Pharmacology, Toxicology and Addiction MedicineTier 1Disease (DEADMAN)

Acute and chronic effects, including overdose, from the use of - cocaine

Description

Cocaine - short-acting sympathomimetic + local anaesthetic (Na-channel blocking) properties
Acute: euphoria, sympathomimetic toxidrome, chest pain (cocaine-associated ACS), seizures, intracranial haemorrhage at high dose
Chronic: cardiomyopathy, nasal septal perforation (insufflation), dependence

Epidemiology

Use inc in Australia in recent years, though less prevalent than methamphetamine
Cocaine-associated chest pain is a recognised, specific ED presentation requiring a tailored approach

Aetiopathogenesis

Blocks reuptake of dopamine, noradrenaline, serotonin -> sympathomimetic effects
Na-channel blockade (local anaesthetic effect) -> contributes to seizures and cardiac conduction effects at high dose
Coronary vasospasm + inc myocardial oxygen demand + prothrombotic effect -> MI even with normal coronary arteries, and even in young patients
Chronic use -> myocardial fibrosis/cardiomyopathy, accelerated atherosclerosis

Diagnosis

Clinical (see toxidromes-sympathomimetic) + urine drug screen
ECG + troponin mandatory for any chest pain in a cocaine user - infarction can occur regardless of dose or frequency of use
CT brain if severe headache/neurological signs (haemorrhage risk)

Management

Cocaine-associated chest pain / ACS

Benzodiazepines - first-line, reduce sympathetic drive and chest pain
Nitrates, aspirin as per standard ACS care
Avoid unopposed beta-blockade (including for arrhythmia/HTN) - unopposed alpha effect risks worsening coronary vasospasm; use benzodiazepines +/- phentolamine +/- calcium channel blocker instead
Primary PCI as per standard STEMI pathway if infarction confirmed

Dependence

Psychosocial interventions - no approved pharmacotherapy for cocaine dependence

Associations

MI, aortic dissection, intracranial haemorrhage, seizures
Nasal septal perforation with chronic insufflation
Often co-used with alcohol (forms cocaethylene - more cardiotoxic, longer half-life) or opioids ("speedballing")

Natural history & complications

Acute effects are short-lived (30-60 min) given short half-life - repeated dosing ("bingeing") common, compounding cardiovascular risk
Cardiovascular risk from a single use is real and not confined to heavy chronic users

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