Gamma hydroxybutyrate toxicity
(Redirected from GHB)
Contents
Background
- Abbreviation: GHB
- Central nervous system depressant
- GABA-B agonist (as opposed to GABA-A agonists - alcohol, benzodiazepines, etc)
- Abused for:
- Body building or sleep enhancement
- euphoric, sexual, stimulant, and relaxant effects
- Surreptitious drugging to facilitate sexual assault
- Also used therapeutically in the treatment of narcolepsy[1]
Pharmacokinetics
- effect starts in 15-20min, peaks in 30-60 min,
- lipid soluble, no protein binding so crosses BBB readily
- elimination is dose-dependent with half life of 20-50 min
- The duration of GHB's clinical effects depends upon the dose, and ranges from 2.5 to 4 hours
Pharmacology
- Is a metabolite and precursor of GABA
- Interacts with GHB-specific receptors and also acts as a direct agonist of GABA-B receptors
- Affects multiple neurotransmitter systems, including those of opioids, dopamine, serotonin, glutamate, and acetylcholine
- Gamma butyrolactone (GBL) and 1,4 butanediol (BD) are GHB analogs that are rapidly metabolized to GHB after ingestion, with the same toxic and recreational effects
Clinical Features
Classic Presentation: Young adult presents comatose and is intubated for airway protection and subsequently awakens while in the emergency department. When awake, can be safely discharged
- CNS and respiratory depression
- also cardiac and GI symptoms
- often found to have co-intoxicants
- usually young white male from nightclub
- may present with nausea and vomiting, respiratory depression, bradycardia, seizure
- may also have ataxia, nystagmus, somnolence and aggression
- respiratory/CNS depression resolves abruptly
- respiratory depression worse with other CNS depressants (alcohol, benzodiazepines, etc)
- periods of apnea and hyperventilation
- decreases respiratory rate but tidal volume increases so minute volume stable
- can also have seizure but EEG shows no epileptiform changes
- bradycardia, hypotension
- ekg change occasionally but rare
- also get vomiting, hypothermia
Clinical Course
- recover in 2-6 hrs
- may be extubated and sent home
- if longer than 6hr, look for other cause
- can have cross tolerance with other drugs-alcohol and others that effect liver p450 cytochome oxidase system
Differential Diagnosis
Sedative/hypnotic toxicity
- Absinthe
- Barbiturates
- Benzodiazepines
- Chloral hydrate
- Gamma hydroxybutyrate (GHB)
- Baclofen toxicity
- Opioids
- Toxic alcohols
Drugs of abuse
- 25C-NBOMe
- Alcohol
- Amphetamines
- Bath salts
- Cocaine
- Ecstasy
- Gamma hydroxybutyrate (GHB)
- Heroin
- Inhalant abuse
- Hydrocarbon toxicity
- Difluoroethane (electronics duster)
- Marijuana
- Phencyclidine (PCP)
- Psilocybin ("magic mushrooms")
- Synthetic cannabinoids
Evaluation
- Not detectable on routine toxicology screens
Management
- supportive
- look for coingestants and occult trauma
- charcoal not helpful since rapidly absorbed and since can vomit and aspirate
- protein bound so can use dialysis*but so short course usually do not need.
Antidotes
- flumazenil/ narcan helps in animals but not in humans[citation needed]
- physostigmine may reverse coma, but if co-ingestant present, may be dangerous-potential to lower seizure threshold
Disposition
See Also
References
- ↑ Mamelak M, Scharf MB, Woods M. Treatment of narcolepsy with gamma-hydroxybutyrate. A review of clinical and sleep laboratory findings. Sleep. 1986;9(1 Pt 2):285-289. doi:10.1093/sleep/9.1.285