Alcohol withdrawal, seizure risk

A. Parenteral. Administer slowly intravenously (rate < 50 mg/mln children, < 1 mg/kg/min) until seizures are controlled or the loading dose of 10-15 mg/kg is achieved. For status epilepticus, give 15-20 mg/kg IV over 10-15 minutes and not to exceed 100 mg/minute (children have required as much as 30 mg/kg in the first 24 hours to treat status epilepticus). Slow the infusion rate if hypotension develops. Intermittent infusions of 2 mg/kg every 5-15 minutes may diminish the risk of respiratory depression or hypotension. For alcohol withdrawal seizures, initial dose of 260 mg, then 130 mg every 30 minutes until signs of mild intoxication (see below). 

Abrupt alcohol withdrawal leads to a characteristic syndrome of motor agitation, anxiety, insomnia, and reduction of seizure threshold. The severity of the syndrome is usually proportionate to the degree and duration of alcohol abuse. However, this can be greatly modified by the use of other sedatives as well as by associated factors (eg, diabetes, injury). In its mildest form, the alcohol withdrawal syndrome of tremor, anxiety, and insomnia occurs 6-8 hours after alcohol consumption is stopped (Figure 23-2). These effects usually abate in 1-2 days. In some patients, more severe withdrawal reactions occur, with patients at risk of hallucinations or generalized seizures during the first 1-3 days of withdrawal. Alcohol withdrawal is one of the most common causes of seizures in adults. Several days later, individuals can develop the syndrome of delirium tremens, which is characterized by total disorientation, hallucinations, and marked abnormalities of vital signs. 

Tiapride appears to be useful in alcohol withdrawal as an alternative to the benzodiazepines (2). It facilitates the management of ethanol withdrawal, but its use in patients at risk of severe reactions in acute withdrawal should be accompanied by adjunctive therapy for hallucinosis and seizures. Since it may prove difficult to identify such patients and since there is also a small risk of the neuroleptic malignant syndrome (particularly with parenteral administration), the usefulness of tiapride in this setting is likely to be limited. The potential risk of tardive dyskinesia at the dosage used in alcoholic patients following detoxification (300 mg/day) requires evaluation and necessitates medical supervision. It is unlikely to produce problems of dependence or abuse. 

Tramadol, phenothiazine antipsychotics and the majority of antidepressants, as well as a number of other drugs, can lower the seiznre threshold and are associated with an increased risk of convnlsions [6]. Again, these drugs may accumulate in patients with liver impairment such as cirrhosis or acute liver failure, and care must be taken if choosing to use them. This is especially important in alcoholics, who have an increased risk of seizures from acute alcohol withdrawal [7]. Examples of drugs that can lower the seizure threshold and should be used with caution/avoided are ... 

Side effects typically effect the CNS, appearing within 2 weeks of therapy and disappearing after drug withdrawal. They include somnolence, headache, tremor, dysarthria, vertigo, confusion, nervousness, irritability, psychotic states, paranoid reactions, catatonic reactions, twitching, ankle clonus, hyperreflexia, visual disturbances, paresis, and seizures. Large doses or concomitant ingestion of alcohol increases the risk of seizures. Cycloserine is contraindicated in individuals with a history of epilepsy and should be used with caution in individuals with a history of depression. 

Seizures have been reported in patients receiving tramadol. The risk of seizure is increased with doses of tramadol above the recommended range. Concomitant use of tramadol increases the seizure risk in patients taking tricyclic antidepressants, selective serotonin reuptake inhibitors, or other opioids. Tramadol may enhance the seizure risk in patients taking MAO inhibitors, neuroleptics, or other drugs that reduce the seizure threshold. Risk of convulsions may also increase in patients with epilepsy, those with a history of seizures, or in patients with a recognized risk for seizure (such as head trauma, metabolic disorders, alcohol and drug withdrawal, CNS infections). 

A careful haseline physical examination, ECG, and laboratory work-up are essential. Underlying ECG changes (U waves, prolonged QT interval, or flattened T waves) secondary to hypokalemia or bradycardia and atrioventricular block from starvation may be present. AU antidepressants can cause seizures thus a careful risk-benefit assessment is warranted if the patient has predisposing factors such as a personal or family history of seizures, cerebrovascular disease, or alcohol or sedative-hypnotic withdrawal. 

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