Alcohol withdrawal and delirium tremens: quick reference

Rapid summary

Alcohol withdrawal occurs after an abrupt reduction or cessation of prolonged and heavy alcohol intake. The condition can develop despite a measurable or high blood alcohol concentration, particularly in patients with marked tolerance.

The most important measures in severe or complicated withdrawal are:

1. A benzodiazepine in a sufficient and repeated dose, titrated against clinical effect.
2. Parenteral thiamine early, preferably before or at the same time as carbohydrate administration.
3. Rapid identification of seizures, delirium tremens, infection, trauma and metabolic disturbance.
4. Monitoring at the appropriate level of care, with readiness for respiratory support.
5. Treatment of the alcohol use disorder and planned follow-up, not merely detoxification.

Benzodiazepines reduce the severity of withdrawal and the risk of seizures and delirium [1,2]. In delirium tremens the aim should be a calm, mildly somnolent but rousable patient, while ventilation, circulation and underlying disease are monitored [3].

The management of complicated withdrawal varies between regions and units. Follow the local protocol for choice of drug, dosing, route of administration and criteria for intermediate care or intensive care.

Time course after the last intake

The times given are approximate. Symptoms can begin before the blood alcohol concentration has reached zero, and several syndromes can overlap [1,4].

More than 90 percent of withdrawal seizures occur within 48 hours. Seizures later than this, focal seizures or status epilepticus should raise strong suspicion of another or an additional cause [1]. Delirium tremens most often begins after one to three days but can start earlier in patients with previous complicated withdrawal [4].

Untreated delirium tremens has historically carried a high mortality. With modern sedation, supportive treatment and treatment of the precipitating illness the prognosis is considerably better [3,5].

Pathophysiology

Alcohol enhances inhibitory signalling via gamma-aminobutyric acid, GABA, and inhibits excitatory glutamate signalling, in part via NMDA receptors. With prolonged alcohol exposure the nervous system adapts through reduced GABA-mediated inhibition and increased glutamatergic activity. When the alcohol level suddenly falls, the compensatory excitation remains, producing tremor, sympathetic activation, hallucinations, seizures and delirium [1,6].

Repeated withdrawal episodes can, through so-called kindling, make later episodes more severe and lower the seizure threshold [6]. This explains why a history of previous withdrawal seizures or delirium tremens is one of the strongest risk markers for a new complicated withdrawal.

Benzodiazepines enhance the function of the GABA-A receptor and are cross-tolerant with alcohol. They therefore treat the central mechanism underlying withdrawal, unlike, for example, beta blockers, alpha-2 agonists and antipsychotics, which mainly affect individual symptoms.

Initial management

ABCDE and immediate tests

Assess the withdrawal and other life-threatening conditions at the same time.

• Secure a patent airway and adequate ventilation.
• Measure oxygen saturation, respiratory rate, pulse, blood pressure and temperature.
• Check the plasma glucose immediately.
• Assess level of consciousness, orientation, focal neurology and signs of trauma.
• Insert an intravenous cannula in moderate or severe withdrawal.
• Record an ECG in marked autonomic involvement, electrolyte disturbance, chest pain, arrhythmia or when antipsychotic treatment is planned.

Reasonable initial laboratory tests are full blood count, sodium, potassium, creatinine, liver function tests, bilirubin, INR, glucose, magnesium, phosphate and calcium. Add further tests according to the clinical picture: blood gas, ketones, lipase, CRP, cultures, ammonia, toxicological analyses and a pregnancy test.

The blood alcohol concentration can support the history but neither confirms nor excludes withdrawal. Withdrawal symptoms despite a high alcohol concentration indicate marked tolerance and an increased risk of further deterioration [7].

Treatment goals

The goal is not to normalise a rating scale score at any cost. The goal is to:

• stop seizures and prevent new seizures
• reduce agitation, anxiety and autonomic hyperactivity
• achieve calm or mild somnolence without unnecessarily deep sedation
• avoid aspiration, trauma, overheating and circulatory instability
• identify and treat concurrent illness
• prevent Wernicke's encephalopathy.

