Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.
Stimulant, cannabis and novel psychoactive substance harms
Psychiatry · UK scope · Sources checked 27 Aug 2026 · Clinical review pending
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Treat the toxidrome, not the street name
Chest pain, severe hypertension, arrhythmia, hyperthermia, seizure, collapse, extreme agitation, psychosis, hyponatraemic symptoms or reduced consciousness after stimulant, cannabis or NPS exposure can deteriorate rapidly, while the actual compound and dose may be unknown.
Action: Call emergency services, assess airway, breathing, circulation, glucose, temperature and consciousness, use a low-stimulation environment, obtain ECG and urgent cause-directed tests, and seek local toxicology or National Poisons Information Service guidance. Actively cool hyperthermia, manage seizures and agitation through the acute protocol, and give naloxone whenever an opioid toxidrome is possible.
Overview
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.
Stimulants increase monoaminergic activity and arousal; cannabis acts mainly through cannabinoid receptors; the NPS category spans chemically unrelated stimulants, synthetic cannabinoids, hallucinogens, dissociatives, sedatives and synthetic opioids. A product sold under one name may contain another compound or several. Clinical care therefore starts with the toxidrome and physiology rather than certainty about the label. Record timing, route, repeated dosing, setting, co-use, sleep deprivation and what the person was trying to achieve, then examine temperature, hydration, pupils, muscle tone, consciousness, cardiovascular and mental state.
Acute stimulant toxicity produces a sympathomimetic picture: agitation, anxiety, sweating, dilated pupils, tachycardia, hypertension and hyperthermia. Severe outcomes include arrhythmia, acute coronary syndrome, aortic dissection, stroke, seizure, serotonin toxicity, rhabdomyolysis and renal failure. Cocaine-related chest pain is a medical emergency even in a young person. MDMA can cause hyperthermia in hot crowded environments, while excessive hypotonic fluid plus antidiuretic effects can cause hyponatraemia; the distinction matters because indiscriminate water intake can worsen cerebral oedema.
Practice
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PsychiatryOriginal SBA
Synthetic-cathinone neurological deterioration
A young adult becomes confused and vomits after taking a powder sold as mephedrone at a festival and reports drinking several litres of water. Which immediate assessment is most important alongside ABC?
Sources and review status6 sources · checked 27 Aug 2026 · clinical review pending+
Sources
Sources and review status
National guidance is shown before implementation-dependent detail. Apply principles in context and verify current guidance when a decision affects care. Source check completed 27 Aug 2026; clinical approval remains outstanding.
Editorial contact: Doctor’s Passport editorial team. Source-check date is separate from clinical approval. Report a content problem ·
Cannabis may cause relaxation or altered perception but also panic, impaired coordination, tachycardia, paranoia and psychosis, especially with high-potency products and personal vulnerability. Regular use can lead to dependence and worsen the course of established psychosis. Cannabinoid hyperemesis presents with recurrent severe nausea and vomiting, abdominal pain and learned hot bathing; acute care treats dehydration and alternative diagnoses, while cessation prevents recurrence. Synthetic cannabinoid receptor agonists have less predictable pharmacology and can produce collapse, respiratory depression, severe behavioural disturbance, seizures, cardiovascular events and withdrawal.
Novel psychoactive substances require broad differential thinking. Synthetic cathinones resemble other stimulants but can cause prolonged agitation, psychosis, hyperthermia and cardiovascular toxicity. GHB and related drugs can cause rapid coma and a severe short-interval withdrawal syndrome in dependent users. Ketamine is associated with dissociation, injury and chronic bladder or upper urinary tract damage. Potent synthetic opioids such as nitazenes may contaminate powders or counterfeit tablets; if breathing is depressed, give naloxone regardless of the substance the person thought they had taken.
After acute stabilisation, formulate dependence, mental health and social function. Ask about craving, impaired control, tolerance, withdrawal, time spent, harms and failed attempts to stop. NHS treatment for cocaine relies on psychological therapies, couples work where appropriate and contingency management rather than an opioid-style substitute. Cannabis and NPS plans use motivational and cognitive-behavioural approaches, sleep and anxiety care, relapse prevention and practical risk reduction. Offer infectious-disease care for injecting, sexual-health support, naloxone when opioid exposure is plausible, and coordinated psychosis treatment without excluding the person from either service.
