Liver transplant: anaesthetic phases

Surgical approach

• Orthotopic liver transplantation: native liver removed and donor liver implanted in anatomical position
  • Incision: typically bilateral subcostal ± midline extension (Mercedes) or J-shaped subcostal
  • Key vascular steps: hepatic artery, portal vein, hepatic veins/IVC; biliary anastomosis (duct-to-duct or Roux-en-Y)
• Three operative phases
  • Pre-anhepatic (dissection): mobilisation of native liver; control of inflow/outflow; large collateral/variceal bleeding risk
  • Anhepatic: native liver out; venous clamping (IVC/portal) ± veno-venous bypass; no hepatic metabolism/clearance
  • Neohepatic (reperfusion): portal vein unclamp then hepatic artery; haemodynamic instability/reperfusion syndrome; biliary reconstruction; haemostasis/closure
• Techniques affecting physiology
  • Classic: IVC cross-clamp (greater preload reduction)
  • Piggyback: preserves IVC flow (less haemodynamic disturbance); may still have partial IVC occlusion
  • Veno-venous bypass (portal + IVC drainage to axillary/femoral return): reduces venous congestion and maintains preload; adds anticoagulation/air/thrombosis risks

Anaesthetic management (headline)

• Type of anaesthesia
  • General anaesthesia with controlled ventilation; regional techniques usually avoided (coagulopathy, haemodynamic lability)
• Airway
  • Cuffed endotracheal tube; consider rapid sequence induction if ascites/GERD/delayed gastric emptying
• Duration
  • Variable by centre/complexity; re-do transplant and portal vein thrombosis can be longer
• Pain
  • Large upper abdominal incision; multimodal analgesia (opioid + paracetamol if appropriate; cautious NSAIDs); consider wound infiltration/rectus sheath/TAP if coagulation allows
• Key monitoring/lines
  • Arterial line (often 2 sites), large-bore IV access, rapid infuser, central venous access (multi-lumen), temperature, urinary catheter
  • Cardiac output monitoring and/or TOE depending on local practice and patient factors (pulmonary HTN, cardiomyopathy, instability)
  • Near-patient testing: ABG, lactate, electrolytes, glucose; viscoelastic testing (TEG/ROTEM) and fibrinogen

Aims across all phases

• Maintain organ perfusion while minimising bleeding and transfusion-related harm
• Anticipate rapid physiological transitions at clamping and reperfusion
• Optimise: temperature, calcium, acid–base, potassium, glucose, coagulation, and volume status
• Use goal-directed blood product therapy guided by viscoelastic tests + clinical bleeding
• Prevent/identify: air embolus, massive haemorrhage, arrhythmias, right heart failure, intracranial complications (encephalopathy), renal injury

Phase 1: Pre-anhepatic (dissection) — physiology and anaesthetic priorities

• What is happening physiologically
  • Large blood loss risk from adhesions, collateral vessels, portal HTN, coagulopathy, thrombocytopenia
  • Low SVR/high CO state common in cirrhosis; relative hypovolaemia despite oedema/ascites
  • Renal vulnerability (HRS, diuretics, vasodilation); hyponatraemia may be present
• Haemodynamic strategy
  • Maintain MAP to ensure coronary/cerebral/renal perfusion; accept lower CVP strategy to reduce bleeding (centre-dependent)
  • Early vasopressor support (noradrenaline) often preferable to excessive crystalloid
  • Consider vasopressin/terlipressin infusion if refractory vasoplegia/portal HTN physiology (local protocols)
• Coagulation and transfusion
  • Baseline labs + repeat: Hb, fibrinogen, INR/APTT, platelets; interpret with viscoelastic testing (balanced haemostasis possible despite abnormal INR)
  • Treat active bleeding with targeted products: fibrinogen/cryoprecipitate first if low clot amplitude; platelets if low count/function; FFP for factor deficiency with bleeding
  • Antifibrinolytic (e.g., tranexamic acid) if hyperfibrinolysis on TEG/ROTEM or diffuse oozing; balance against thrombosis risk (hepatic artery/portal vein)
• Metabolic/other
  • Correct ionised hypocalcaemia (citrate load from transfusion) to support contractility and coagulation
  • Maintain normothermia (forced air warming, fluid warmers, warmed blood) to reduce coagulopathy
  • Glucose monitoring: risk of hypoglycaemia (poor hepatic reserve) or hyperglycaemia (stress, dextrose infusions)

