Withdrawal, Wernicke risk and a cirrhotic liver

Alcohol withdrawal delirium (delirium tremens) in a dependent drinker, starting about 36 hours after the last drink, with tremor, diaphoresis, tachycardia, hypertension, visual hallucinations, disorientation and a CIWA-Ar of 24. DT typically begins 48–96 hours after the last drink but can start earlier; the presence of hallucinations and disorientation rather than tremor alone marks the severe end of the spectrum, with a mortality of several per cent if untreated.

Competing explanations

• Hepatic encephalopathy: asterixis, a clear precipitant (bleeding, infection, constipation, hypokalaemia) and often a higher ammonia. Here ammonia is only mildly raised, there is no asterixis, and there is florid autonomic overactivity, which encephalopathy does not cause. The two can coexist, and his potassium of 3.3 and gastrointestinal bleed are both precipitants.
• Wernicke's encephalopathy: ophthalmoplegia, nystagmus, ataxia and global confusion; absence does not exclude it, and any at-risk drinker with confusion should be treated presumptively.
• Gastrointestinal haemorrhage and hypovolaemia: tachycardia and confusion may be due to blood loss; check haemoglobin, lactate and urine output, and resuscitate.
• Sepsis, subdural haematoma (low platelets, falls), hypoglycaemia, hyponatraemia (131) and postictal state: all need excluding with bedside glucose, bloods and imaging where indicated.

A CIWA-Ar score is meaningless in a patient who is disorientated, encephalopathic or intubated - it can only be used in a patient who can answer; in delirium, treat empirically.

Benzodiazepine choice. Chlordiazepoxide is the usual first-line drug, but it is a long-acting agent with active metabolites that accumulate in cirrhosis and in the elderly, prolonging sedation and worsening encephalopathy. In Child–Pugh B, lorazepam is preferred: it undergoes glucuronidation, which is relatively preserved in liver disease, has no active metabolites and a shorter half-life. Use it as a symptom-triggered regimen - for example lorazepam 2 mg orally or IV, repeated every 1–2 hours according to the sedation and withdrawal score, then tapered over 3–5 days - rather than a fixed high-dose loading schedule. Give thiamine 100 mg IV before any glucose-containing fluid, and in a malnourished drinker use parenteral Pabrinex (two pairs three times daily for 2–3 days) to prevent Wernicke's encephalopathy. Replace magnesium and potassium, and monitor for hypoglycaemia.

Monitoring. Hourly in the first 24 hours: sedation level, respiratory rate, pulse, blood pressure, temperature, fluid balance and neurological observations. Repeat electrolytes, magnesium, phosphate, renal function, INR, glucose and ammonia; watch for aspiration, seizures, arrhythmia and gastrointestinal rebleeding. Keep the environment quiet and well lit, with reorientation and 1:1 nursing.

What to avoid. Antipsychotics are not a substitute for benzodiazepines in withdrawal; they lower the seizure threshold and add to QT risk, and haloperidol in liver disease can precipitate encephalopathy. Do not use physical restraint. Avoid paracetamol above 2 g/day and avoid sedatives with anticholinergic load. Involve hepatology and gastroenterology early, because the bleed and the withdrawal are being treated simultaneously and each worsens the other.

Assess the mental state properly before labelling it. Depressive and anxiety symptoms in the first two to four weeks of abstinence are often withdrawal-related and improve; do not diagnose major depression on the ward. Reassess at four weeks with a structured interview and a suicide risk assessment, since drinkers with cirrhosis have a high suicide risk and access to medication.

Pharmacological relapse prevention with the liver in mind

• Baclofen is the best-supported option in alcohol-related cirrhosis and is not hepatotoxic; start at 5 mg three times daily and titrate, adjusting for renal function and sedation.
• Acamprosate is reasonable if renal function is intact (it is renally excreted) and is useful for maintaining abstinence.
• Naltrexone should be avoided or used only with close monitoring of liver enzymes in advanced cirrhosis.
• Disulfiram is absolutely contraindicated in liver disease and in anyone who may drink impulsively.
• Treat any confirmed depression with an SSRI such as sertraline at a low starting dose, monitoring for hyponatraemia in someone with ascites, and avoid drugs with high hepatic metabolism where possible.

Non-pharmacological and social

• Refer to an addiction service and to Alcoholics Anonymous or a comparable peer group; motivational work and relapse-prevention sessions focused on triggers, craving and his social network.
• Hepatology follow-up with variceal surveillance, nutrition review and micronutrient replacement, and a written plan for what to do if he drinks again.
• Involve his family with his consent, address housing and employment, and give the GP a clear shared-care plan. Document the Wernicke risk so that any future presentation receives thiamine immediately.