Cocaine toxicity

💡 Key Point: Cocaine is widely available in the UK and often under-reported by patients unless asked directly. Always consider it in young patients presenting with unexplained chest pain, stroke, or agitation.

🧠 Aetiology & Pathophysiology

• Cocaine toxicity results from potent central and peripheral sympathomimetic effects due to inhibition of dopamine, noradrenaline, and serotonin reuptake.
• The surge in catecholamines causes vasoconstriction, hypertension, tachycardia, and coronary vasospasm, predisposing to myocardial ischaemia and arrhythmia.
• Chronic use accelerates atherosclerosis and induces myocardial fibrosis and cardiomyopathy.
• The euphoric and reinforcing effects arise from dopamine stimulation in the mesolimbic reward pathway (nucleus accumbens and prefrontal cortex).
• At high doses, cocaine also acts as a local sodium-channel blocker, explaining its anaesthetic properties and potential for conduction delays or seizures in overdose.

💉 Routes of Administration

• Snorting: Most common. Causes mucosal vasoconstriction → chronic rhinitis, septal perforation, and anosmia.
• Smoking (“crack”): Rapid onset, short duration → higher addictive potential; may cause pulmonary oedema or barotrauma.
• IV injection: Produces intense but brief “rush”; risks include septicaemia, endocarditis, DIC, and pulmonary emboli.
• Topical use: Rarely used in ENT/ophthalmic surgery for its anaesthetic and vasoconstrictive effect.

⚡ Clinical Effects

• Cardiovascular: Coronary artery spasm → chest pain, myocardial infarction; arrhythmia; aortic dissection; hypertension.
• Neurological: Seizures, agitation, hyperreflexia, or stroke (ischaemic or haemorrhagic).
• Psychiatric: Euphoria, anxiety, panic, hallucinations, and cocaine-induced psychosis or paranoia.
• Other systemic features: Hyperthermia, mydriasis, rhabdomyolysis, metabolic acidosis, and acute kidney injury.
• Withdrawal: Dysphoria, fatigue, hypersomnia, and intense craving but without severe physiological danger (unlike alcohol or benzodiazepines).

🧪 Investigations

• Blood tests: FBC, U&E, glucose, troponin (at 0 & 12 h), CK (for rhabdomyolysis).
• ECG: Monitor for ischaemia, conduction delay, or QT prolongation.
• Chest X-ray: Assess for aortic dissection, pulmonary oedema, or pneumomediastinum in smokers of “crack.”
• CT head: If focal neurological signs or altered consciousness.
• Urine toxicology: Confirms recent use (detectable 1–3 days after ingestion).

🩹 Management Overview

⚠️ Principles: Treat the sympathomimetic crisis — control agitation, hyperthermia, and hypertension — while avoiding unopposed β-blockade.

🏥 Disposition

• Admit to coronary care / high-dependency unit if chest pain, arrhythmia, or neurological deficit.
• Observe asymptomatic users for at least 6 hours; delayed vasospasm can occur.
• Psychiatric review for suicidal ideation or substance-use counselling before discharge.

🧩 Differential Diagnoses

• Amphetamine or MDMA (ecstasy) intoxication.
• Pheochromocytoma crisis.
• Thyrotoxic crisis.
• Primary psychosis.

📚 References

• NICE CKS: Stimulant Drug Toxicity
• StatPearls: Cocaine Toxicity Management
• Hollander JE, Hoffman RS. Gaps in the management of cocaine-associated chest pain. N Engl J Med 1992;327:351–6.
• Wood DM, Dargan PI. Acute cocaine toxicity. BMJ 2020;371:m4224.

Summary: Cocaine causes catecholamine excess with multisystem effects — most critically, coronary vasospasm and arrhythmia. Treatment is primarily supportive, targeting vasodilation, sedation, and temperature control, while avoiding unopposed β-blockade. Long-term management should include addiction support and cardiovascular screening.