Gamma-hydroxybutyrate (GHB) is the most dangerous and well-known drug to abuse, is unfamiliar to many psychiatric professionals. Recent cases of severe GHB withdrawal delirium have occurred in psychiatric settings, making it necessary for psychiatric professionals to be informed about the management of these patients.
GHB, a naturally occurring metabolite of gamma-aminobutyric acid (GABA), is an inhibitory neurotransmitter that mediates sleep cycles, cerebral metabolism, memory and emotional control. Synthetic GHB, originally used by body builders for its putative anabolic effects, has more recently been abused for its sedative, euphoriant and aphrodisiac effects and as a “rave” and “date rape” drug.
GHB was previously available in health food stores and gyms, and it was marketed for its purported muscle building and fat burning effects. In 1990, the Food and Drug Administration (FDA) banned the manufacture and distribution of GHB after receiving several reports of abuse leading to coma and seizures. Precursor compounds such as gamma-butyrolactone (GBL) and 1, 4-butanediol (BD), which can be converted by the body or simple chemical processing into GHB, remained available over the Internet. GHB is easily manufactured by illicit laboratories or by “home brew” recipes that have been published in books and on the Internet. Despite the FDA’s attempts to control distribution of these compounds, they remain widely available to body builders and to drug abusers. For the purpose of this paper, the abbreviation GHB will be used to refer to both GHB and its related precursors.
Although acute effects of GHB overdose have led to coma, seizure, respiratory arrest, and death, withdrawal syndromes from chronic GHB abuse were initially reported to be mild and without complications or sequelae. More recently, several cases of severe GHB withdrawal delirium that necessitated management in intensive care unit settings have been reported. The reasons for the increasing severity of GHB withdrawal are not known; however, one explanation could be that the use of precursors such as GBL and BD have become more popular since GHB was banned by the FDA. In comparison to GHB, GBL is more rapidly absorbed, reaches higher concentrations, and has a more prolonged duration of action. When combined with alcohol, BD demonstrates prolonged toxicity resulting from competition for alcohol dehydrogenase, which is involved in the metabolism of both these compounds. Alcohol is frequently used by GHB abusers in an attempt to detoxify them from GHB; in the case of BD, alcohol may actually exacerbate and extend BD’s toxic effects.
GHB withdrawal delirium
Because the initial symptoms of GHB withdrawal delirium are often auditory and visual hallucinations, disorientation, and severe agitation, these symptoms may be presumed to be psychiatric in nature, and the patient may be transferred to a psychiatric unit. Although milder cases have been managed in this setting, more severely dependent cases may be at risk of physical decompensation and death if not transferred to a critical care setting. In this article, we will describe two patients in severe GHB withdrawal who were transferred to the inpatient psychiatric unit in our facility. Suggestion would be given for assessment, monitoring, and administration of patients at threat of developing this severe GHB withdrawal delirium syndrome.