Although GHB overdose has been associated with random clonic movements and agitation on awakening, no seizure-like EEG activity has been seen in human volunteers or patients. Cardiovascular effects include bradycardia and hypotension from decreased systemic vascular resistance, without change in cardiac index. Limited observations have suggested that physostigmine reverses GHB-induced coma, but that flumazenil and naloxone do not. Management of pure GHB intoxication involves support and airway protection. Atropine can be administered for significant bradycardia that does not improve with stimulation.
Patients often awake suddenly after several hours of observation.
The authors point out that GHB has been studied extensively as a protective agent in resuscitation patients with tissue hypoxia or shock, and suggest that this effect may explain why these patients often recover completely despite profound respiratory depression and hypoxia. Since these patients do well with support alone, we would not recommend the use of physostigmine in GHB overdose. This very well referenced review is worthwhile reading. It is not a substitute for careful analysis of the original literature, and neither provides nor is intended to provide the basis for patient evaluation or treatment. The publisher makes a reasonable effort to assure accuracy, but assumes no liability for any errors or omissions.