Hepatorenal Syndrome and Anaesthesia

Definition

Classification

Pathophysiology

Diagnostic Features

• Acute kidney injury with rising serum creatinine or oliguria.
• No shock or persistent severe hypovolaemia.
• No improvement after withdrawal of diuretics and volume expansion with albumin.
• No nephrotoxic drugs or iodinated contrast exposure.
• No evidence of intrinsic renal disease: significant proteinuria, haematuria, or abnormal renal ultrasound.
• Search actively for precipitating factors: spontaneous bacterial peritonitis, sepsis, GI bleeding, dehydration, over-diuresis, large-volume paracentesis.

Management

1. Treat the precipitant: cultures, early antibiotics for infection, control GI bleed, stop diuretics and nephrotoxins.
2. Restore effective circulating volume: IV albumin, with careful assessment for pulmonary oedema.
3. Vasoconstrictor therapy plus albumin:
   • Terlipressin is preferred where available.
   • Norepinephrine infusion in ICU is an effective alternative.
   • Midodrine plus octreotide may be used when other agents are unsuitable, but is less effective.
4. Renal replacement therapy for refractory hyperkalaemia, acidosis, fluid overload, uraemia, or as a bridge to transplantation.
5. Liver transplantation is definitive treatment.

Anaesthetic Implications

Preoperative assessment and optimization

• Severity of liver disease: Child-Pugh class, MELD score.
• Renal status: serial creatinine, urea, electrolytes, urine output, acid-base status.
• Volume status: ascites, oedema, intravascular depletion, pulmonary oedema.
• Cirrhotic cardiomyopathy: ECG and echocardiography where indicated.
• Coagulopathy and thrombocytopenia.
• Encephalopathy, sepsis/SBP, variceal bleeding, hypoglycaemia.
• Cross-match blood and correct clinically significant anaemia/coagulopathy as appropriate.

• Treat infection and control bleeding.
• Stop diuretics if hypovolaemic or HRS-AKI is suspected.
• Avoid dehydration, prolonged fasting, and hypotension.
• Avoid nephrotoxic drugs: NSAIDs, aminoglycosides, ACE inhibitors/ARBs, and unnecessary contrast.
• Continue vasoconstrictor and albumin therapy in consultation with hepatology/ICU.

Intraoperative management

• Standard ASA monitoring plus invasive arterial pressure monitoring for major/emergency surgery.
• Central access if vasoactive infusion, major fluid shifts, or difficult peripheral access is anticipated.
• Hourly urine output, serial blood gases, electrolytes, glucose, lactate, Hb, and coagulation tests.
• Temperature monitoring and active warming.

1. Maintain renal perfusion and adequate mean arterial pressure.
2. Avoid sudden reduction in systemic vascular resistance at induction.
3. Avoid fluid overload, ascites worsening, and pulmonary oedema.
4. Avoid drugs that worsen renal or hepatic function.
5. Maintain normoxia, normocapnia, normothermia, and normal glucose.

• Titrate induction drugs carefully because cirrhotic patients may develop profound hypotension.
• Propofol can be used cautiously in reduced titrated doses; etomidate may be useful in haemodynamically unstable patients.
• Prefer short-acting agents with minimal dependence on renal clearance, for example fentanyl/remifentanil, cisatracurium/atracurium, and volatile agents such as isoflurane or sevoflurane.
• Avoid or reduce long-acting sedatives, morphine, and renally excreted neuromuscular blockers.
• Use vasopressors early rather than giving repeated large fluid boluses. Norepinephrine is usually appropriate to maintain systemic pressure.
• Avoid nitrous oxide in major abdominal surgery/tense ascites where bowel distension is undesirable.

• Use goal-directed, cautious fluid replacement.
• Balanced crystalloids may be used for initial resuscitation, but avoid both hypovolaemia and saline-induced hyperchloraemic acidosis.
• Albumin is preferred when intravascular volume expansion is needed in HRS/cirrhosis.
• Avoid excessive crystalloid, which causes ascites, tissue oedema, dilutional coagulopathy, and pulmonary oedema.
• Blood products should be given for active bleeding or clinically relevant coagulopathy, not merely to normalize laboratory values.

Regional anaesthesia

• Neuraxial block may cause severe hypotension and may be contraindicated with coagulopathy or thrombocytopenia.
• Avoid epidural/spinal anaesthesia in significant coagulopathy, sepsis, severe hypovolaemia, or unstable HRS.
• Ultrasound-guided peripheral nerve blocks can be considered if coagulation status permits.

Postoperative care

• ICU/HDU monitoring is advisable after major or emergency surgery.
• Continue arterial pressure, urine output, creatinine, electrolytes, acid-base, and fluid-balance monitoring.
• Avoid NSAIDs and nephrotoxic antibiotics.
• Treat hypotension, bleeding, sepsis, hypoxaemia, and electrolyte disturbance promptly.
• Restart diuretics only after restoration of haemodynamic stability.
• Early hepatology, nephrology, and transplant-team involvement is essential.

Conclusion