Makindo Medical Notes

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🌿 About

• Cannabis toxicity results from the acute or chronic use of derivatives of the Cannabis sativa plant. The main psychoactive compound is Δ⁹-tetrahydrocannabinol (THC), which acts on CB₁ receptors in the brain and CB₂ receptors in immune tissues.
• Common preparations include:
  • Marijuana: dried flowers and leaves.
  • Hashish: resin extract.
  • Oils / “Wax” / Edibles: concentrated THC derivatives of variable potency.
• Routes: Smoking → effects within 10–20 min; oral ingestion → delayed onset (1–2 h) but prolonged duration (up to 12 h). Edibles are a common cause of accidental overdose.

💡 Teaching point: THC acts as a partial agonist at central CB₁ receptors, reducing GABA and glutamate release → altered perception, coordination, and mood. Chronic exposure down-regulates CB₁ receptors, explaining tolerance and withdrawal.

🧠 Clinical Features

• Mild / Low dose: Euphoria, altered time perception, laughter, mild ataxia, increased appetite (“munchies”), tachycardia, dry mouth, mild hypertension.
• Moderate / High dose: Panic attacks, severe anxiety, hallucinations, paranoid delusions, depersonalisation, transient psychosis, vomiting.
• Severe / Intravenous or Synthetic Cannabinoids: Cardiovascular collapse, renal failure, pulmonary oedema, DIC, seizures, and hyperthermia. “Spice” and other synthetic products have unpredictable potency.
• Withdrawal syndrome (chronic users): Irritability, insomnia, decreased appetite, low mood, tremor, and anxiety beginning 24–72 h after cessation, lasting up to 2 weeks.

🔬 Investigations

• Urine toxicology: detects THC-COOH for 3–7 days (occasional) or up to 30 days (chronic users).
• Blood tests: U&E, LFTs, glucose, creatine kinase (if agitation or hyperthermia), and screen for co-ingestion (e.g., stimulants, alcohol).
• ECG: check for tachyarrhythmia, QT prolongation (particularly if combined with stimulants).
• CT / MRI: only if neurological deficit or suspicion of alternative pathology (e.g., intracranial haemorrhage, encephalitis).

💊 Management

⚠️ Principle: Supportive care is the cornerstone. Specific antidotes do not exist. Treat agitation, prevent complications, and exclude other causes of collapse.

🩺 Follow-Up Care

• Advise against driving or machinery use for 24 h after intoxication.
• Offer referral to local drug and alcohol services (e.g. Change Grow Live, NHS Talking Therapies).
• Educate on risks of synthetic cannabinoids and edibles.
• Screen for concurrent mental health disorders — particularly anxiety, depression, and psychosis.

🧩 Differential Diagnoses

• Stimulant toxicity (amphetamine, cocaine).
• Anticholinergic poisoning.
• Hypoglycaemia or alcohol intoxication.
• First presentation of a primary psychotic disorder.

📚 References

• NICE CKS: Cannabis Misuse
• NHS: Cannabis – The Facts
• Hall W, Degenhardt L. Adverse health effects of non-medical cannabis use. NEJM 2014;370:2219–27.
• Monte AA et al. Cannabis intoxication and hyperemesis in emergency care. NEJM 2019;380:2309–17.

Summary: Cannabis toxicity typically follows a benign course but can cause significant neuropsychiatric disturbance or cardiovascular collapse, particularly with high-potency or synthetic products. Prompt supportive management and psychosocial follow-up are essential to prevent recurrence and address underlying dependence.