Synopsis
Recognise overlapping acute and chronic harms from stimulants, cannabis and novel psychoactive substances, stabilise severe toxicity, obtain a substance-specific functional history, and provide evidence-based psychosocial and harm-reduction care despite uncertain product contents.
- Ask about the claimed substance, form, route, amount, timing, redosing, setting, sleep, food and fluid intake, alcohol or other drugs, and retain packaging for clinicians where safe.
- Cocaine, amphetamines and synthetic cathinones can cause anxiety, agitation, psychosis, hyperthermia, seizures, hypertension, arrhythmia, myocardial infarction, stroke and rhabdomyolysis.
- Cocaine plus alcohol forms cocaethylene and increases toxicity; do not describe alcohol as a safe way to soften a stimulant comedown.
- MDMA-related collapse may reflect hyperthermia or dilutional hyponatraemia, which need different fluid decisions; measure temperature and sodium urgently.
- Cannabis can cause panic, impaired driving, psychosis and dependence; repeated cyclical vomiting relieved by hot bathing suggests cannabinoid hyperemesis, for which sustained cessation is definitive prevention.
- Synthetic cannabinoid receptor agonists are not simply stronger cannabis: unconsciousness, respiratory depression, aggression, psychosis, seizures, arrhythmia, stroke and acute kidney injury are reported.
- Novel psychoactive substance labels do not predict contents; manage observed physiology, consider mixed exposure and consult toxicology rather than relying on a negative routine urine screen.
- There is no licensed substitution medicine for cocaine, amphetamine, cannabis or most NPS dependence; tailored psychosocial treatment, contingency management where recommended and practical harm reduction are central.
Key red flags
Chest pain, severe breathlessness, syncope, marked hypertension, arrhythmia or focal neurological deficit after stimulant exposure suggests myocardial infarction, aortic disease or stroke.
Core hyperthermia, rigidity, severe agitation, seizure, acidosis or dark urine raises concern for serotonin toxicity, excited delirium physiology, rhabdomyolysis and multiorgan injury.
Headache, vomiting, confusion or seizure after MDMA or excessive water intake can indicate acute hyponatraemia and cerebral oedema.
Persistent hallucinations, persecutory beliefs, suicidal intent, violent behaviour or inability to care for self requires urgent psychiatric and physical assessment.
Reduced consciousness or respiratory depression after any purported recreational product should trigger airway support and naloxone because synthetic opioid contamination is possible.
Investigation priorities
Track temperature, pulse, blood pressure, respiratory state, oxygen saturation and consciousness during evolving toxicity.
Management branches
Recent use is followed by severe agitation, chest pain, hyperthermia, seizure, psychosis or collapse.
- Move to a low-stimulation safe setting and assess ABC, glucose, temperature, ECG, consciousness and injury without confrontational restraint.
- Treat seizures, agitation, hyperthermia, arrhythmia and electrolyte abnormalities through acute protocols with toxicology or critical-care advice.
- Use naloxone and ventilation for an opioid respiratory pattern, investigate mixed poisoning and continue observation for recurrent or delayed toxicity.
The person is stable but the product contents, cause of symptoms or psychiatric diagnosis remains uncertain.
- Build a timeline of all substances, doses, route, redosing, sleep, nutrition and symptom onset, including periods of abstinence.
- Assess dependence, cognition, psychosis, mood, suicide, sexual risk, injection injury, housing, exploitation and safeguarding.
- Use targeted testing only where it answers a clinical question and revise the formulation as symptoms resolve or persist.