Stimulant and Cannabis Toxicity
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Direct answer
Stimulant toxicity produces a sympathomimetic toxidrome of agitation, hypertension, tachycardia, hyperthermia and mydriasis, while cannabis toxicity causes tachycardia, red eyes, anxiety and sometimes psychosis. Cocaine and amphetamines carry the greatest risk of seizures, myocardial ischaemia and rhabdomyolysis, and MDMA adds serotonergic effects and hyponatraemia. Benzodiazepines are the first-line treatment for agitation and seizures, with active cooling and supportive care for hyperthermia.
What you must remember
- Sympathomimetic toxidrome: agitation, hypertension, tachycardia, hyperthermia, diaphoresis and mydriasis, caused by catecholamine excess.
- Cocaine: causes coronary vasospasm, myocardial infarction, aortic dissection and seizures, even in young users, through sodium channel and reuptake blockade.
- Beta-blockers: non-selective agents are avoided in cocaine toxicity, because unopposed alpha stimulation can worsen vasoconstriction and hypertension.
- Amphetamines: cause hyperthermia, rhabdomyolysis, intracranial haemorrhage, arrhythmias and psychosis, with cooling and benzodiazepines as key measures.
- MDMA: causes hyperthermia, serotonergic toxicity, hyponatraemia from excess water intake and liver injury, so sodium and temperature are monitored closely.
- Cannabis: tachycardia, conjunctival injection, dry mouth, anxiety, paranoia and psychosis; in children it causes drowsiness, ataxia and hypotonia, and glucose is checked to exclude hypoglycaemia as the cause.
- Cannabinoid hyperemesis syndrome: cyclic vomiting in chronic heavy users, often relieved by hot showers, and managed by stopping cannabis and giving antiemetics.
- Hyperthermia: active external cooling and benzodiazepines form the core of care, since antipyretics do not reverse the hypermetabolic state.
Stimulants and cannabis compared
Stimulant and cannabis toxicity overlap in agitation and tachycardia, but the danger and the monitoring differ sharply.
| Feature | Cocaine and amphetamines | MDMA | Cannabis |
|---|---|---|---|
| Main action | Catecholamine release and reuptake block | Serotonin and catecholamine release | CB1 receptor agonism |
| Key danger | Myocardial ischaemia, seizures, stroke | Hyperthermia, hyponatraemia | Anxiety, psychosis, vomiting syndrome |
| Typical picture | Sympathomimetic toxidrome | Hyperthermic serotonergic picture | Tachycardia, red eyes, dry mouth |
| Key monitoring | ECG, troponin, creatine kinase | Temperature, serum sodium, creatine kinase | Clinical state; blood glucose in drowsy children |
| Management | Benzodiazepines; avoid non-selective beta-blockers | Benzodiazepines, cooling, careful sodium correction | Supportive care, benzodiazepines for agitation |
Sympathomimetic features with hyperthermia point to the stimulants, while red eyes in a calm, sedated patient point towards cannabis. Stimulant toxicity can kill quickly through hyperthermia, arrhythmia or intracranial haemorrhage, so cardiac and temperature monitoring come first.
Urine drug screens detect many of these drugs but miss newer analogues and say nothing about dose, so the clinical picture guides management more than the result. A positive screen should not be taken as proof of cause, since sepsis or a head injury can coexist with drug use.
Where the exam tries to catch you
Most lost marks come from treating stimulant toxicity as a psychiatric problem or choosing the wrong sedative.
- Trap: giving a non-selective beta-blocker to a cocaine patient with chest pain and hypertension Correct: benzodiazepines are first-line, since beta-blockade can worsen vasoconstriction.
- Trap: attributing MDMA hyperthermia to infection alone Correct: MDMA hyperthermia is a toxic process needing benzodiazepines and active cooling, while sepsis is excluded in parallel.
- Trap: labelling cannabis-induced vomiting as gastroenteritis Correct: cannabinoid hyperemesis syndrome causes cyclic vomiting in chronic heavy users and often improves with hot showers.
- Trap: assuming cannabis-induced psychosis always means schizophrenia Correct: acute cannabis psychosis often settles, although persistent symptoms need psychiatric review.
Frequently asked questions
Why are beta-blockers avoided in cocaine toxicity?
Beta-blockers are avoided in cocaine toxicity because unopposed alpha stimulation can worsen vasoconstriction and hypertension. Benzodiazepines are the first-line treatment for chest pain, agitation and seizures, and some toxicologists use labetalol only in refractory cases.
What is the main danger of MDMA toxicity?
The main danger of MDMA toxicity is hyperthermia, which can progress to rhabdomyolysis, coagulopathy and multi-organ failure. Hyponatraemia from excess water intake and serotonergic effects also occur, so serum sodium and temperature are monitored closely.
What is cannabinoid hyperemesis syndrome?
Cannabinoid hyperemesis syndrome is recurrent cyclic vomiting with abdominal pain in chronic heavy cannabis users, often with relief from hot showers. It is managed by stopping cannabis, giving antiemetics and fluids, and reassuring the patient that the course is usually reversible with abstinence.
Which features suggest cannabis rather than stimulant toxicity?
Red conjunctivae, dry mouth and a relatively calm, sedated state suggest cannabis rather than a stimulant, which causes marked agitation, hypertension and mydriasis. In children, cannabis often causes drowsiness, ataxia and hypotonia, so the history should be taken carefully and blood glucose checked to exclude other causes.
What are the complications of amphetamine toxicity?
Amphetamine toxicity can cause hyperthermia, rhabdomyolysis, intracranial haemorrhage, myocardial ischaemia and psychosis. Management centres on benzodiazepines, active cooling and monitoring of creatine kinase, renal function and electrolytes.