Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011206 (delirium)
 5,996 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The symptoms and clinical management of alcohol, barbiturate and benzodiazepine withdrawal syndromes are discussed in this article. People who suffer alcohol withdrawal should be admitted to hospital if they have medical or surgical complications or severe symptoms; supportive care and pharmacotherapy, especially diazepam loading, are the essential components of treatment. Barbiturate withdrawal requires pharmacotherapy and admission to hospital for patients who have taken more than 0.4 g/d of secobarbital or an equivalent amount of another barbiturate for 90 days or longer, or 0.6 g/d or an equivalent dose for 30 days or longer, or who have had withdrawal seizures or delirium; phenobarbital loading is recommended. Regular benzodiazepine therapy that has lasted at least 3 months should be gradually stopped. Short-acting agents should be replaced with long-acting ones, such as diazepam, to avoid withdrawal symptoms. Most of these patients can be managed on an outpatient basis.
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PMID:Alcohol, barbiturate and benzodiazepine withdrawal syndromes: clinical management. 289 72

A 29-y-old man had taken small daily doses of barbiturates as hypnotics (50 mg pentobarbital, 30 mg phenobarbital) for 4y with no evident intoxication. When he attempted suicide by ingestion of 15 g amobarbital, treatment with charcoal hemoperfusion resulted in rapid disappearance of drug from the blood. Generalized convulsions and delirium ensued; these were responsive to phenobarbital. An electroencephalogram (EEG) showed diffuse 5-Hz theta activity. Tc-99m hexamethylpropyleneamineoxime (HMPAO) single photon emission computed tomographic (SPECT) imaging of the brain demonstrated a diffuse bilateral decrease in blood flow to the cerebral cortex. These investigations were performed interictally on day4 without sedative drugs, prior to initiation of anticonvulsants, and at a time when barbiturates were no longer detected in the serum. An EEG on day 15 no longer showed abnormal slowing. On the other hand, Tc-99m HMPAO SPECT of the brain demonstrated residual cerebral hypoperfusion on day 20, with nearly full recovery of cerebral perfusion on day 51. Barbiturate withdrawal syndrome is presumed to require a history of abuse; however in patients with a history of treatment with barbiturates physicians treating acute barbiturate poisoning should be alert for the possibility of barbiturate withdrawal syndrome even in the absence of barbiturate abuse.
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PMID:Transient diffuse cerebral hypoperfusion in Tc-99m HMPAO SPECT of the brain during withdrawal syndrome following acute barbiturate poisoning. 1245 39