Risk assessment

Risk factors for severe or complicated withdrawal

Risk is increased with:

• previous delirium tremens
• previous withdrawal seizures
• several previous withdrawal episodes
• prolonged and very high alcohol intake
• withdrawal symptoms despite a measurable or high alcohol concentration
• clear autonomic hyperactivity on arrival
• concurrent infection, sepsis, trauma, surgery or other acute illness
• old age or frailty
• decompensated liver cirrhosis or other serious organ disease
• hypokalaemia, hypomagnesaemia, thrombocytopenia or marked malnutrition
• concurrent withdrawal from benzodiazepines or other sedatives
• use of several substances
• limited scope for observation, adherence or social support.

Previous delirium tremens or withdrawal seizures are particularly important risk markers [1].

PAWSS

The Prediction of Alcohol Withdrawal Severity Scale, PAWSS, is intended to predict complicated withdrawal before it has developed. It should not be confused with CIWA-Ar, which grades ongoing symptoms. In a prospective validation among medical inpatients, PAWSS with a cut-off of 4 had a sensitivity of 93.1 percent and a specificity of 99.5 percent for complicated withdrawal [8]. The scale was developed after a systematic review of risk factors and an initial pilot study [9].

The results are promising, but the scale does not replace clinical judgement and should be used according to local protocol.

CIWA-Ar

CIWA-Ar grades ten symptoms, including nausea, tremor, sweating, anxiety, agitation, perceptual disturbances, headache and orientation. It can be used for repeated assessments and symptom-triggered treatment in a communicative and otherwise assessable patient.

Important limitations:

• CIWA-Ar does not diagnose alcohol withdrawal.
• The scale does not reliably predict future seizures or delirium.
• It does not distinguish delirium tremens from delirium of another cause.
• It requires the patient to be able to understand and answer questions.
• Pain, infection, anxiety, psychosis, nausea and trauma can produce falsely high scores.
• It is unsuitable in intubation, marked confusion, language barriers or reduced consciousness.
• It is not well validated in the severely physically ill or in intensive care patients [4,10].

In delirium tremens or intensive care, a general sedation scale such as RASS is often more useful than CIWA-Ar.

Choice of level of care

Outpatient management can only be considered with

• mild withdrawal
• no previous seizures or delirium tremens
• no serious physical or psychiatric comorbidity
• stable vital signs
• a reliable patient
• a sober and drug-free support person
• safe housing
• the possibility of daily follow-up and rapid return.

Admission is recommended with

• previous complicated withdrawal
• current seizures, hallucinations or delirium
• moderate or severe withdrawal
• marked autonomic involvement
• pregnancy
• old age or frailty
• serious liver, lung, cardiac or renal disease
• suspected infection, pancreatitis, bleeding or trauma
• electrolyte disturbance or malnutrition
• concurrent withdrawal from other sedatives
• suicide risk, psychosis or lack of social safety.

Patients with decompensated cirrhosis or significant liver dysfunction are as a rule not suitable for outpatient detoxification [11].

Benzodiazepines

Benzodiazepines are first-line treatment in moderate, severe or complicated alcohol withdrawal. In a Cochrane review of 64 studies and 4,309 participants, benzodiazepines reduced the risk of withdrawal seizures compared with placebo, relative risk 0.16, 95 percent confidence interval 0.04 to 0.69 [2]. There is no reliable evidence that any single benzodiazepine is generally more effective than the others.

Choice of drug

Diazepam has active metabolites and can accumulate in cirrhosis and in the elderly. Oxazepam and lorazepam are metabolised mainly by glucuronidation and have no long-acting active metabolites, which reduces but does not eliminate the risk of oversedation [1,11].

Oxazepam has a slower onset than intravenous diazepam and is therefore not the first choice for rapid control of seizures or marked agitation.

Symptom-triggered treatment

In symptom-triggered treatment, a further dose is given after a structured assessment, followed by frequent reassessments. In studies from specialised detoxification units this reduces the total benzodiazepine dose and the duration of treatment.

A meta-analysis of six randomised trials with 664 patients found that symptom-triggered treatment shortened treatment by an average of 60.4 hours and reduced the dose by 10.5 mg lorazepam equivalents. The studies mainly comprised low-risk patients in specialised settings. There was insufficient evidence for conclusions about mortality, seizures or delirium, and transferability to acute hospitals was limited [12].

