This substance may be used therapeutically but can also be subject to abuse.

 

Treatment for narcolepsy

Treatment for alcoholism

Anesthetic agent

Euphoric

“Date rape” agent

“Growth Hormone booster”

“Aphrodisiac”

“Muscle builder” (although effectiveness has never been proven)

 

Emergency stabilization may be required for respiratory depression and/or pulmonary aspiration, immediate assessment and management of respiratory compromise is a priority. Due to fast onset of action, gastrointestinal decontamination is not recommended.

 

There is no proven antidote for poisoning. Extracorporeal elimination techniques would not be anticipated to be of clinical benefit in the majority of patients as most will satisfactorily recover with adequate airways management alone.

 

Supportive care is the mainstay of management, with primary emphasis on airway management and cardiovascular support. Airway protection including endotracheal intubation and/or assisted ventilation may be necessary due to respiratory depression and aspiration risk. Seizures may rarely occur and, in the presence of coma, indicate anoxia: manage the airway and ensure adequate ventilation. Should repetitive seizure occur in a well ventilated patient treat with a benzodiazepine, or if still refractory, a barbiturate. Myoclonic jerking is a recognized re-emergence phenomenon and single episodes do not require treatment. Other complications such as bradycardia, hypotension, hypothermia, and gastrointestinal upset should be treated along usual guidelines.

 

A sedative-hypnotic withdrawal syndrome is recognized after chronic abuse of this compound and may last 3 to 21 days. Benzodiazepines are usually effective to relieve symptoms, but high doses may be required. Severe cases of GHB withdrawal may be refractory to benzodiazepines and benefit from treatment with baclofen or barbiturates. Consultation with a medical toxicologist or poison center is recommended for cases of refractory GHB withdrawal.

 

Weakness, headache, fatigue, and nausea lasting 3 days after ingestion may occur. However, if significant CNS depressant effects persist beyond 8 hours, alternative causes should be investigated.

 

Emergency Stabilization

Decontamination

Antidote(s)

Enhanced Elimination

Supportive Care

Ensure the airway is protected if compromised (intubation may be necessary).

 

Establish secure intravenous access if hypotensive.

 

Airway

Breathing

Blood pressure

Heart rate/rhythm

Core body temperature

Blood oximetry

 

Absorption is too rapid for decontamination to be effective.

Supportive care is likely to be successful without decontamination.

There are no specific antidotes for this overdose.[1]

 

Agents including naloxone, flumazenil, and physostigmine have been investigated as potential antidotes. None have shown consistent results in reversing intoxication.

 

Physostigmine is viewed as an unproven experimental antidote for this intoxication. It was initially investigated as a reversal agent in patients under GHB-induced anesthesia.[2][3] However, use following poisoning has produced differing results, with the majority of patients not showing response.[4][5][6] Reviews of the literature have shown there is not sufficient evidence to support the use of physostigmine in acute GHB overdose.[6][7] At this stage physostigmine is not recommended.[1]

 

Additionally, naloxone and flumazenil have been used following human poisoning, both have had limited effect on reversing toxicity.[8][9][10][11][12] Neither of these compounds can be recommended.[1]

 

There is limited information regarding use of hemodialysis, hemoperfusion, hemodiafiltration, or hemofiltration to enhance elimination. GHB has minimal protein binding, a low molecular weight,[13] and a relatively small volume of distribution,[14][15][16] suggesting use of extra-corporal techniques may enhance its elimination. However, it would not be anticipated to be of benefit in the majority of patients as GHB has a rapid clearance and short duration of clinical effects.

 

Closely monitor:

Respiratory compromise is the most critical problem in severe poisoning. Intense respiratory support, when needed, constitutes the most vital supportive measure. Rapid sequence induction with endotracheal intubation and/or assisted ventilation may be required.[1]

 

Monitoring for respiratory failure should include:

Manage respiratory failure following standard treatment protocols.