Phase 2: Anhepatic — physiology and anaesthetic priorities

• Defining features
  • No liver function: no lactate clearance, no citrate metabolism, reduced drug metabolism, no bile production
  • Venous return may fall due to IVC/portal clamping (more with classic technique; less with piggyback; mitigated by veno-venous bypass)
• Haemodynamics
  • Expect hypotension at clamping: treat with vasopressors + volume as needed; consider TOE if unstable to assess RV/LV filling and function
  • Veno-venous bypass: watch for air embolus, circuit clotting, hypothermia, haemolysis; anticoagulation strategy is centre-specific
• Acid–base/electrolytes
  • Progressive metabolic acidosis and rising lactate (reduced clearance + ongoing production); optimise perfusion/oxygen delivery, consider bicarbonate only for severe acidaemia with instability
  • Citrate accumulation from transfusion → hypocalcaemia (and potentially metabolic alkalosis later when citrate is metabolised after reperfusion)
  • Potassium may rise (transfusion, acidosis, renal dysfunction); aim to have K+ controlled before reperfusion
• Coagulation
  • Reduced synthesis of clotting factors continues; fibrinolysis may increase; use TEG/ROTEM to guide therapy
• Drug considerations
  • Reduced clearance of opioids/benzodiazepines/relaxants; prefer agents with organ-independent metabolism where possible (e.g., atracurium/cisatracurium)

Phase 3: Neohepatic (reperfusion and post-reperfusion) — physiology and anaesthetic priorities

• Reperfusion sequence and timing
  • Portal vein unclamp (often first) → rapid influx of cold, acidotic, hyperkalaemic preservative/venous blood; then hepatic artery anastomosis reperfused
  • Highest risk period: first 5–10 minutes after reperfusion
• Post-reperfusion syndrome (PRS)
  • Typical definition: fall in MAP ≥30% from baseline lasting ≥1 minute within 5 minutes of reperfusion (definitions vary by centre)
  • Mechanisms: sudden ↓SVR (vasodilators), myocardial depression, acute RV strain (embolus/thrombus/air), acidosis, hyperkalaemia, hypocalcaemia, hypothermia
  • Management: anticipate and treat promptly with vasopressors (noradrenaline bolus/infusion, adrenaline bolus for severe), calcium bolus, correct K+/acidosis, optimise preload, increase FiO2, deepen anaesthesia only if appropriate
• Electrolytes and acid–base after reperfusion
  • Hyperkalaemia risk peaks at reperfusion: treat with calcium, insulin/dextrose, bicarbonate if severe acidaemia, hyperventilation, and consider dialysis/haemofiltration if refractory
  • Acidosis may worsen transiently; lactate should start to fall if graft functioning (not immediate in all cases)
  • Ionised calcium often falls (citrate + binding); treat to maintain contractility/coagulation
• Coagulation after reperfusion
  • May improve as graft produces factors, but early period can show hyperfibrinolysis and platelet dysfunction; repeat TEG/ROTEM frequently
  • Beware thrombosis risk (hepatic artery thrombosis, portal vein thrombosis) if over-correction or indiscriminate procoagulants
• Haemodynamics and cardiac complications
  • Consider TOE if severe instability to distinguish: vasoplegia vs hypovolaemia vs LV dysfunction vs RV failure/PE/air
  • Arrhythmias: bradycardia/asystole (hyperkalaemia, cold load), AF/VT; treat underlying cause and follow ALS principles
• End of case priorities
  • Haemostasis, normothermia, stable vasopressor requirement, acceptable gas exchange, controlled electrolytes, adequate urine output/renal plan
  • Decide extubation vs ICU ventilation: most go to ICU intubated; selected fast-track extubation in stable patients (centre-specific)

Monitoring and access (typical set-up)

• Arterial pressure monitoring
  • Radial A-line for continuous BP and frequent sampling; consider femoral A-line if poor waveform/vasoplegia or for backup
• Central access
  • Large-bore multi-lumen CVC for vasoactive infusions and rapid administration; avoid subclavian if coagulopathic (non-compressible)
  • Consider additional large-bore peripheral cannulae; rapid infuser and level 1-type warming
• Advanced monitoring
  • TOE useful for PRS, RV failure, air/thrombus, preload assessment; ensure no contraindication (e.g., significant oesophageal varices/strictures—risk-benefit decision)
  • CO monitoring (pulse contour, oesophageal Doppler, PA catheter in selected severe pulmonary HTN) depending on local practice
• Point-of-care testing
  • ABG: Hb, lactate, glucose, electrolytes, ionised Ca2+; repeat frequently (often every 30–60 min and around key events)
  • TEG/ROTEM: guide fibrinogen, platelets, FFP, antifibrinolytics

Phase-linked transfusion/haemostatic strategy (practical)

• Pre-anhepatic: anticipate major haemorrhage
  • Activate major haemorrhage protocol early if escalating loss; ensure blood availability (RBC, FFP, platelets, cryo/fibrinogen concentrate)
  • Maintain fibrinogen (often first factor to fall); treat hypocalcaemia during high transfusion rates
• Anhepatic: manage acidosis/citrate and prepare for reperfusion
  • Aim: K+ in safe range, ionised Ca2+ normal, temperature normal, Hb appropriate, coagulation optimised
• Neohepatic: avoid both bleeding and thrombosis
  • Recheck TEG/ROTEM soon after reperfusion; treat hyperfibrinolysis if present; avoid indiscriminate procoagulants
  • If severe refractory coagulopathy/bleeding: consider specialist therapies per protocol (e.g., PCC, fibrinogen concentrate, rFVIIa as rescue) with thrombosis awareness