Symptom-triggered dosing is unsuitable as the sole strategy when the patient:

• cannot communicate reliably
• has delirium or is intubated
• has previous withdrawal seizures that occurred without clear preceding symptoms
• has conditions that distort the rating score
• cannot be assessed sufficiently often.

Front-loading

Front-loading means repeated doses of a long-acting drug under close monitoring until the withdrawal is controlled. The method is particularly relevant in severe withdrawal or a high risk of complications. The prolonged effect then provides a pharmacological self-tapering.

Front-loading requires repeated checks of respiration, level of consciousness, blood pressure and clinical effect. The risk of accumulation is greater in old age, cirrhosis and with concurrent opioid or sedative effect [6].

Fixed schedule and tapering

A fixed schedule can be suitable when:

• the rating scale cannot be used reliably
• staffing does not allow sufficiently frequent assessments
• the patient has a high risk of complications
• a symptom-triggered protocol is supplemented with scheduled baseline treatment.

Once the withdrawal is under control, an individual oxazepam schedule can be prescribed, often distributed over the 24 hours. The daily dose can then usually be reduced progressively and treatment stopped within approximately 3 to 7 days. Longer treatment increases the risk of accumulation, falls, confusion, dependence and diversion.

A general reduction of 25 to 40 percent per day can be used in some local schedules, but must be adapted to the previous dose requirement, the half-life of the drug, liver function, comorbidity and residual symptoms. After extensive front-loading with diazepam a separate tapering schedule is not always needed.

Monitoring for adverse effects

Check in particular for:

• a falling respiratory rate
• hypoventilation or rising carbon dioxide
• increasing somnolence
• aspiration
• ataxia and risk of falls
• hypotension
• paradoxical agitation
• concurrent opioid or sedative effect.

Fear of respiratory depression must not lead to inadequate treatment of an ongoing delirium tremens. The solution is a higher level of care and closer monitoring, not leaving the central withdrawal mechanism untreated.

Withdrawal seizures

Withdrawal seizures are usually generalised tonic-clonic and most often occur within 12 to 48 hours. They can occur without marked preceding autonomic symptoms. More than half of patients have several seizures, and a smaller proportion develop status epilepticus [1,4].

Acute management

• Follow the usual ABCDE approach.
• Terminate an ongoing seizure with a benzodiazepine according to the local seizure protocol.
• Check the plasma glucose.
• Correct hypoxia and relevant electrolyte disturbances.
• Continue withdrawal treatment even after the seizure has stopped.
• Monitor for further seizures and for the development of delirium tremens.

In a randomised trial, intravenous lorazepam reduced the risk of a further seizure within six hours compared with placebo. Benzodiazepines are the best-supported drug class for preventing recurrent withdrawal seizures [13].

Antiepileptic drugs

Phenytoin does not prevent recurrent pure withdrawal seizures and should not be given for this indication alone [13]. It may still be relevant if the patient also has epilepsy or another established indication.

A Cochrane review of 56 studies and 4,076 participants did not find sufficient support for routinely replacing benzodiazepines with carbamazepine, valproate or other antiepileptic drugs [14]. Gabapentin and carbamazepine may have a role in selected cases of mild withdrawal, but the evidence is weaker in severe or complicated withdrawal [15].

Investigate the seizure particularly with

• a first seizure
• focal onset
• focal neurology
• status epilepticus
• more seizures than expected
• a seizure more than 48 hours after the last intake
• fever or meningism
• head trauma
• persisting impairment of consciousness
• suspected mixed poisoning or concurrent sedative withdrawal.

CT of the brain is performed on indication. EEG should be considered when non-convulsive status is suspected, with a new seizure pattern or with unexplained persisting reduced consciousness [1].

Thiamine and Wernicke's encephalopathy

When thiamine should be given

Give parenteral thiamine early in:

• alcohol withdrawal in a malnourished patient
• prolonged high alcohol intake
• delirium or other confusion
• difficulty walking or ataxia
• ocular motor abnormalities or nystagmus
• prolonged vomiting
• hypothermia or hypotension without a clear explanation
• planned intravenous glucose, enteral nutrition or parenteral nutrition
• suspected Wernicke's encephalopathy.

