Posted: July 1st, 2024

A 22-year-old male presents to the emergency department with altered mental status

Acute Gamma-Hydroxybutyrate (GHB) Intoxication: A Case Study and Analysis

Case Presentation

A 22-year-old male presents to the emergency department with altered mental status. His friends report he consumed an unknown quantity of a clear liquid at a nightclub approximately two hours ago. The patient is minimally responsive to verbal stimuli and exhibits periods of agitation alternating with deep sedation.

Medical History: No significant past medical history. No known allergies.
Social History: Occasional recreational drug use, including MDMA and cannabis.

Physical Examination:
Temperature: 36.8°C (98.2°F)
Heart Rate: 52 beats per minute
Respiratory Rate: 10 breaths per minute
Blood Pressure: 105/65 mmHg
Oxygen Saturation: 96% on room air

General: Obtunded, alternating between agitation and sedation.
Neurological: Glasgow Coma Scale 10 (E2, V3, M5). Pupils 3mm and reactive.
Cardiovascular: Bradycardic, regular rhythm. No murmurs.
Respiratory: Shallow breathing, clear lung fields.
Gastrointestinal: Soft, non-tender abdomen.

Laboratory Results:
Serum electrolytes, liver function tests, and complete blood count within normal limits.
Serum ethanol level: Negative
Urine drug screen: Negative for common drugs of abuse

Toxicological Analysis

The clinical presentation strongly suggests acute gamma-hydroxybutyrate (GHB) intoxication. GHB, a central nervous system depressant, has gained popularity as a recreational drug in nightclub settings. Its rapid onset of action and short half-life contribute to its appeal among young adults seeking euphoria and disinhibition (Busardò and Jones, 2019).

Key features of this case aligning with GHB toxicity include:

1. Altered mental status: The patient’s fluctuation between agitation and sedation is characteristic of GHB intoxication. This pattern, often described as a “GHB roller coaster,” results from the drug’s effect on GABA-B receptors and rapid pharmacokinetics (Schep et al., 2021).

2. Cardiovascular effects: Bradycardia, as observed in this patient, is a common finding in GHB overdose. The drug’s action on the cardiovascular system can lead to significant hemodynamic changes.

3. Respiratory depression: The patient’s decreased respiratory rate warrants close monitoring, as respiratory failure represents a significant risk in severe GHB intoxication.

4. Rapid onset: The timeline of symptom onset (approximately two hours post-ingestion) aligns with GHB’s pharmacokinetic profile.

5. Negative toxicology screen: Standard urine drug screens do not detect GHB, explaining the negative result despite clear clinical intoxication (Busardò and Jones, 2019).

Management Approach

The management of acute GHB intoxication primarily involves supportive care, as no specific antidote exists. The following interventions should be implemented:

1. Airway management: Close monitoring of the patient’s respiratory status is crucial. Intubation may be necessary if significant respiratory depression occurs or if the patient cannot protect their airway.

2. Hemodynamic support: While this patient’s blood pressure remains adequate, fluid resuscitation might be required in cases of hypotension. Atropine can be considered for severe bradycardia.

3. Neurological monitoring: Frequent reassessment of the patient’s level of consciousness using the Glasgow Coma Scale helps track the clinical course and guide interventions.

4. Seizure precautions: Although seizures are uncommon in isolated GHB toxicity, appropriate measures should be in place due to the patient’s altered mental status.

5. Diagnostic testing: While routine toxicology screens are negative for GHB, specialized testing can be performed if available. However, treatment decisions are typically based on clinical presentation rather than confirmatory testing (Wong et al., 2018).

6. Observation: Given GHB’s short half-life (20-50 minutes), most patients recover fully within 4-8 hours. Continuous monitoring in a safe environment is essential until complete resolution of symptoms.

7. Addressing hypoxia: Supplemental oxygen should be provided to maintain adequate oxygenation, with arterial blood gas analysis performed if clinically indicated.

8. Managing agitation: During periods of agitation, a calm environment and verbal de-escalation techniques are preferred. Physical restraints should be avoided if possible, as they may increase the risk of rhabdomyolysis (Busardò and Jones, 2019).

9. Preventing complications: Measures to prevent aspiration, such as positioning the patient in the recovery position when not intubated, are important.

10. Psychosocial intervention: Once the patient has recovered, a thorough assessment of their substance use patterns and provision of harm reduction strategies should be conducted.

This case highlights the importance of recognizing the clinical features of GHB intoxication and implementing prompt, supportive care. Healthcare providers in emergency settings must maintain a high index of suspicion for GHB use, especially in young adults presenting with characteristic alterations in consciousness and vital signs. The rapid resolution of symptoms with appropriate supportive measures underscores the effectiveness of this management approach in most cases of acute GHB toxicity.

References

Busardò, F.P. and Jones, A.W., 2019. GHB pharmacology and toxicology: acute intoxication, concentrations in blood and urine in forensic cases and treatment of the withdrawal syndrome. Current neuropharmacology, 17(1), pp.52-79.

Schep, L.J., Knudsen, K., Slaughter, R.J., Vale, J.A. and Mégarbane, B., 2021. The clinical toxicology of gamma-hydroxybutyrate, gamma-butyrolactone and 1, 4-butanediol. Clinical Toxicology, 59(1), pp.3-14.

Wong, C.G., Gibson, K.M. and Snead, O.C., 2018. From the street to the brain: neurobiology of the recreational drug γ-hydroxybutyric acid. Trends in pharmacological sciences, 39(7), pp.632-654.

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