Acute toxicity 🚩
Stimulants (cocaine, amphetamine, methamphetamine) drive catecholamine excess: agitation, hyperthermia, tachycardia, hypertension, and emergencies — ACS/arrhythmia, seizures, intracerebral haemorrhage, aortic dissection. Management: benzodiazepines first for agitation/adrenergic drive; active cooling; treat end‑organ effects. Avoid β‑blocker monotherapy in cocaine (theoretical unopposed α‑vasoconstriction) — benzodiazepines are the anchor.
Stimulant‑induced psychosis — two questions, not one
Heavy use → persecutory delusions, hallucinations (incl. tactile/formication), severe paranoia — clinically indistinguishable cross‑sectionally from primary psychosis. Apply the timeline (Concept 28): onset with use, resolution with abstinence → substance‑induced. But don't reflexively dismiss a first psychotic presentation as "just drugs" — some declare a primary psychotic disorder. Hold "what syndrome?" AND "is the substance causing it?" simultaneously.
The disorder — treatment reality
No established agonist maintenance with the evidence base of opioids. First‑line is psychosocial: CBT, contingency management, family/community interventions. Guidelines don't recommend routine stimulant substitution (dexamphetamine/methylphenidate/modafinil) for cocaine/stimulant use disorder.
Pitfalls
- β‑blocker monotherapy in cocaine toxicity.
- Committing to "drug‑induced" vs "primary" psychosis prematurely — reassess with the abstinence course.
Pearls
- 🎯 Benzodiazepines are the workhorse for sympathomimetic toxicity.
- 🩺 Stimulant psychosis = two diagnoses considered, resolved by the abstinence timeline.
Next → The organising principle behind all of this — the timeline — with cannabis (Concept 45).