Key points
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.
Aetiology
01
Reward and reinforcement
Euphoria, alertness, relief from distress or social belonging can reinforce repeated exposure despite progressively shorter benefit and greater harm.
02
Product variability
Unregulated synthesis, adulteration and mislabelling make active compound, potency and duration unpredictable between products sold under one name.
03
Psychosocial vulnerability
Trauma, mental illness, unstable housing, deprivation, nightlife or custodial environments may increase exposure and reduce access to safer coping and care.
Pathophysiology
1
Monoamine excess
Cocaine, amphetamines and cathinones increase dopamine, noradrenaline or serotonin signalling, producing arousal alongside cardiovascular and thermal toxicity.
2
Cannabinoid signalling
THC alters perception, memory, coordination and salience through cannabinoid receptors, with psychotic effects amplified by potency and vulnerability.
3
Synthetic receptor activity
Many synthetic cannabinoids are potent full receptor agonists, contributing to effects more severe and less predictable than partial agonist THC.
4
Heat and muscle injury
Agitation, vasoconstriction and sustained muscle activity generate hyperthermia, rhabdomyolysis, acidosis and subsequent renal or multiorgan failure.
Clinical features and red flags
Sympathomimetic toxicity
Agitation, sweating, mydriasis, tachycardia, hypertension and hyperthermia suggest stimulant or cathinone toxicity but do not identify a specific compound.
Substance-induced psychosis
Hallucinations, paranoia and disorganisation temporally related to use or sleep deprivation may persist beyond intoxication and require longitudinal review.
Cannabinoid hyperemesis
Recurrent vomiting with chronic cannabis exposure and compulsive hot bathing is suggestive, after urgent gastrointestinal and metabolic causes are assessed.
Synthetic cannabinoid toxicity
Rapid shifts between unresponsiveness, agitation, psychosis, seizures and cardiovascular instability are more severe and unpredictable than typical cannabis effects.
Post-stimulant crash
Fatigue, hypersomnia, dysphoria, anxiety, craving and suicidal thinking may follow prolonged stimulant use and need direct risk assessment.
Red flags requiring action
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.
Investigations
01Serial physiological observationsFirst step
Why
Track temperature, pulse, blood pressure, respiratory state, oxygen saturation and consciousness during evolving toxicity.
Interpretation and limitations
Hyperthermia or deterioration mandates escalation; a settled appearance after short observation may not exclude a long-acting or re-dosed NPS.
02Electrocardiogram and cardiac markers
Why
Evaluate chest pain, arrhythmia, syncope or significant stimulant cardiovascular exposure.
Interpretation and limitations
Treat suspected acute coronary syndrome clinically; young age and a non-diagnostic first ECG do not remove risk.
03Glucose, electrolytes and organ-injury tests
Why
Detect hypoglycaemia, hyponatraemia, acidosis, rhabdomyolysis, renal injury and hepatic injury.
Interpretation and limitations
Sodium guides management of MDMA-associated neurological symptoms, while creatine kinase and renal trends reflect hyperthermic muscle injury.
04Substance and mental-state history
Why
Relate psychosis, panic, mood change and cognition to exposure, abstinence, sleep and previous episodes.
Interpretation and limitations
Symptoms persisting during verified abstinence or predating use raise the probability of an independent mental disorder, though both can coexist.
Differential diagnosis
01
Primary psychosis or mania
A prior episode, persistence during abstinence and symptoms independent of exposure support an autonomous disorder that can still be substance worsened.
02
Serotonin or anticholinergic toxicity
Medicine combinations can produce agitation, hyperthermia and autonomic change, with neuromuscular and bowel findings helping distinguish toxidromes.
03
Sepsis or endocrine crisis
Infection, thyrotoxicosis, hypoglycaemia and other acute metabolic disease can mimic stimulant physiology and require prompt diagnosis and specific treatment.
04
Opioid contamination
Unexpected respiratory depression after a claimed stimulant or tablet may reflect fentanyl or nitazene exposure and warrants naloxone.
Management
01Acute toxicityStabilise observed physiologyFirst stepRecent use is followed by severe agitation, chest pain, hyperthermia, seizure, psychosis or collapse.+
1Move to a low-stimulation safe setting and assess ABC, glucose, temperature, ECG, consciousness and injury without confrontational restraint.
2Treat seizures, agitation, hyperthermia, arrhythmia and electrolyte abnormalities through acute protocols with toxicology or critical-care advice.
3Use naloxone and ventilation for an opioid respiratory pattern, investigate mixed poisoning and continue observation for recurrent or delayed toxicity.
02Diagnostic reviewName harms before compoundsThe person is stable but the product contents, cause of symptoms or psychiatric diagnosis remains uncertain.+
1Build a timeline of all substances, doses, route, redosing, sleep, nutrition and symptom onset, including periods of abstinence.
Complications
01
Cardiovascular catastrophe
Arrhythmia, myocardial infarction, aortic dissection, cardiomyopathy and stroke can occur unexpectedly in otherwise young and apparently healthy stimulant users.
02
Thermal multiorgan failure
Severe hyperthermia and rhabdomyolysis can progress to acidosis, disseminated coagulation, renal failure, hepatic failure, cardiovascular collapse and death.
03
Persistent psychiatric illness
Psychosis, anxiety, depression, cognitive impairment and suicide risk may continue beyond intoxication or recur with renewed exposure.
04
Route-related disease
Injecting, smoking and intranasal use cause blood-borne infection, lung injury, vascular damage, skin infection and nasal tissue injury.
Monitoring and follow-up
Follow chest symptoms, blood pressure, sleep, weight, dental health, cognition and mood according to the stimulant pattern and route.
Review psychosis, paranoia, panic, depression and suicide risk during intoxication, the comedown and a period of reduced use or abstinence.
For cannabinoid hyperemesis, track vomiting episodes, renal and electrolyte recovery and whether cannabis cessation prevents recurrence.
Ask repeatedly about changing products and routes because an apparently stable street name may acquire different potency or opioid contamination.
Measure treatment engagement, days of use, high-risk episodes, functioning and harm reduction rather than requiring immediate abstinence as the only success.
Special situations
Temperature changes priority
Agitation with core hyperthermia is a physiological emergency; verbal behaviour alone can understate impending muscle and organ injury.
Water can also harm
After MDMA, headache, vomiting and confusion may be hyponatraemic encephalopathy, so generic advice to drink large volumes is unsafe.
Synthetic is not predictable
Synthetic cannabinoid or cathinone products vary between packets and can switch toxidromes despite the same branding.
A negative screen is limited
Standard toxicology panels miss many NPS and detection does not establish timing, impairment or causality.
Psychosis needs both pathways
Substance use can precipitate or worsen psychosis, but neither a psychosis diagnosis nor ongoing use justifies exclusion from the other service.
Common pitfalls
01
Assuming the street name proves the active compound and ignoring an observed opioid or sedative toxidrome.
02
Managing severe stimulant agitation as a behavioural problem without measuring temperature, glucose and cardiovascular physiology.
03
Advising unlimited water intake after MDMA without considering hyponatraemia.
04
Describing synthetic cannabinoids as ordinary high-strength cannabis despite their distinct seizure, coma and cardiovascular harms.
05
Diagnosing a primary psychotic disorder or dismissing symptoms as intoxication without a longitudinal timeline.
06
Promising a substitute medicine for stimulant or cannabis dependence when psychosocial treatment is the evidence-based core.
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.
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.
05Targeted toxicology
Why
Support management when results can change care, surveillance or safeguarding.
Interpretation and limitations
Routine screens omit many NPS and do not prove current impairment; consult toxicology for appropriate samples and interpretation.
2
Assess dependence, cognition, psychosis, mood, suicide, sexual risk, injection injury, housing, exploitation and safeguarding.
3Use targeted testing only where it answers a clinical question and revise the formulation as symptoms resolve or persist.
03Ongoing careLink psychosocial and harm reductionUse is recurrent, dependent or causing physical, psychiatric or social harm.+
1Offer local drug-service care using motivational, cognitive-behavioural, contingency or family approaches matched to the substance and person.
2Treat coexisting mental illness and physical complications concurrently, including cannabis cessation for recurrent hyperemesis and psychosis risk.
3Agree concrete harm reduction: avoid using alone or mixing drugs, lower exposure after abstinence, sterile equipment, hydration without overhydration, naloxone and emergency signs.