Alcohol withdrawal

For patient information, click here

Epidemiology

 * Alcohol abuse or dependence afflicts up to 15 million persons in the United States. It accounts for 100,000 deaths and an economic burden of over 100 billion dollars per year.   The lifetime prevalence of alcohol abuse is approximately 14% and of alcohol dependence is 8%.  Approximately 500,000 patients/year develop withdrawal that is severe enough to prompt pharmacologic management.
 * Between 13% and 71% of persons admitted for detoxification have evidence of withdrawal.
 * Approximately 3% of chronic alcoholics develop withdrawal seizures. Five percent of patients with alcohol withdrawal develop delirium tremens (DTs), which is associated with approximately 5% mortality.

Pathophysiology

 * Prolonged exposure to alcohol results in inhibition of the inhibitory GABA A-type and NMDA-type glutamate receptors located in the CNS. Without the alcohol, greater CNS excitability results.
 * Elevated norepinephrine has been found in the CSF of withdrawing patients. It is postulated that 2-receptors are decreased resulting in less inhibition of presynaptic norepinephrine release.

Diagnostic Criteria

 * 1) History of cessation or reduction in heavy and prolonged alcohol use.
 * 2) 2 or more of:
 * autonomic hypereactivity
 * hand tremor
 * insomnia
 * nausea and vomiting
 * transient tactile
 * visual or auditory hallucinations
 * psychomotor agitation
 * anxiety
 * grand mal seizures
 * Note history of blackouts, morning shakes, prior detoxifications or DTs and frequency, amount and type of alcohol.

Clinical Findings

 * Minor withdrawal symptoms result from sympathetic over activity and are tremulousness, anxiety, nausea, vomiting, diaphoresis, palpitations, insomnia and headache. They usually come on within 6 hours of cessation of alcohol intake.  (still with alcohol in the bloodstream).  These symptoms usually resolve in 24-48 hours.
 * Withdrawal seizures occur within 48 hours of cessation. Some have reported seizures occurring after only 2 hours of abstinence.
 * Hallucinations occur within 12-24 hours of cessation. The typical hallucinations are visual (pink elephants) but auditory and tactile can occur.  These hallucinations are not to be confused with DTs.  DTs may have associated hallucinations, but usually begin 48-96 hours after the last drink and are associated with a clouded sensorium.
 * Delirium Tremens: The patient in DTs is disoriented, hallucinating and with evidence of autonomic hyperactivity, e.g. tachycardia, diaphoresis, hyperpyrexia, hypertension. The 5% mortality associated with this disorder is generally from arrhythmias or a complication of complicating comorbid medical condition brought on by the added stress of alcohol withdrawal.  Preexisting pulmonary disease, liver disease, temp >104 and older age are associated with an increased risk of death from DTs.
 * Fluid and electrolyte status is often affected. Dehydration is almost a universal finding as a result of increased insensible losses, restricted access to free water and diuretic effect of alcohol.  Potassium, magnesium and phosphate depletion is common.

Treatment

 * No clinical findings can reliably predict who will or will not develop withdrawal. Risk factors for DTs: Previous DTs or detoxifications, Age >30, high degree of alcohol dependence, duration of abuse, the presence of moderate symptoms (CIWA >14) left untreated and concurrent medical illness are all strongly predictive.  These findings should prompt intervention. Time abstinent may be a helpful negative predictor. In one large study, patients who were asymptomatic 36 hours after their last drink did not develop symptoms.
 * All patients with alcohol abuse should receive 1mg Folate QD, Magnesium/ phosphate/potassium/fluid volume repletion and Thiamine 100 mg IV/IM x1 then 100 mg QD.
 * Treatment of alcohol related seizures is on an as needed basis with benzodiazepines. They tend to be transient phenomenon.  Phenytoin is ineffective in the management of withdrawal seizures, but may be indicated if another seizure disorder or status epilepticus is present.  Long term medical suppression or prophylaxis is not indicated for withdrawal seizures.  Neuroleptics lower the seizure threshold and should not be used in these patients; however, haloperidol has been used safely in conjunction with benzodiazepines (BDZs).
 * BDZs are the cornerstone of therapy for minor withdrawal, seizures and DTs. Fixed schedule therapy, front-loading therapy and symptom-triggered therapy have all been evaluated with similar efficacy.  Symptoms triggered therapy was associated with less total administration of drug and shorter length of stay but has only been evaluated in patients without acute comorbid illness or seizures and should be restricted to only this limited group of patients.
 * Guidelines at BIDMC suggest use of the front loaded regimen preferably with long acting BDZs. Use of short acting BDZs is reserved for patients with liver dysfunction and/or medical instability.  Treatment efficacy is assessed using the CIWA Scale (see below).
 * In the medically stable patient with no liver dysfunction 10 mg PO/IV is administered every hour till CIWA <10 or sedated. If the patient is stable but has liver disease, give 2 mg Lorazepam IV/PO Q 1H till CIWA <10 or sedated.  Calculate the total dose used and give this Q6H for 24 hrs.  Use that latter regimen for the unstable patient.
 * If CIWA is stable x24 hours then decrease the dose by 20%/day. If there is a history of DTs or seizures or the patient is unstable decrease the dose by 10%/day.  Give prn doses of lorazepam recurrence of withdrawal (CIWA >10).