosis, hyperkalaemia, hypotension), arrhythmias, bleeding (heparin/thrombolysis), hypothermia, AKI, compartment syndrome
    • Have calcium, insulin/dextrose, sodium bicarbonate (selected), vasopressors ready; communicate before clamp release

Definition and importance

  • Acute limb ischaemia: sudden decrease in limb perfusion threatening limb viability (typically <14 days symptom onset)
  • High morbidity/mortality: risk of limb loss, systemic complications from reperfusion, and underlying cardiovascular disease

Aetiology

  • Embolus (classically sudden onset, no prior claudication): AF, mural thrombus post-MI, valvular disease, aneurysm
  • In-situ thrombosis (often on background PAD): plaque rupture, low flow states, dehydration, hypercoagulable states
  • Graft/stent occlusion: thrombosis or technical failure
  • Trauma/iatrogenic: arterial injury, dissection, closure device complication
  • Other: aortic dissection, popliteal aneurysm thrombosis, compartment syndrome causing secondary ischaemia

Clinical features and classification

  • Symptoms/signs: the 6 Ps
    • Pain (often severe), Pallor, Pulselessness, Paraesthesia, Paralysis, Poikilothermia (cold)
  • Rutherford classification (practical perioperative relevance)
    • I Viable: no sensory/motor loss; arterial/venous Doppler audible → urgent but not immediate
    • IIa Marginally threatened: minimal sensory loss (toes), no motor deficit; arterial Doppler often inaudible → urgent revascularisation
    • IIb Immediately threatened: more than toes sensory loss, mild–moderate motor deficit → immediate revascularisation (time critical)
    • III Irreversible: profound anaesthesia, paralysis/rigor; major tissue loss inevitable → primary amputation; reperfusion may be fatal

Initial management (ED/ward) relevant to anaesthesia

  • Resuscitate: ABCDE, oxygen if needed, IV access, analgesia (opioid titration), treat sepsis/shock
  • Anticoagulation: IV UFH bolus then infusion unless contraindicated; reduces thrombus propagation and improves microcirculation
  • Limb care: keep limb dependent (not elevated), keep warm (systemically), avoid external heat to limb (burn risk), no compression
  • Investigations: FBC, U&E/creatinine, coagulation, group & save/crossmatch, ABG/VBG (lactate, K+), ECG, troponin if indicated
  • Imaging: CTA or duplex if it will not delay limb-saving intervention; consider renal function/contrast nephropathy risk

Preoperative assessment (anaesthetic focus)

  • Assess urgency and limb viability; clarify planned procedure (embolectomy vs bypass vs thrombolysis vs amputation) and location (theatre vs IR)
  • Cardiovascular risk: ALI patients often have significant IHD/CCF/AF; obtain baseline ECG, consider echo if time and instability
  • Physiology: dehydration, sepsis, metabolic acidosis, hyperkalaemia (especially with prolonged ischaemia), rhabdomyolysis
  • Anticoagulants/antiplatelets: document timing/doses (DOAC/warfarin/LMWH/UFH, aspirin, clopidogrel); impacts neuraxial and bleeding
  • Aspiration risk: pain, opioids, emergency surgery → treat as full stomach; plan RSI where appropriate

Intraoperative management

  • Induction: haemodynamically stable induction; consider etomidate/ketamine in shock; avoid hypotension that worsens limb and end-organ perfusion
  • Ventilation: maintain normocapnia and oxygenation; avoid severe hypocapnia (vasoconstriction) and acidosis (arrhythmogenic, worsens pulmonary vasoconstriction)
  • Haemodynamics: aim adequate MAP for coronary/cerebral perfusion and collateral limb flow; vasopressors often required (noradrenaline ± vasopressin)
  • Fluids/blood: balanced crystalloids; avoid overload in cardiac disease; crossmatch if bypass/bleeding risk; cell salvage may be useful in open surgery
  • Temperature: active warming; hypothermia worsens coagulopathy and vasoconstriction
  • Analgesia: opioid titration; consider regional where safe; ketamine infusion can help severe ischaemic pain; plan post-op analgesia early
  • Antibiotics: per local vascular protocol (especially if graft, fasciotomy, or amputation)

