Hepatic Encephalopathy (HE)

Grade it before induction - West Haven criteria, plus a look for asterixis, hyperreflexia, and an inverted sleep-wake pattern. Serial ammonia levels track the patient poorly; follow the exam.

Airway and aspiration - Grade 3-4 HE has no reliable airway protection, and ascites raises intra-abdominal pressure on top of it. Plan RSI. Patients at risk for aspiration or respiratory compromise get intubated prophylactically and go to the ICU.

Sedatives hit harder - Hepatically cleared drugs linger, so reduce doses across the board. Avoid benzodiazepines, particularly when alcohol withdrawal is also in play, and avoid known hepatotoxic drugs.

Find the trigger first - GI bleed, infection, constipation, dehydration from diuretics or paracentesis, electrolyte derangement, renal failure, or a new sedative. Elective cases wait until the precipitant is fixed.

Intraoperative housekeeping - Follow electrolytes and urine output. Both drive HE and both move fast in a cirrhotic on diuretics.

Coagulation before neuraxial - INR and platelet count. Synthetic failure drops factors V and VII, hypersplenism drops platelets, and portal hypertension engorges the epidural veins, which raises the bloody-tap risk.

Protect hepatic perfusion - Anesthesia and surgery cut hepatic blood flow and oxygen delivery by as much as 30-40%. Hypotension on top of that is ischemia-reperfusion injury and postoperative liver dysfunction.

Ask about a shunt - HE follows TIPS in 24-53% of cases. Find out whether a shunt exists and how the patient behaved after it.

Acute liver failure crossover - When HE comes from acute liver failure, cerebral edema is what kills: head elevation, mannitol, hyperventilation. Run dextrose — hypoglycemia is common and harmful. Correct coagulopathy only for active bleeding or an invasive procedure.

Emergence - Expect delayed awakening and plan for it. A patient who does not wake needs the metabolic workup, not more time.

Hepatic encephalopathy (HE) is a reversible neuropsychiatric syndrome that appears when the liver can no longer clear gut-derived neurotoxins, or when portosystemic shunting lets them bypass the liver entirely. Gut bacteria generate ammonia from urea, protein, and glutamine; failing hepatocytes and collateral shunts strip out first-pass clearance, and hyperammonemia follows.

Ammonia crosses the blood-brain barrier into astrocytes, where glutamine synthesis, increased GABA activity, and impaired energy utilization produce the clinical picture — inverted sleep-wake cycle first, then confusion and asterixis, then coma. Cerebral edema and seizures travel with it in acute liver failure.

HE complicates 30-45% of patients with cirrhosis and 24-53% of patients after TIPS. Almost every episode has a trigger: GI bleeding, infection, constipation, dehydration from diuretics or large-volume paracentesis, electrolyte derangement, renal failure, or sedatives — exactly the list a perioperative course can supply.