Oral thiamine is insufficient as initial treatment when Wernicke's encephalopathy is suspected, because absorption is unreliable.

Dosing

Swedish local protocols vary. Follow the local protocol. A common Swedish approach is:

The scientific evidence for the exact optimal dose and duration of treatment is weak. A Cochrane review found insufficient randomised evidence to determine the best dose, frequency or route of administration [16]. In a later randomised trial there was no reliable difference in neurological or cognitive outcomes between different parenteral dose levels, but substantial methodological problems limit the conclusions [17]. Since untreated Wernicke's encephalopathy can cause permanent memory impairment and the treatment is relatively safe, high-dose regimens are still used when there is clinical suspicion.

Thiamine and glucose

Give thiamine before or at the same time as glucose when this can be done without delay. Never delay acute glucose treatment in hypoglycaemia. The evidence that a single dose of glucose would immediately precipitate Wernicke's encephalopathy consists mainly of case reports. Prolonged carbohydrate administration without thiamine can, however, worsen an existing deficiency [18].

Practical rule:

• at a normal glucose level, give thiamine first or at the same time
• in hypoglycaemia, give glucose immediately and thiamine as soon as possible.

Clinical diagnosis

The classic triad of confusion, ataxia and ocular motor disturbance is complete in a minority. Suspect Wernicke's encephalopathy if at least two of the following are present:

• nutritional deficiency
• ocular motor signs
• cerebellar dysfunction
• altered mental state or memory disturbance.

A normal CT of the brain does not exclude Wernicke's encephalopathy. Treat on clinical suspicion.

Magnesium

Magnesium is required for several thiamine-dependent enzyme reactions. Check and correct hypomagnesaemia, particularly in severe withdrawal, arrhythmia, seizures or an inadequate response to thiamine. Magnesium should not, however, be given routinely as specific withdrawal treatment when the magnesium level is normal. A Cochrane review found insufficient evidence that magnesium in itself prevents or treats alcohol withdrawal [19].

Delirium tremens

Diagnosis

Delirium tremens is alcohol withdrawal with delirium. The patient has an acute and fluctuating disturbance of attention and consciousness, together with cognitive change and usually clear signs of withdrawal.

Common findings:

• disorientation
• severely reduced attention
• fluctuating consciousness
• psychomotor agitation
• tremor
• sweating
• tachycardia and hypertension
• fever or hyperthermia
• visual, auditory or tactile hallucinations
• disturbed circadian rhythm.

Hypoactive delirium occurs and should raise particular suspicion of infection, metabolic encephalopathy, drug effects or another concurrent illness.

Practical management

Sedative hypnotics that are cross-tolerant with alcohol are more effective than neuroleptics as the main treatment. In a meta-analysis, mortality risk was higher with neuroleptic-based treatment than with sedative hypnotics [3].

Antipsychotics

Haloperidol or another antipsychotic can in particular cases be used as an adjunct in severe hallucinosis or agitation that persists despite adequate GABAergic treatment.

It should:

• never replace a benzodiazepine
• be used cautiously early in the course, when the seizure tendency is high
• be preceded by assessment of the QT interval and electrolytes when the situation allows
• be avoided or dosed with particular caution in parkinsonism, Lewy body dementia or marked QT prolongation.

Antipsychotics can lower the seizure threshold, prolong the QT interval and mask a withdrawal that is still inadequately treated [1].

Treatment failure and intensive care treatment

Suspect treatment failure when the patient remains severely agitated, autonomically unstable or delirious despite repeated and adequate benzodiazepine doses. Always begin by checking:

• that the doses have actually been administered
• that the correct route of administration is being used
• concurrent infection or sepsis
• head trauma or intracranial haemorrhage
• hypoxia or hypercapnia
• electrolyte and acid-base disturbance
• hepatic encephalopathy
• another withdrawal state or poisoning
• pain, urinary retention or another treatable stressor.

