Liver failure in icu

Surgical approach (when relevant)

• Liver failure in ICU is primarily a medical/critical care problem; surgery is only relevant if a cause/complication requires intervention or if transplantation is undertaken.
• Potential surgical/interventional procedures encountered
  • Source control: laparotomy/laparoscopy for perforation/ischaemic bowel; drainage of intra-abdominal sepsis
  • Biliary obstruction/cholangitis: ERCP ± stent; percutaneous transhepatic biliary drainage
  • Variceal haemorrhage: endoscopic banding/sclerotherapy; balloon tamponade (bridge); TIPSS (IR) as rescue/bridge
  • Acute liver failure (ALF) with cerebral oedema: invasive monitoring (ICP bolt in selected centres) rather than surgery
  • Liver transplantation (definitive for ALF or decompensated chronic liver disease): hepatectomy + implantation; venovenous bypass sometimes; major bleeding risk

Anaesthetic management (when relevant)

• Context: ICU patient with liver failure may require anaesthesia for endoscopy, IR (TIPSS), laparotomy, or transplantation.
• Type of anaesthesia
  • Usually GA with controlled ventilation; regional techniques often contraindicated/limited by coagulopathy, thrombocytopenia, sepsis, haemodynamic instability
• Airway
  • ETT preferred (aspiration risk: encephalopathy, variceal bleed, full stomach, ileus); SGA generally avoid in active GI bleeding/raised aspiration risk
• Duration and pain (procedure-dependent)
  • Endoscopy/IR: 0.5–3 h, variable pain; laparotomy: 2–6 h, high pain; transplantation: 6–12+ h, high pain
• Key intra-anaesthetic priorities
  • Haemodynamics: vasoplegia common; noradrenaline first-line; consider vasopressin/terlipressin (esp. variceal bleed/HRS physiology); avoid fluid overload
  • Coagulopathy: use viscoelastic testing (TEG/ROTEM) to target products; avoid prophylactic correction unless bleeding/procedure requires
  • Glucose: frequent checks; treat hypoglycaemia; avoid wide swings
  • Electrolytes/acid-base: correct K+/Ca2+/Mg2+; manage lactate and metabolic acidosis; anticipate citrate toxicity with massive transfusion
  • Drug handling: reduced hepatic clearance and altered protein binding; titrate to effect; prefer short-acting agents with organ-independent metabolism where possible
  • Renal protection: avoid nephrotoxins; maintain perfusion; consider RRT coordination
  • Neuro: encephalopathy/raised ICP risk in ALF—avoid hypoxia/hypercapnia; maintain CPP; consider hypertonic saline strategy where used locally

Definitions and classification

• Acute liver failure (ALF): acute hepatic injury with impaired synthetic function (INR ≥ 1.5) and hepatic encephalopathy in a patient without pre-existing cirrhosis (classically within 26 weeks).
• Acute-on-chronic liver failure (ACLF): acute decompensation of cirrhosis with organ failures and high short-term mortality (definitions vary: EASL-CLIF).
• Decompensated chronic liver disease: cirrhosis with complications (ascites, variceal bleed, encephalopathy, jaundice, HRS).
• Severity scoring used in ICU/transplant discussions
  • MELD-Na: predicts mortality and transplant priority (bilirubin, INR, creatinine, sodium).
  • Child-Pugh: chronic liver disease severity (bilirubin, albumin, INR, ascites, encephalopathy).
  • King’s College Criteria (KCC): prognostic/transplant criteria in ALF (paracetamol vs non-paracetamol).
  • SOFA/CLIF-SOFA: organ failure burden in ACLF.

Aetiology (high-yield ICU causes)

• ALF causes
  • Paracetamol (acetaminophen) toxicity (commonest in UK).
  • Viral hepatitis (A, B, E), HSV (esp. pregnancy/immunosuppressed).
  • Drug-induced liver injury: anti-TB drugs, valproate, antibiotics, herbal agents.
  • Ischaemic hepatitis (“shock liver”): hypotension/hypoxia, cardiac arrest, severe sepsis.
  • Vascular: Budd–Chiari, hepatic artery thrombosis.
  • Pregnancy-related: acute fatty liver of pregnancy, HELLP.
  • Metabolic/other: Wilson’s disease (young, Coombs-negative haemolysis), malignancy infiltration.
• ACLF precipitants
  • Sepsis (including spontaneous bacterial peritonitis), GI bleeding, alcohol binge, drug/toxin, dehydration/over-diuresis, portal vein thrombosis, surgery.

