Ms. J, 42, was admitted to the OB-GYN service for a routine vaginal hysterectomy to treat dysfunctional uterine bleeding. In the presurgical history, she described having a few drinks daily. Shortly after a successful uncomplicated procedure, the patient became tremulous and was given several doses of lorazepam.
Two days after surgery, the patient became delirious. She complained of tactile and visual hallucinations, her level of consciousness waxed and waned, and she showed significant autonomic instability. A psychiatry consult was ordered. The consult team recommended IV fluids, IV diazepam, and haloperidol, supplemented with a multivitamin and 100 mg/d of thiamine. When the patient’s delirium resolved within 4 days, a more detailed discussion revealed a history of alcohol abuse and withdrawal seizures.
It is not uncommon for a patient to develop acute alcohol withdrawal and delirium tremens (DTs) while recovering from routine surgery. Delirium tremens remains a medical emergency, even though advances have reduced its associated mortality rates (Box).1-7
Psychiatrists who know the risk factors for DTs—also termed alcohol withdrawal delirium—can identify and protect patients who are susceptible to this life-threatening complication. We describe the clinical features of DTs, potential predisposing factors, theories behind its mechanisms, and strategies for preventing and managing DTs in patients experiencing alcohol withdrawal.
Clinical features
Disorientation and confusion are the hallmark features of DTs. Other clinical manifestations include vivid hallucinations, extreme tremulousness, autonomic hyperactivity, sweating, tachycardia, and agitation. Men experiencing DTs seem to demonstrate a greater degree of autonomic hyperactivity than women.8
Symptoms usually arise in the alcoholic patient between the third and fifth days of abstinence but have been known to occur several weeks after a patient’s last drink. Symptoms usually resolve within a few days9 but have been known to resolve within hours in some patients and to persist for several months in others.10
Differential diagnosis. Clinicians often fail to differentiate alcohol hallucinosis from DTs. Alcohol hallucinosis—which occurs in 3 to 10% of patients with severe alcohol withdrawal11 —manifests as auditory, visual, or tactile hallucinations with a clear sensorium. Patients experiencing DTs also may experience hallucinations but with confusion, disorientation, and severe autonomic hyperactivity. Unlike DTs, alcohol hallucinosis is not fatal.9
DTs also should be differentiated from:
- other causes of delirium, such as medication or infection. If the cause is identified and removed, the delirium should gradually resolve.
- Wernicke’s encephalopathy—caused by glucose exposure in the thiamine-deficient alcoholic—which is characterized by confusion, ophthalmoplegia, and ataxia.
Completing a thorough history and physical exam, talking to family members, and reviewing past medical charts are often the best ways to differentiate DTs from other conditions.
What causes DTs?
Vitamin deficiencies were initially thought to cause alcohol withdrawal.3 More recent evidence points toward multiple neuroadaptive changes in the brain associated with chronic alcohol exposure.12 Although numerous neurotransmitter systems may play a role in alcohol withdrawal, recent research has focused on glutamate13 and gamma-aminobutyric acid (GABA).14
DTs: MORTALITY RATE AS HIGH AS 15%
Approximately 1.5 to 2 million Americans seek treatment for alcohol abuse or dependence each year.1 As many as 71% of these patients manifest symptoms of alcohol withdrawal.2 Of those individuals who experience alcohol withdrawal, delirium tremens (DTs) may occur in up to 5%.3-5 Utilizing these percentages, it can be estimated that as many as 50,000 to 70,000 individuals develop DTs each year in the United States alone.
Although the incidence of DTs can be assumed to be relatively low, the condition should be considered a medical emergency. Studies list mortality rates for DTs as high as 15% and as low as 2 to 3%.7,8
The brain seems to compensate for alcohol’s enhancement of GABA (inhibitory) neurons by up-regulating excitatory neurons (glutamate). Alcohol has been shown to have some effects on neurons.15 The implication is that withdrawing alcohol triggers an “excitatory state” until the brain can readjust the fine balance between excitation and inhibition, a process that takes weeks to months. Some changes may never reverse because of the neurotoxic effects of alcohol and alcohol withdrawal.
Repeated alcohol exposure and withdrawal may lead to neuroadaptive changes in the brain and to more severe withdrawal symptoms, such as DTs. Repeated alcohol withdrawal episodes can produce a kindling effect. As outlined by Becker, kindling occurs “when a weak electrical or chemical stimulus, which initially causes no overt behavioral responses, results in the appearance of behavioral effects, such as seizures, when it is administered repeatedly.”16 Thus, repeated alcohol withdrawal worsens future episodes and eventually leads to alcohol withdrawal seizures.
Whereas most of these theories apply to alcohol withdrawal, they are also compatible with the neuronal mechanisms that may underlie DTs. Alcohol withdrawal and DTs share the presence of a “hyperactive state.” Most likely, DTs is the progression to more severe or pronounced neuroadaptive changes seen in mild to moderate alcohol withdrawal. One could certainly imagine that the possible neurotoxic effects of alcohol, alcohol withdrawal, and repeated detoxifications could sensitize the CNS to the more severe symptoms seen in DTs. Infection and metabolic abnormalities may also enhance the progression. Unfortunately, why some but not all patients experiencing alcohol withdrawal progress to DTs is unknown.