Erfan Bashar
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Delirium — Management

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Educational scope notice: This is a study note for medical students, not medical advice, diagnosis, or treatment guidance. Clinical management should follow local protocols and current guidelines. Drug doses are intentionally omitted; exact regimens follow local protocols.

Management follows a strict hierarchy: remove the cause, stabilise the patient with environmental and supportive measures, and consider drugs only where distress or danger remains. Treating delirium without finding its cause fails, because delirium is always the consequence of something else.

The first step is identifying and eliminating the underlying trigger, whether infection, metabolic derangement, drug effect, withdrawal, retention, or pain. Alongside it comes stabilisation: correcting dehydration, electrolyte imbalance, and nutritional deficiency. Nurses carry much of this work, because they spend the most time with the patient and notice the early drift first.

Environment before drugs

Environmental measures sound modest and matter greatly. Reorient frequently to time, place, and person, with clocks, calendars, daylight, and familiar objects. Reduce staff changes and ambient noise. Mobilise early, protect night-time sleep, keep hydration and nutrition going, and remove restraints and catheters wherever possible. Each of these reverses one of the precipitating factors, which is why multicomponent prevention programmes built on exactly these measures cut delirium odds roughly in half.

Drugs: a narrow, qualified place

The guiding rule is to avoid sedating confused patients wherever possible, because sedation clouds the picture and can worsen the episode. In particular, phenobarbital and long-acting benzodiazepines are avoided in general delirium for their paradoxical effects.

That rule has one major exception. Alcohol withdrawal delirium, delirium tremens, is treated with benzodiazepines, which remain the mainstay. Longer-acting agents such as diazepam or chlordiazepoxide are generally preferred, while lorazepam or oxazepam is chosen when hepatic function is impaired. The claim that giving alcohol treats delirium tremens is wrong; benzodiazepines are the standard of care.

Where drugs are needed for severe distress, agitation, or psychosis that non-drug measures have not settled, guidance allows a short trial of low-dose haloperidol, usually for 1 week or less, started at the lowest clinically appropriate dose and reviewed quickly, with caution in Parkinson disease and Lewy-body dementia. Distress may be less evident in hypoactive delirium, which can still involve psychotic symptoms, so the absence of agitation never rules out suffering. Antipsychotics do not treat the cause, and trial evidence for shortening delirium is inconclusive: in ventilated and shocked intensive-care patients, haloperidol or ziprasidone did not shorten delirium compared with placebo. They are a bridge for dangerous agitation rather than a treatment for delirium itself, and intensive-care guidance recommends against routine use. Atypical antipsychotics, cholinesterase inhibitors, valproate, and melatonin have all been tried on mechanistic grounds, but none carries definitive evidence in delirium, and melatonin’s plausible role is limited to the sleep-wake disturbance.

Prevention deserves the last word because so much delirium is clinician-made. Early identification of at-risk patients, especially frail elderly ones, with reorientation, mobilisation, sleep protection, and hydration, prevents cases that restraints, catheters, polypharmacy, and chaotic wards would otherwise create. Hospital care designed for the elderly patient is itself the treatment.

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