Alcohol withdrawal symptoms occur when patients stop drinking or significantly decrease their alcohol intake after a long-term dependence. Withdrawal has a broad range of symptoms from mild tremors to a condition called delirium tremens which results in seizures and could progress to death if not recognized and treated promptly.
Ethanol is the primary alcohol ingested by chronic users. It is a central nervous system (CNS) depressant that the body becomes reliant on over time. It does this by inhibiting the excitatory portion (glutamate receptors) of the CNS and enhancing the inhibitory portions (GABA receptors) of the CNS. When the depressant is stopped, the central nervous system becomes overexcited as the inhibition is taken away. Thus, the body gets an excitatory overload which results in the symptoms of withdrawal.
GABA (gamma-aminobutyric acid) is the major inhibitory neurotransmitter in the central nervous center. GABA has very specific binding sites available for ethanol thus increasing the inhibition of the central nervous system when present. Chronic ethanol exposure to GABA creates constant inhibition or depressant effects on the brain. Ethanol also binds to glutamate, which is one of the excitatory amino acids in the central nervous system. When it binds to glutamate, it inhibits the excitation of the central nervous system, thus worsening the depression of the brain.
Alcohol withdrawal can range from very mild symptoms to the severe form, which is named delirium tremens. The hallmark is autonomic dysfunction resulting from the excitation of the central nervous system. Mild signs/symptoms can arise within six hours of alcohol cessation. If symptoms do not progress to more severe symptoms within 24 to 48 hours, the patient will likely recover. However, the time to presentation and range of symptoms can vary greatly depending on the patient, their duration of alcohol dependence, and volume typically ingested. Most cases should be described by their severity of symptoms, not time since their last drink. Noting the last drink is very important however in any patient with an alcohol dependence history who may be presenting with other complaints. You can help prevent withdrawal by staying on top of this! Some features that may heighten your suspicion that a patient could suffer severe withdrawal include a history of prior delirium tremens, as well as a history of low platelets (thrombocytopenia) or low potassium levels (hypokalemia).
Mild symptoms can be insomnia, tremulousness, hyperreflexia, anxiety, gastrointestinal upset, headache, palpitations.
Moderate symptoms include alcohol withdrawal seizures (rum fits) that can occur 12 to 24 hours after cessation of alcohol and are typically generalized in nature. There is a 3% incidence of status epilepticus in these patients. About 50% of patients who have had a withdrawal seizure will progress to delirium tremens.
Delirium tremens is the most severe form of alcohol withdrawal, and its hallmark is that of an altered sensorium with significant autonomic dysfunction and vital sign abnormalities. It includes visual hallucinations, tachycardia, hypertension, hyperthermia, agitation, and diaphoresis. Symptoms of delirium tremens can last up to seven days after alcohol cessation and may last even longer.
These symptoms mimic those of withdrawal from long-term benzodiazepine or barbiturate use, so important historical features to note when a patient presents with autonomic dysfunction suspicious for a withdrawal syndrome should always include a medication list and social history. Also, consider these risk factors for any patient presenting with seizures of unknown etiology.
The diagnosis of alcohol withdrawal can be made by taking an excellent history and performing a thorough physical examination. It is a clinical diagnosis based on mild, moderate, or severe symptoms. Patients with suspicion for alcohol withdrawal should be evaluated for other underlying disease processes such as dehydration, infection, cardiac issues, electrolyte abnormalities, gastrointestinal bleeding, and traumatic injury. Basic laboratory studies (electrolytes, blood counts) may be drawn, but will likely be nondiagnostic. Many chronic alcoholics will have a baseline ketoacidosis due to their poor nutritional status, and labs may show acidemia with ketone production similar to a diabetic but with euglycemia or hypoglycemia due to lack of glycogen stores in their liver.
Some literature recommends checking an alcohol level at the time of onset of symptoms as patients who are symptomatic while still having a positive alcohol level with symptoms of autonomic dysfunction/withdrawal will have a higher morbidity/mortality and their short-term prognosis can be poor.
Patients with prolonged altered sensorium or significant renal abnormalities should have an evaluation for the potential ingestion of another toxic alcohol. Patients who become financially strapped due to alcoholism could ingest other alcohols to become intoxicated. These can include isopropyl alcohol, commonly known as rubbing alcohol which can lead to acidemia without ketosis as well as hemorrhagic gastritis. Ethylene glycol (antifreeze) ingestion can lead to altered sensorium, seizures, and severe renal dysfunction with acidemia that may require initiation of hemodialysis. Methanol is rarely ingested as an ethanol substitute but can result in multisystem organ failure, blindness, and seizures.
Other common household substances can also contain a significant amount of alcohol if ingested in large quantities including mouthwash and cough syrup. Some of these items may also contain a lot of salicylates or acetaminophen so consider checking aspirin and acetaminophen levels in patients presenting with alcohol withdrawal.
Patients should be kept calm in a controlled environment to try to reduce the risks of progression from mild symptoms to hallucinations. With mild to moderate symptoms, patients should receive supportive therapy in the form of intravenous rehydration, correction of electrolyte abnormalities, and have comorbid conditions as listed above ruled out. Due to the risk of a comorbid condition called Wernicke-Korsakoff syndrome, patients can also receive a “banana bag” or cocktail of folate, thiamine, dextrose containing fluids, and a multivitamin.
The hallmark of management for severe symptoms is the administration of long-acting benzodiazepines. The most commonly used benzodiazepines are intravenous diazepam (Valium) or intravenous lorazepam (Ativan) for management. Patients with severe withdrawal symptoms may require escalating doses and intensive care level monitoring. Early consultation with a toxicologist is recommended to assist with aggressive management as these patients may require benzodiazepine doses at a level higher than the practitioner is comfortable with to manage their symptoms.
Withdrawal seizures can typically be managed with benzodiazepines as well, but may require adjunct therapy with phenytoin, barbiturates, and may even require intubation and sedation with propofol (Diprivan), ketamine (Ketalar), or in the most severe cases dexmedetomidine (Precedex).
Oral chlordiazepoxide (Librium) and oxazepam (Serax) are very commonly used for prevention of withdrawal symptoms.
Toxic alcohol co-ingestions should be managed with the assistance of a toxicologist.
Patients with a history of alcohol dependence may have confounding social or underlying psychiatric issues that you should also be aware of once they are stabilized. They will likely require a multidisciplinary approach before discharge.