ICU · gi-nutrition

Acute Hepatic Encephalopathy — Comprehensive ICU Management (West Haven, Lactulose, Rifaximin, Cerebral Oedema, Nutrition)

Also known as Hepatic encephalopathy · HE · Acute hepatic encephalopathy · West Haven classification · Portosystemic encephalopathy · Lactulose · Rifaximin · Ammonia neurotoxicity · Astrocyte swelling · Covert and overt HE · TIPS-related encephalopathy

Hepatic encephalopathy (HE) = a reversible syndrome of impaired brain function in patients with advanced liver disease and/or portosystemic shunting, produced by gut-derived neurotoxins (predominantly ammonia) that the failing liver cannot clear. ACUTE (episodic) HE is the common ICU presentation: a cirrhotic patient who was previously well develops overt confusion, somnolence or coma over hours-days, almost always driven by a PRECIPITANT. The fellowship-level intensivist must master FIVE domains. (1) RECOGNISE AND GRADE using the West Haven classification: grade 1 (mild confusion, euphoria/anxiety, sleep reversal, +/- asterixis), grade 2 (lethargy, disorientation, personality change, asterixis present), grade 3 (somnolent but rousable, gross disorientation, incomprehensible speech), grade 4 (coma). Grades 1-2 = 'covert/mild'; grade 2-4 = 'overt'. (2) UNDERSTAND THE PATHOPHYSIOLOGY: ammonia (produced in the gut by bacterial deamination of urea/protein) is normally cleared by the hepatic urea cycle; in cirrhosis it is shunted past the liver (portosystemic shunting) and reaches the brain, where it diffuses across the blood-brain barrier into ASTROCYTES. Astrocyte glutamine synthetase condenses ammonia + glutamate - GLUTAMINE; glutamine is osmotically active, accumulates, draws in water - ASTROCYTE SWELLING (Alzheimer type II astrocytosis). When this overwhelms compensatory osmolyte (myo-inositol) release - CYTOTOXIC CEREBRAL OEDEMA - raised ICP. Cerebral oedema is COMMON in acute liver failure (Type A) but UNCOMMON in cirrhotic (Type C) HE (the brain has time to adapt osmotically) — though it can occur in high-grade or rapidly evolving HE. (3) FIND AND TREAT THE PRECIPITANT — the 1 priority, because episodic HE rarely occurs without one: INFECTION is 1 (spontaneous bacterial peritonitis, pneumonia, bacteraemia, UTI — culture EVERYTHING and treat empirically), followed by gastrointestinal bleed, CONSTIPATION, electrolyte derangement (HYPO NATRAEMIA 1 electrolyte cause; hypokalaemia — hypokalaemia promotes renal ammonia production), SEDATIVES/benzodiazepines (GABAergic — precipitate HE; avoid unless treating alcohol withdrawal), ALCOHOL (intoxication or withdrawal), and TIPS (transjugular intrahepatic portosystemic shunt — increases portosystemic shunting; HE in ~20-40% post-TIPS). (4) AMMONIA-LOWERING THERAPY: LACTULOOSE first-line — a non-absorbable disaccharide converted by gut bacteria to organic acids, lowering colonic pH and converting absorbable NH3 to non-absorbable NH4+ (ion trapping) plus a cathartic effect; in deep encephalopathy give it via NG or enema with oral dosing repeated hourly until stools appear, then titrate to the endpoint of 2-3 soft bowel motions/day (the ENDPOINT is stool frequency/consistency, NEVER a target ammonia). RIFAXIMIN 550 mg BD is ADDITIVE to lactulose for recurrent/overt HE — a minimally absorbed gut rifamycin antibiotic that reduces ammonia-producing bacteria (Bass 2010 NEJM RCT: rifaximin + lactulose reduced breakthrough HE by 58% over 6 months vs lactulose + placebo). (5) SUPPORTIVE AND AVOIDANCE MEASURES: AVOID BENZODIAZEPINES unless treating alcohol withdrawal (they are GABA-ergic and precipitate/worsen HE; if sedation is unavoidable use a SHORT-ACTING agent like oxazepam or lorazepam — and only after flumazenil-reversibility has been considered); provide NUTRITION with a HIGH-PROTEIN diet 1.2-1.5 g/kg/day — protein is NOT restricted (Cordoba 2004 RCT: a normal-protein diet was as safe as a low-protein diet and avoided the protein catabolism that itself generates ammonia); manage cerebral oedema if it develops (head of bed 30 degrees, hypertonic saline, mannitol if ICP monitored). PROGNOSIS: overt HE carries 1-year mortality ~40-50% in cirrhosis; the severity of HE and the underlying liver failure (Child-Pugh/MELD), recurrence, and response to therapy determine outcome. The two examinable 'do-NOT' rules: do NOT routinely check or chase a 'target ammonia' level to guide therapy (it is supportive, not diagnostic or a treatment target — titrate lactulose to stools); and do NOT restrict dietary protein (protein restriction worsens sarcopenia, increases ammonia-generating catabolism, and does not improve HE).

Checked against its sources on 3 Sept 2026