Pathophysiology relevant to ICU

• Circulation: hyperdynamic state (low SVR, high CO) + relative hypovolaemia; vasoplegia worsens with sepsis; cirrhotic cardiomyopathy may limit stress response.
• Renal: hepatorenal physiology (renal vasoconstriction, low effective arterial volume) predisposes to AKI; ATN common with sepsis/bleeding.
• Respiratory: hepatopulmonary syndrome (intrapulmonary shunt, hypoxaemia) and portopulmonary hypertension; ascites/pleural effusions impair mechanics.
• Haemostasis: “rebalanced” haemostasis—both bleeding and thrombosis risk; INR reflects reduced procoagulants but not anticoagulants; platelet dysfunction + thrombocytopenia; hyperfibrinolysis may occur.
• Metabolism: hypoglycaemia (reduced gluconeogenesis), lactic acidosis (impaired clearance), hypothermia.
• CNS: hepatic encephalopathy; in ALF risk of cerebral oedema/raised ICP (ammonia-driven astrocyte swelling + inflammation).
• Immune: immune dysfunction with high infection risk (bacterial/fungal) despite inflammatory phenotype.

Assessment and monitoring in ICU

• History/exam: timeline (acute vs chronic), toxins/drugs (paracetamol), alcohol, viral risks, pregnancy; bleeding, confusion, sepsis signs; stigmata of chronic liver disease.
• Core investigations
  • Bloods: LFTs, bilirubin, INR/PT, fibrinogen, FBC/platelets, U&E/creatinine, glucose, ABG/VBG with lactate, ammonia (trend), group & screen/crossmatch.
  • Infection: cultures (blood/urine/ascitic fluid), CXR, procalcitonin as per local practice.
  • Aetiology: paracetamol level (timed), viral serology, autoimmune markers, ceruloplasmin/urinary copper if suspected, pregnancy tests.
  • Imaging: ultrasound Doppler (portal/hepatic veins), CT if needed; consider echocardiography (cirrhotic cardiomyopathy, PoPH).
• Monitoring
  • Arterial line for frequent gases/glucose and BP; central access for vasoactives; consider cardiac output monitoring if refractory shock.
  • Neuro: frequent GCS/encephalopathy grading; pupils; consider continuous EEG if seizures suspected; ICP monitoring only in selected ALF patients in specialist centres.
  • Fluid balance: strict I/O, daily weight; assess volume responsiveness carefully (dynamic indices, echo).