 

Aspiration is a significant risk. Protection and careful monitoring of the airway is required if aspiration is suspected. Oxygen should be administered and artificial ventilation may be required.[1]

 

Manage pulmonary aspiration using standard protocols.

 

Profound coma is characteristic and generally short-term. Airway protection may be required, endo-tracheal intubation and even ventilation may on occasion be necessary.[17]

 

Closely monitor level of consciousness.

 

Manage coma following standard treatment protocols.

 

Myoclonic jerking is recognized as a re-emergence phenomenon (sometime mistaken for seizure activity) and does not require treatment. However, tonic-clonic seizures may occur and should be treated with standard protocols. Anoxia is an important precipitant and adequate airways and ventilation must be ensured.

 

Observe the patient closely for onset of seizure activity.

 

 

Bradycardia may occur in moderate to severe intoxication. Pharmacological intervention is rarely required in patients with hemodynamically stable bradycardia. Atropine may be useful in the presence of hemodynamically-unstable bradycardia.[1]

 

Monitor:

 

Manage bradycardia following standard treatment protocols.

 

Metabolic acidosis is reported in severe cases. Acid-base abnormalities should be sought and appropriately treated. In severe, refractory acidosis, hemodialysis may be required.[18]

 

Monitor:

Manage metabolic acidosis following standard treatment protocols.

 

A sedative-hypnotic withdrawal syndrome related to gamma hydroxybutyrate is recognized with symptoms resolving in some 3 to 21 days.[19][20][21][22][23][24] Initial treatment of choice appears to be benzodiazepine administration. Treatment with benzodiazepines has been reported as being sufficient to achieve regression of symptoms,[25] however, adequate doses must be administered initially to halt the progression of withdrawal. Benzodiazepine requirement should be assessed hourly. If necessary, second line management options include barbiturates, baclofen, or propofol.[21][23][26][27][28][29][30] Consultation with a medical toxicologist or poison center is recommended for cases of refractory GHB withdrawal.

 

Monitor for:

Manage withdrawal following standard treatment protocols.

 

Patients may, if initially symptomatic, be discharged following 4 hours of observation. Symptomatic patients may discharged subsequent to becoming stable and asymptomatic.[31] Children should not be discharged at night.

 

Medical follow-up is unlikely to be required, as long as recovery from any complications is complete. Psychiatric intervention may be necessary depending on the circumstances of the exposure.

 

Following appropriate supportive care the prognosis is good.

 

CNS depression[10][18][36][39][40][41][42][43][44][45][46][47][48][49][50][51][52][53][54][55]

Agitation/combativeness[5][8][10][34][38][39][42][43][44][46][56][57][58][59]

Disorientation[52][60][61][62][63]

Dizziness[12][34][38][43][62][64][65]

Ataxia[8][34][46][49][53][57][63][66]

Confusion[38][43][49][52][64]

Hallucinations[38][63][64][66]

Hypotonia[17][39][44][49][67]

Hyporeflexia[4][68][69][70]

Slurred speech[57][63][66]

Confusion[39][63][71]

Incoordination[38][57]

Dysarthria[34][61]

Headache[56][61]

Euphoria[20][52]

Amnesia[34][52]

Vertigo[17]

Disinhibition[61]

Delusions[62]

Bruxism (teeth grinding)[5]

Extrapyramidal side effects[66]

Dystonias[66]

Athetoid posturing[5]

Tremor[17][57]

Myoclonus[17][34][42][54]

Seizure[18][36][40][42][43][44][50][67][72][73][74][75][76]

Coma[10][18][33][38][53][56][58][60][61][67][72][73][74][77][78][79][80]

 

Bradycardia[4][5][12][18][17][34][37][38][40][42][43][46][51][57][58][61][52][63][55][70][74][75][78][79][81][82]

Hypotension[5][11][17][34][40][43][61][63][67][73][79][82]

Tachycardia[18][34][38][58][52][55][73][83]

Hypertension[8][18][34][38][49][73][81][83]

Chest tightness[61][64]

Palpitations[61]

