Key Facts

Cocaine and other stimulants are among the most commonly misused substances in the UK. Cocaine-related harm has risen dramatically over the past decade, driven by increased purity and availability. Stimulant misuse carries significant cardiovascular, neurological, and psychiatric risks.

Epidemiology

• Cocaine: ~875,000 users in past year (England and Wales); highest rates in 20-29 age group
• Cocaine purity: average has increased from ~20% to >60% over the past decade
• Cocaine deaths: approximately 840/year (England and Wales); increasing trend
• Amphetamines: ~130,000 past-year users; declining trend but methamphetamine emerging
• MDMA (ecstasy): ~500,000 past-year users; typically intermittent recreational use

Aetiology

• Cocaine: derived from coca plant (Erythroxylum coca); two forms:
  • Powder cocaine (cocaine hydrochloride): snorted or injected
  • Crack cocaine (freebase): smoked; rapid onset, intense but brief high → highly reinforcing
• Amphetamines: synthetic stimulants; oral, intranasal, injected
• Methamphetamine (crystal meth): more potent, neurotoxic; emerging in UK, particularly in chemsex context
• Reinforcement: powerful dopaminergic reward → rapid development of psychological dependence

Pathophysiology

• Cocaine: blocks dopamine transporter (DAT), noradrenaline transporter (NET), serotonin transporter (SERT) → increased synaptic monoamines
  • Also blocks sodium channels (local anaesthetic effect) → cardiac arrhythmias
  • Vasospasm: coronary and cerebral arteries → ACS, stroke
• Amphetamines: reverse-transport mechanism → release of presynaptic dopamine, noradrenaline, serotonin stores
• Methamphetamine: additional neurotoxic effects on dopaminergic neurons
• Chronic use: dopamine receptor downregulation → anhedonia, depression, cognitive impairment

Acute Cocaine/Stimulant Intoxication

• Cardiovascular: tachycardia, hypertension, chest pain, palpitations, arrhythmias
• Neurological: mydriasis, tremor, hyperreflexia, seizures, headache, stroke
• Psychiatric: euphoria, grandiosity, agitation, paranoia, hallucinations (tactile — "cocaine bugs"/formication)
• General: hyperthermia, diaphoresis, anorexia

Complications of Acute Use

• Cocaine-associated acute coronary syndrome: chest pain within hours of use; coronary vasospasm ± thrombosis; may cause MI in young patients with normal coronary arteries
• Aortic dissection: acute tearing chest pain, hypertension
• Stroke: both ischaemic and haemorrhagic; especially with crack cocaine
• Seizures: usually generalised tonic-clonic; self-limiting
• Hyperthermia and rhabdomyolysis: particularly with MDMA and methamphetamine
• Serotonin syndrome: with MDMA; agitation, myoclonus, hyperthermia, autonomic instability

Stimulant Withdrawal ("crash")

• Onset within hours to days of cessation
• Dysphoria, depression, fatigue, hypersomnia
• Increased appetite
• Psychomotor retardation
• Intense craving
• Not medically dangerous but significant suicide risk

Red Flags

• Chest pain: assume cardiac aetiology; ECG and troponin
• Severe hypertension (>180/120 mmHg): risk of hypertensive emergency, dissection, stroke
• Hyperthermia >40°C: life-threatening; aggressive cooling required
• Seizures: may progress to status epilepticus
• Paranoid psychosis with aggression: may require emergency sedation
• Body packing: cocaine-filled packets in GI tract; rupture → massive overdose

Bedside

• ECG: ST changes (ACS), arrhythmias, QTc prolongation, Brugada pattern
• Observations: HR, BP (hypertensive emergency?), temperature, SpO2, GCS
• Capillary glucose: cocaine can cause hyper- or hypoglycaemia
• Urine drug screen: cocaine metabolite (benzoylecgonine) detectable for 2-4 days; amphetamines detectable for 1-3 days