Reperfusion: pathophysiology and management

  • Mechanism: washout of anaerobic metabolites and cellular contents from ischaemic limb → systemic acidosis, hyperkalaemia, myoglobin, inflammatory mediators
  • Clinical effects at reperfusion: hypotension (vasodilation), brady/ventricular arrhythmias, cardiac arrest, pulmonary oedema (inflammatory), worsening coagulopathy
  • Preparation before reperfusion/clamp release
    • Inform anaesthetist before restoring flow; ensure A-line waveform and recent ABG (K+, pH, lactate)
    • Optimise volume status and vasopressor readiness; consider increasing FiO2 temporarily
    • Treat hyperkalaemia proactively if suspected/prolonged ischaemia: calcium chloride/gluconate, insulin/dextrose, salbutamol; consider bicarbonate if severe acidaemia
  • Rhabdomyolysis/AKI prevention: maintain perfusion, avoid nephrotoxins, monitor urine output; consider alkalinisation/diuresis only with senior input and clear indication (evidence mixed)

Compartment syndrome (perioperative relevance)

  • Risk increased with prolonged ischaemia, reperfusion, thrombolysis, aggressive fluid resuscitation, and combined arterial/venous injury
  • Diagnosis: pain out of proportion, pain on passive stretch, tense compartments, sensory changes; pulses may be present
  • Anaesthetic pitfall: dense regional analgesia may mask evolving compartment syndrome; ensure robust surveillance plan if blocks used
  • Treatment: urgent fasciotomy; anticipate blood loss, fluid shifts, and significant post-op pain

Postoperative care

  • Destination: HDU/ICU often appropriate (reperfusion risk, vasopressors, metabolic derangement, major comorbidity, fasciotomy/amputation)
  • Monitoring: serial ABGs (K+, pH, lactate), ECG monitoring for arrhythmias, urine output/creatinine, CK, coagulation if thrombolysis/heparin
  • Analgesia: multimodal; consider PCA; regional catheters only with anticoagulation plan and neurovascular checks
  • Anticoagulation/antiplatelets: continue per vascular/haematology plan; be explicit about neuraxial catheter removal timing if used
You are called to anaesthetise a patient with acute limb ischaemia for emergency embolectomy. What are your immediate priorities?

Structure: urgency/viability → resuscitation → anticoagulation/bleeding risk → anaesthetic plan → reperfusion preparation.

  • Confirm diagnosis/urgency and limb viability (Rutherford IIb = immediate theatre; III = amputation/avoid reperfusion)
  • ABCDE: treat shock/sepsis, oxygen if needed, two large-bore IV, analgesia, temperature management
  • Check anticoagulation: UFH started? DOAC/warfarin/antiplatelets? implications for neuraxial and bleeding
  • Baseline investigations: ECG, FBC/U&E/coag, group & crossmatch, ABG/VBG (K+, pH, lactate), glucose
  • Plan monitoring: early arterial line; consider CVC if vasoactive infusions likely; urinary catheter
  • Anaesthetic technique: usually GA with RSI (full stomach); titrate induction to haemodynamics; prepare vasopressors
  • Reperfusion plan: warn team before flow restored; have calcium, insulin/dextrose, salbutamol, bicarbonate (selected) ready; repeat ABG after reperfusion
Describe the pathophysiology of reperfusion syndrome in acute limb ischaemia and how it presents under anaesthesia.

Key concept: systemic effects of washout + inflammatory response after restoring flow to ischaemic tissue.

  • Washout of metabolites: lactic acidosis and CO2 load → fall in pH, increased ventilatory requirement
  • Hyperkalaemia from cell lysis → peaked T waves, conduction delay, ventricular arrhythmias/asystole
  • Myoglobin release (rhabdomyolysis) → pigment nephropathy and AKI risk, especially with hypovolaemia
  • Systemic vasodilation/inflammatory mediators → hypotension, increased capillary leak; may precipitate pulmonary oedema in vulnerable patients
  • Coagulopathy/bleeding risk may be exacerbated by acidosis, hypothermia, and anticoagulation/thrombolysis
How would you manage severe hyperkalaemia occurring at the moment of reperfusion/clamp release?

Treat the ECG first, then shift potassium, then remove potassium; correct contributing factors.

  • Call for help; stop potassium-containing fluids; check ECG and confirm with ABG if possible without delaying treatment
  • Stabilise myocardium: IV calcium chloride (central) or calcium gluconate (peripheral); repeat if ECG changes persist
  • Shift K+ intracellular: insulin + dextrose; nebulised/IV salbutamol; consider sodium bicarbonate if severe acidaemia
  • Support circulation: treat hypotension with vasopressors and fluids as appropriate; optimise ventilation/oxygenation
  • Remove K+: diuresis if appropriate; consider renal replacement therapy post-op if refractory/AKI
  • Communicate with surgeon: consider staged reperfusion or temporary re-occlusion if catastrophic instability (case-dependent)
Discuss your choice of anaesthetic technique for acute limb ischaemia surgery. When might regional anaesthesia be inappropriate?

Balance urgency, anticoagulation, physiological derangement, and need for postoperative neurovascular assessment.