ECG changes

Atrial fibrillation[5][36]

Asystole[18]

 

Respiratory depression[8][10][12][18][17][33][34][38][42][43][46][58][52][74][79][85]

Bradypnea[4][5][11][12][39][60][61][68][34][63][72][73][79][86]

Aspiration[39][41][43][47][58][77][79]

Periodic (Cheyne-Stokes) respirations[44][87][88]

Cyanosis[18][39]

Tachypnea[73]

Pneumothorax[70]

Pulmonary edema[85][89]

Apnea[5][10][17][33][41][44][51][58][52][62][63][64][70][72][77][79][81][82][85][86]

 

Nausea[43]

Vomiting[33][34][36][39][40][42][52][62][53][67][70][73][74][82][90]

Salivation[44][91]

Abdominal pain[62]

 

Hypothermia[4][5][36][42][43][46][61][52][62][63][67][70][73][79]

Metabolic or respiratory acidosis[8][10][18][46][67][70][79][85][86][92]

Hyperglycemia[58][81][85]

 

Miosis[8][11][12][26][39][43][56][58][61][52][64][75][81][85]

Mydriasis[12][18][38][43][48][56][57][61][54]

Nystagmus[49][56][57][63][66]

 

Hypokalemia[42][43][60][85]

Hypernatremia (if large doses of the sodium salt ingested)[93]

 

Rhabdomyolysis[42][43][44][56][55][71]

 

Sweating[8][10][34][46][52][63][55]

 

Nausea and vomiting[21][25]

Diarrhea[21][94]

Abdominal pain[95]

Hallucinations[19][21][22][23][29][96][97][98][99][100][101][102][103][104][105][106][107][108][109][110]

Tremor[19][20][21][22][25][29][95][96][97][98][101][104][105][107][108][109][110][111][112][113][114][115]

Sweating[19][21][22][25][29][96][98][101][103][104][105][106][107][109][113][114]

Anxiety[19][20][21][22][25][29][94][95][104][111][113]

Paranoia[19][21][29][99][101][102][103][104][107][110][113]

Agitation[21][23][102][103][105][106][108][112][115][116]

Aggression/combativeness[21][97][100][107][113]

Disorientation[19][21][22][23][97][102][104][110]

Confusion[19][21][22][102][104][108][115]

Insomnia[20][22][29][96][98][102][104][106][110][111][114]

Depression[29][104][114]

Tachycardia[19][21][22][23][25][29][95][96][97][98][102][104][105][112]

Hypertension[19][21][22][29][95][96][102][104][106][107]

Cardiac palpitations[95][108][114]

Dyspnea[108]

Tachypnea[101]

Miosis[102]

Nystagmus[19][95][105][110]

 

The toxic dose in children has not been established.

 

Toxicity of gamma hydroxybutyrate:[17][20][26][31][93]

 

 

Other substances may be abused concomitantly with this compound greatly increasing toxicity.[1][118][119]

 

Sodium hydroxide may be inappropriately used in the preparation of gamma hydroxybutyrate forming a caustic mixture.[33]

 

Blood concentrations do not aid patient management.

 

Gamma hydroxybutyrate (GHB) is a water-soluble four carbon molecule normally found in the human body. It is formed from the precursor molecule gamma butyrolactone (GBL) and is metabolized to succinic semialdehyde and the neurotransmitter gamma-aminobutyric acid (GABA).[31] The greatest concentration of GHB in humans is in the basal ganglia.

 

 

HUMAN

Gamma hydroxybutyrate (GHB) acts as:

Has a general anesthetic effect caused via:

 
ANIMAL
GHB alters dopaminergic activity:

However, the direction is dependent on several undefined variables.

 

GHB has binding affinity for two receptor sites in the central nervous system

 

This substance may be available in a stated dosage, however this should be treated with some caution particularly if obtained illicitly, due to variables such as uncontrolled manufacturing process, inappropriate packaging, and product bulking.

 

Attempts to avoid detection:

 

Testing: