GHB Poisoning


Gamma-hydroxybutyrate (GHB) and its precursors Gamma- butyrolactone (GBL) and 1,4 butanediol (1,4-BD) are drugs of abuse.  GHB is both a metabolite and precursor of GABA and acts as a CNS and respiratory depressant in high doses.  

Initially researched as a potential anaesthetic agent in the 1960s, its intoxicating properties have led it to become recreationally abused. Australian statistics suggest 0.8% of Australians over the age of 14 have used GHB at some stage in their life.1  

GHB metabolites

GHB & Precursor Structures


GHB is well absorbed orally with peak concentrations reached 25 to 60 minutes post ingestion. The ingestion of food with GHB has been shown to increase the time to peak concentration and decrease the peak of plasma concentration. 

It crosses the placenta and the blood brain barrier.

Metabolism is hepatic with a reported half-life between 20 to 52 minutes, with the majority of the dose being completely eliminated within 4 to 8 hours.1

Risk Assessment

Case studies suggest a relatively consistent toxidrome with symptoms typically occurring within 15-45 minutes1:

< 10mg/kgeuphoria, anterograde amnesia, hypotonia
20-30mg/kgdrowsiness, sleep, myoclonus
> 50mg/kgcoma, bradycardia, respiratory depression

GHB effects by dose

  • Vomiting, miosis and sweating are commonly reported.  
  • Paradoxical agitation and combativeness have been reported, often occurring when intubation is attempted. Patients are described as alternating between agitation and somnolence.1  
  • While seizure like activity have been reported, it has been suggested that this is likely a misdiagnosis of the myoclonus which is expected in toxicity.1 
  • Death if it occurs is typically due to respiratory failure.
  • Co-ingestions of alcohol or other respiratory depressants may greatly enhance toxicity.



Decontamination with activated charcoal is not indicated as the drug is consumed in liquid form and is rapidly absorbed.

Supportive Measures

Supportive care is the mainstay of therapy1with an emphasis on respiratory support. Given the relatively rapid recovery intubation and ventilation is often not required, but may be necessary for patients with significant aspiration.  

The bradycardia seen in GHB toxicity is rarely haemodynamically significant and should not require pharmacotherapy. 

Mild hypotension usually responds to crystalloid therapy.  

Myoclonic movements do not require any treatment.


In mild cases of intoxication without co-ingestions, observation for 2 hours should be adequate to assess signs and symptoms at peak toxicity.  

CNS depression, if present, usually persists for 1 to 3 hours with complete recovery expected within 4 to 8 hours.

Additional Information

Large overdoses of GHB precursors, particularly GBL, can be associated with a metabolic acidosis with can be severe in significant ingestions2.

GHB withdrawal can occur in patients who have a history of significant abuse (normally daily use). Symptoms are similar to alcohol withdrawal and can be severe. Unlike alcohol withdrawal treatment requires blockade of both GABA-A and GABA-B receptors and should be discussed with the toxicology team.


  1. Schep L, Knudsen K, Slaughter R, Vale J and Megarbane.  ‘The clinical toxicology of gamma-hydroxybutyrate, gamma butyrolactone and 1,4-butanediol.’ Clin Toxicol2012;50:458-70.
  2. Roberts, D.M., et al., Extreme gamma-butyrolactone overdose with severe metabolic acidosis requiring haemodialysis. Ann Emerg Med, 2011, 58(1): p. 83-5.