  • GA is common: emergency, full stomach, variable duration, potential for major haemodynamic swings and reperfusion events
  • Neuraxial may be useful for infra-inguinal surgery/analgesia but often inappropriate due to
    • Therapeutic UFH infusion/bolus, thrombolysis, dual antiplatelet therapy, or uncertain anticoagulant history
    • Time-critical IIb limb where delays are unacceptable
    • Severe sepsis/shock (sympathectomy-related hypotension)
  • Peripheral nerve blocks: can reduce opioids but may mask compartment syndrome; require explicit monitoring strategy
A patient with ALI is on an IV heparin infusion. What are the key anaesthetic implications?

Think: bleeding, neuraxial safety, monitoring, and coordination with surgery.

  • Bleeding risk: surgical field bleeding; need for crossmatch and readiness for transfusion; monitor coagulation (aPTT/anti-Xa per local protocol)
  • Neuraxial/regional: therapeutic UFH is a major contraindication to neuraxial; if considering, must follow timing guidance and involve seniors
  • Lines/monitoring: arterial line helpful; avoid traumatic instrumentation; careful with IM injections
  • Perioperative plan: clarify whether heparin will be stopped/continued and whether intra-op bolus is planned; document timing
How do you recognise and manage compartment syndrome after revascularisation? What is the relevance of regional anaesthesia?

Compartment syndrome is a clinical diagnosis; delay causes irreversible muscle/nerve injury.

  • Recognition: severe pain out of proportion, pain on passive stretch, tense compartments; sensory loss; late motor weakness; pulses may remain
  • Management: urgent surgical fasciotomy; treat as emergency; optimise analgesia and haemodynamics; anticipate bleeding and fluid shifts
  • Regional relevance: dense blocks/epidurals can mask pain; if used, ensure frequent objective assessment and low threshold for pressure measurement/surgical review
What are the main differential diagnoses for a painful cold leg and how would they change your anaesthetic approach?

Differentiate vascular occlusion from mimics; some are medical emergencies with different priorities.

  • Acute limb ischaemia (arterial occlusion): anticoagulate, urgent revascularisation
  • Acute DVT/phlegmasia: swollen painful limb; anticoagulation/thrombolysis; less typical pulselessness; consider PE risk
  • Compartment syndrome (trauma/reperfusion): pain on stretch; urgent fasciotomy; avoid masking with dense regional
  • Cellulitis/necrotising infection: sepsis resuscitation, source control, broad-spectrum antibiotics; major haemodynamic instability possible
  • Neurological (stroke/spinal): weakness/sensory loss without vascular signs; changes urgency and anticoagulation decisions
Previous FRCA-style question: 'Outline the anaesthetic considerations for emergency lower limb revascularisation for acute ischaemia.'

A complete answer should cover patient factors, surgery factors, technique, monitoring, and reperfusion/complications.

  • Patient: elderly, high prevalence of IHD/CCF/AF, diabetes/CKD; assess functional status, current ischaemic pain/opioid use, sepsis/dehydration
  • Urgency/procedure: embolectomy vs bypass vs thrombolysis vs amputation; expected blood loss; need for heparin/thrombolytics
  • Pre-op tests: ECG, labs incl. K+/lactate, group & crossmatch; consider ABG and bedside echo if unstable
  • Anaesthesia: GA often with RSI; regional only if safe and not delaying; plan analgesia and neurovascular assessment
  • Monitoring: A-line, temperature, urine output; consider CVC; frequent ABGs around reperfusion
  • Intra-op goals: maintain perfusion pressure, avoid hypothermia/acidosis, manage anticoagulation, anticipate blood loss
  • Reperfusion: anticipate hypotension, hyperkalaemia, acidosis, arrhythmias; have drugs ready; communicate with surgeon
  • Post-op: HDU/ICU, monitor K+/pH/lactate/CK/renal function; watch for compartment syndrome; continue anticoagulation plan
Previous FRCA-style question: 'What are the causes and management of metabolic acidosis during vascular surgery?' (apply to ALI reperfusion)

In ALI, acidosis is commonly from lactate washout and shock; management is primarily cause-directed.

  • Causes: tissue hypoperfusion/shock, reperfusion lactate washout, hypoventilation, renal failure, sepsis
  • Consequences: reduced myocardial contractility, arrhythmias, reduced response to catecholamines, hyperkalaemia shift
  • Management: improve perfusion (fluids/vasopressors), optimise oxygenation/ventilation, treat sepsis, correct severe hyperkalaemia
  • Bicarbonate: consider only in severe acidaemia with haemodynamic compromise after addressing cause; monitor CO2 load and sodium/osmolality

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