Organ support and ICU management

• Airway/ventilation
  • Intubate for airway protection (grade 3–4 encephalopathy), uncontrolled agitation, severe hypoxaemia, refractory acidosis, or procedures.
  • Ventilation targets: avoid hypoxia; avoid hypercapnia in ALF with cerebral oedema risk (CO2 increases CBF/ICP). Maintain normocapnia unless directed by neuro strategy.
  • PEEP: balance oxygenation vs venous return/ICP; use lung-protective ventilation if ARDS.
• Circulation
  • Resuscitation: cautious crystalloids; avoid chloride load if possible; albumin often used in cirrhosis-specific indications (SBP, HRS, large-volume paracentesis).
  • Vasopressors: noradrenaline first-line; add vasopressin if refractory vasoplegia; terlipressin used for variceal bleed and HRS (monitor ischaemia/hyponatraemia).
  • Inotropes: consider dobutamine if low CO/cirrhotic cardiomyopathy with hypoperfusion.
• Renal support
  • Differentiate prerenal/HRS vs ATN; treat triggers (sepsis, bleeding), stop nephrotoxins, optimise MAP.
  • HRS management (specialist guidance): albumin + vasoconstrictor (terlipressin or noradrenaline in ICU); consider TIPS as bridge in selected; definitive = transplant.
  • RRT: use for refractory hyperkalaemia, acidosis, fluid overload, uraemia; in ALF consider earlier CRRT to help ammonia control and fluid/temperature management.
• Neurological complications (encephalopathy and cerebral oedema in ALF)
  • General measures: head-up 30°, avoid neck venous obstruction, treat fever, avoid hyponatraemia, maintain adequate MAP/CPP, avoid sedative accumulation.
  • Ammonia reduction: lactulose (mainly chronic HE; limited in ileus), rifaximin (chronic), treat constipation; CRRT can reduce ammonia in ALF.
  • Cerebral oedema strategy (specialist ALF): hypertonic saline to maintain higher-normal Na+ (local targets), mannitol bolus if acute ICP rise and osmolality allows; avoid hypotonic fluids.
  • Seizures: treat promptly (levetiracetam often preferred); consider EEG if unexplained low GCS.
• Coagulopathy and bleeding
  • Do not correct INR routinely in non-bleeding patients; INR poorly predicts bleeding risk in cirrhosis.
  • If bleeding or high-risk procedure: use TEG/ROTEM-guided therapy; consider fibrinogen replacement (cryoprecipitate/fibrinogen concentrate) if low; platelets if thrombocytopenic with bleeding/procedure.
  • FFP: large volumes needed; may worsen portal hypertension/volume overload; reserve for active bleeding/procedures with significant coagulopathy.
  • Vitamin K: give if deficiency possible (cholestasis, malnutrition) but expect limited effect in severe failure.
  • Thrombosis prophylaxis: consider pharmacological VTE prophylaxis if platelets/coagulation allow; cirrhosis is not “auto-anticoagulated”.
• Infection management
  • Low threshold for broad-spectrum antibiotics in ACLF/ALF with shock or suspected infection; de-escalate with cultures.
  • SBP: diagnostic paracentesis if ascites + deterioration; treat per protocol; albumin reduces renal failure risk in SBP.
  • Fungal infection risk in prolonged ICU/transplant candidates—consider early discussion with microbiology.
• GI bleeding (variceal) in ICU
  • Resuscitate with permissive transfusion strategy: target Hb often ~70–80 g/L unless specific indications; correct hypocalcaemia; warm patient.
  • Early vasoactive therapy: terlipressin; antibiotics prophylaxis; urgent endoscopy for banding.
  • Airway: early intubation often appropriate for massive haematemesis/encephalopathy.
  • Rescue: balloon tamponade as bridge; TIPSS for refractory bleeding.
• Nutrition and metabolic care
  • Avoid prolonged fasting; early enteral feeding if possible; protein restriction is rarely indicated—aim adequate protein unless refractory encephalopathy with specialist input.
  • Glucose: frequent monitoring; dextrose infusion may be required in ALF.
  • Electrolytes: correct phosphate (refeeding risk), magnesium, potassium; manage hyponatraemia cautiously (avoid rapid correction).
• Specific therapy in paracetamol toxicity
  • N-acetylcysteine (NAC): give according to protocol; benefits even in established liver injury; monitor for anaphylactoid reactions.
  • Consider early referral to liver transplant centre if criteria met or deteriorating (INR, lactate, pH, encephalopathy, creatinine).

When to refer/consider transplantation (high-yield)

• Early discussion with specialist liver/transplant centre for all ALF with encephalopathy or rapidly worsening synthetic function.
• King’s College Criteria (KCC) — Paracetamol ALF
  • Arterial pH < 7.30 (after resuscitation) OR
  • All of: INR > 6.5, creatinine > 300 µmol/L, and grade 3–4 encephalopathy.
  • Lactate criteria are used in many centres (e.g., persistent lactate elevation after fluid resuscitation) as additional prognostic markers.
• KCC — Non-paracetamol ALF
  • INR > 6.5 regardless of encephalopathy grade OR
  • Any 3 of: age <10 or >40, jaundice-to-encephalopathy >7 days, INR >3.5, bilirubin >300 µmol/L, aetiology: non-A non-B hepatitis, idiosyncratic drug reaction.
• Contraindications/limitations (centre-specific): uncontrolled sepsis, irreversible neurological injury, severe cardiopulmonary disease, active malignancy, ongoing substance misuse, inability to engage with care.

Drug handling and sedation/analgesia in liver failure (ICU practical)

• Principles: reduced hepatic clearance, reduced albumin (↑ free drug), increased volume of distribution (ascites), increased sensitivity to CNS depressants; titrate to effect and use short-acting agents.
• Sedation
  • Propofol: useful (extrahepatic clearance) but hypotension risk; avoid prolonged deep sedation if neuro assessment needed.
  • Midazolam: prolonged effect; avoid or use very small doses with close monitoring.
  • Dexmedetomidine: can facilitate neuro assessment; watch bradycardia/hypotension.
• Analgesia
  • Opioids: increased sensitivity; prefer fentanyl/alfentanil/remifentanil (short-acting); avoid large morphine doses (active metabolites, histamine).
  • Paracetamol: avoid in ALF; in stable chronic liver disease can be used at reduced total daily dose per local policy.
  • NSAIDs: generally avoid (renal impairment, GI bleeding, platelet dysfunction).
• Neuromuscular blockade
  • Atracurium/cisatracurium preferred (Hofmann/elimination); rocuronium duration may be prolonged; sugammadex works but consider renal function and cost/availability.