Bloods

• Troponin: serial — cocaine-associated ACS
• FBC: leucocytosis (stress response)
• U&Es: renal function (rhabdomyolysis risk)
• CK: rhabdomyolysis (may be massively elevated)
• LFTs: cocaine-induced hepatotoxicity (rare)
• Coagulation screen: DIC in severe toxicity
• ABG/VBG: metabolic acidosis (lactic acidosis, rhabdomyolysis)
• Blood alcohol level: concurrent use common

Imaging

• Chest X-ray: pulmonary oedema, pneumomediastinum (crack cocaine), aspiration
• CT head: if seizures, focal neurology, or stroke suspected
• CT angiography: if aortic dissection suspected
• Abdominal X-ray/CT: if body packing suspected
• Echocardiography: if endocarditis or cardiomyopathy suspected

Special Tests

• Coronary angiography: for cocaine-associated ACS with ST-elevation
• Lumbar puncture: if subarachnoid haemorrhage suspected (thunderclap headache, CT-negative)
• MRI brain: for stroke characterisation

Non-pharmacological

• Calm environment: reduce sensory stimulation for agitated patients
• Active cooling: remove clothing, fans, cool IV fluids, ice packs for hyperthermia >39°C
• Supportive care: IV fluids, monitoring, observation

Pharmacological — Acute Intoxication/Emergency

• Agitation and seizures:
  • Diazepam 5-10 mg IV (repeat as needed) or lorazepam 1-2 mg IV: first-line for agitation, seizures, and cardiovascular complications
  • Benzodiazepines address most complications by reducing sympathetic drive
• Cocaine-associated chest pain/ACS:
  • GTN sublingual/IV: coronary vasodilation
  • Aspirin 300 mg: antiplatelet effect
  • Diazepam 5-10 mg IV: reduces sympathetic drive and BP
  • Avoid beta-blockers: risk of unopposed alpha-adrenergic stimulation → worsening hypertension and coronary vasospasm
  • Phentolamine 5-10 mg IV: alpha-blocker; if hypertension refractory to benzodiazepines
  • Primary PCI: if STEMI confirmed
• Severe hypertension: benzodiazepines first-line; add GTN or phentolamine if needed
• Hyperthermia: active cooling; dantrolene considered if refractory
• Serotonin syndrome (MDMA): cyproheptadine 12 mg PO initially, then 4 mg 2-hourly; benzodiazepines, cooling

Non-pharmacological — Longer-term Treatment

• CBT: most evidence-based psychosocial intervention for stimulant misuse (NICE CG51)
• Contingency management: incentive-based treatment; NICE TA114 recommends for stimulant misuse
• Motivational interviewing: enhance motivation to change
• Harm reduction: avoid injecting, avoid using alone, start with small amounts of unknown batches

Surgical

• Body packing: if packet rupture suspected — emergency laparotomy; whole bowel irrigation with PEG solution if intact packets

Referral Criteria

• Emergency department: acute toxicity, chest pain, seizures, psychosis
• Cardiology: cocaine-associated ACS, arrhythmias
• Drug and alcohol services: for ongoing psychosocial treatment
• Psychiatry: stimulant-related psychosis, severe depression during withdrawal, suicidality

Outcomes

• Acute cocaine toxicity: most patients recover with supportive care; mortality <5% with appropriate treatment
• Cocaine-associated MI: younger patients; often recoverable but cardiomyopathy may develop
• Stimulant psychosis: usually resolves within days to weeks of cessation; ~10-15% may develop chronic psychotic disorder
• Treatment outcomes: CBT + contingency management → ~30-40% achieve sustained abstinence at 6 months

Complications

• Sudden cardiac death: arrhythmias (VT/VF), even in young healthy individuals
• Dilated cardiomyopathy: chronic cocaine use → progressive heart failure
• Nasal septum perforation: chronic cocaine snorting
• Crack lung: pulmonary haemorrhage, eosinophilic pneumonia, thermal airway injury
• Cognitive impairment: executive dysfunction, impaired decision-making with chronic use
• Socioeconomic harm: financial ruin, relationship breakdown, criminal justice involvement

Stimulant Comparison

Cocaine-Associated Chest Pain: Key Management Points