Phenobarbital

Phenobarbital can be used as an alternative or an adjunct by physicians experienced with the drug and with adequate monitoring. It has a long half-life, a narrow therapeutic range and an additive respiratory depressant effect together with benzodiazepines.

A meta-analysis of eight emergency department studies with 1,507 patients found no reliable reduction in intensive care admission, hospital admission or adverse effects compared with benzodiazepines. The methodological quality of the studies was low to moderate and the risk of bias substantial [20]. Phenobarbital should therefore not be uncritically regarded as superior to benzodiazepines.

Propofol

Propofol can be used in severe refractory withdrawal in an intubated patient in the intensive care unit. It affects both the GABA and the glutamate systems but causes hypotension and respiratory depression. A systematic review of five retrospective cohorts found varying times to symptom control and often longer duration of ventilation and of intensive care. The evidence is of low quality and strongly influenced by the fact that propofol is given to the sickest patients [21].

Propofol is not in itself a reason to intubate. It is an option when the patient already needs, or is likely to need, mechanical ventilation.

Dexmedetomidine

Dexmedetomidine can reduce sympathetic activation and provide sedation without marked respiratory depression. It does not, however, treat the underlying GABAergic mechanism and does not reliably prevent seizures or delirium. It may therefore only be used as an adjunct.

A meta-analysis from 2024 showed no statistically reliable reduction in intubation, relative risk 0.57 with a 95 percent confidence interval of 0.25 to 1.30. The risk of bradycardia was increased, relative risk 2.68 [22]. An earlier meta-analysis judged the evidence to be low to very low and found no reliable overall benefit in duration of intensive care [23].

Clonidine and beta blockers

Clonidine and beta blockers can attenuate tachycardia and hypertension but:

• do not treat the central withdrawal state
• do not prevent seizures
• do not prevent delirium tremens
• can mask clinical deterioration.

They should be used only as adjuncts once adequate GABAergic treatment has been ensured.

Supportive treatment

Fluids and nutrition

Assess dehydration clinically. Tachycardia and sweating do not automatically mean that large volumes of intravenous fluid are needed. Take account of heart failure, cirrhosis, renal failure and the risk of hyponatraemia.

After prolonged poor nutritional intake there is a risk of refeeding syndrome. Check phosphate, potassium and magnesium in particular before and during the start of nutrition. Give thiamine before or at the same time as nutrition.

Environment and nursing care

• A calm and easily surveyable environment.
• Reduced stimulation in marked agitation.
• Normal light levels during the day and darkness at night.
• A clock, a calendar and repeated orientation.
• Glasses and hearing aids if the patient uses them.
• Continuous supervision when there is a risk of falls or absconding.
• Avoid physical restraint if safer alternatives exist.

Physical restraint can increase agitation, hyperthermia, rhabdomyolysis and the risk of injury. If it is nonetheless immediately necessary it should be brief, documented and combined with active sedation and close supervision.

Always exclude other causes

Delirium in a person with alcohol dependence is not automatically delirium tremens. Concurrent illness is common and affects the prognosis. In an intensive care cohort, sepsis, impaired consciousness and seizures were common reasons for admission, and a greater number of concurrent organ failures was linked to a worse outcome [24].

Consider in particular:

• subdural haematoma or other head trauma
• ischaemic or haemorrhagic stroke
• meningitis, encephalitis, pneumonia, urinary tract infection or sepsis
• hypoglycaemia
• hyponatraemia
• hypomagnesaemia, hypokalaemia or hypophosphataemia
• hepatic encephalopathy
• Wernicke's encephalopathy
• pancreatitis
• alcoholic ketoacidosis
• uraemia
• hypoxia or hypercapnia
• thyrotoxicosis
• poisoning with or withdrawal from benzodiazepines, opioids, GHB, pregabalin or other substances
• an adverse drug reaction or anticholinergic syndrome
• status epilepticus.

Withdrawal and another illness can occur at the same time. Treatment with a benzodiazepine should therefore not bring the diagnostic workup to a halt.

Imaging and lumbar puncture

CT of the brain should be considered particularly with:

• a first seizure
• focal neurology
• a focal seizure
• known or suspected head trauma
• anticoagulant treatment
• prolonged impairment of consciousness
• an atypical time course
• a lack of improvement despite adequate treatment.

Lumbar puncture is performed when infection or inflammation of the central nervous system is clinically suspected, after the usual assessment of contraindications.

Liver cirrhosis and hepatic encephalopathy

Withdrawal, delirium tremens and hepatic encephalopathy can overlap. Tremor, confusion and sleep disturbance occur in both conditions. Marked autonomic hyperactivity, hallucinations and the time course from the history suggest withdrawal, whereas asterixis, slower psychomotor function and other signs of decompensation may suggest hepatic encephalopathy.

In advanced liver disease:

• choose oxazepam or lorazepam where the clinical situation allows
• avoid uncritical repeated dosing of diazepam
• titrate according to clinical effect
• treat possible hepatic encephalopathy in parallel
• look for infection and gastrointestinal bleeding
• monitor respiration and level of consciousness closely.

High-dose benzodiazepine can worsen hepatic encephalopathy, but a genuinely severe withdrawal must still be treated. When the diagnosis is uncertain, what is usually required is a higher level of care, not therapeutic passivity [10,11].

Red flags and common pitfalls

• Underdosing the benzodiazepine in delirium tremens. Untreated central excitation can cause seizures, hyperthermia, arrhythmia and death.
• Giving a benzodiazepine without adequate monitoring. A high dose requires readiness for airway support.
• Using CIWA-Ar in a delirious, intubated or non-communicative patient.
• Letting a high CIWA-Ar score automatically trigger more benzodiazepine even though pain, sepsis or another illness explains the score.
• Using antipsychotics as the main treatment.
• Using clonidine, dexmedetomidine or beta blockers as a substitute for GABAergic treatment.
• Delaying glucose in hypoglycaemia in order to give thiamine first.
• Missing Wernicke's encephalopathy because the full classic triad is absent.
• Giving phenytoin as routine treatment of a pure withdrawal seizure.
• Dismissing a first seizure as withdrawal without investigation.
• Missing concurrent infection, bleeding, pancreatitis or trauma.
• Prescribing a benzodiazepine for continued tapering without a clear prescription, a support person and follow-up.
• Ending the admission after detoxification without relapse prevention.

Before discharge

Detoxification treats the withdrawal but not the alcohol use disorder. Before discharge the following should be in place:

• stable vital signs
• no new seizures or signs of delirium
• a completed or clearly planned short benzodiazepine taper
• continued thiamine according to risk and local protocol
• a nutrition plan
• a medication review
• assessment of suicide risk and psychiatric comorbidity
• contact with addiction services or other appropriate follow-up
• information about the risk of relapse and of further withdrawal
• consideration of drug treatment for alcohol dependence.

Naltrexone and acamprosate are established treatment options for alcohol dependence, while the choice of drug must be adapted to liver and renal function, opioid treatment, treatment goals and Swedish reimbursement rules and practice. In advanced liver disease particular caution is required, and often consultation with an addiction or liver specialist [11,25].

A brief in-hospital intervention should be respectful and concrete. Ask about the patient's goals, give clear medical information, offer treatment and arrange actual follow-up. Advice to stop drinking on its own is rarely sufficient.

Practical checklist for the on-call physician

1. Establish the time of the most recent clear reduction in alcohol intake.
2. Ask about previous delirium tremens and withdrawal seizures.
3. Perform ABCDE, plasma glucose and a focal neurological examination.
4. Assess for trauma, infection, other poisoning and sedative withdrawal.
5. Give parenteral thiamine early.
6. Start a benzodiazepine according to local protocol if the withdrawal is moderate, severe or high-risk.
7. If CIWA-Ar is used, ensure that the patient is communicative and that the score genuinely reflects withdrawal.
8. If a seizure has occurred, give a benzodiazepine and investigate alternative causes.
9. In delirium, treat as possible delirium tremens but continue the differential diagnostic workup at the same time.
10. With a high dose requirement, a lack of effect or a falling level of consciousness, contact anaesthesia or intensive care early.
11. Prescribe repeated checks of respiration, consciousness, vital signs and electrolytes.
12. Plan addiction treatment before discharge.

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