Clinical Features of Cocaine Toxicity
Cocaine toxicity presents as a sympathomimetic toxidrome characterized by tachycardia, hypertension, hyperthermia, seizures, diaphoresis, and increased psychomotor activity due to its effects on the sympathetic nervous system, CNS stimulation, and local anesthetic properties. 1
Cardiovascular Manifestations
- Tachycardia - Results from postsynaptic β-adrenergic receptor agonism due to catecholamine reuptake inhibition 1
- Hypertension - Caused by peripheral postsynaptic α-adrenergic receptor agonism 1
- Dysrhythmias - Including wide-complex tachycardia, QRS prolongation, QT interval prolongation, and potentially fatal arrhythmias like ventricular tachycardia and asystolic cardiac arrest 1
- Coronary vasospasm - Even small intranasal doses can cause vasoconstriction, which may be more pronounced in patients with preexisting coronary artery disease 1
- Acute coronary syndrome - The most frequent cocaine-related reason for hospitalization in adults 1
- Myocardial ischemia/infarction - Results from increased oxygen demand, decreased supply via vasoconstriction, and thrombosis 1, 2
Neurological Manifestations
- Seizures - Due to CNS stimulation and lowered seizure threshold 1, 3
- Altered mental status - Ranging from agitation to psychosis 1, 4
- Increased psychomotor activity - A hallmark of sympathomimetic toxidrome 1
- Intracerebral hemorrhage - A potentially fatal complication 4, 5
Other Clinical Features
- Hyperthermia - Can be rapidly life-threatening and requires aggressive management 1
- Diaphoresis - Part of the sympathomimetic toxidrome 1
- Respiratory complications - Including respiratory distress and failure 5
- Renal damage - Can occur with severe toxicity 5
- Gastrointestinal symptoms - Including abdominal pain and bowel ischemia 4, 5
Electrocardiographic Changes
- QRS prolongation - Due to sodium channel blockade during phase 0 of the cardiac action potential 1
- QT interval prolongation - From blockade of cardiac potassium channels 1
- ST segment and T wave changes - May mimic myocardial infarction 2
- Brugada pattern - Has been reported in severe cocaine toxicity 1
Laboratory Findings
- Elevated cardiac biomarkers - May indicate myocardial injury, though not as reliable as in non-cocaine users 2
- Metabolic acidosis - In severe cases 3
- Elevated creatine kinase - Due to rhabdomyolysis in severe cases 3
Pathophysiological Mechanisms
- Catecholamine reuptake inhibition - Leads to accumulation of norepinephrine, epinephrine, dopamine, and serotonin 1
- Sodium channel blockade - Causes QRS prolongation and wide-complex tachycardia 1
- Potassium channel blockade - Results in QT interval prolongation 1
- Increased platelet activation and aggregation - Contributes to thrombosis risk 1
- Elevated inflammatory markers - Including C-reactive protein, von Willebrand factor, and fibrinogen 1
High-Risk Features
- Hyperthermia - Associated with increased toxicity and mortality 1
- Wide-complex tachycardia - Indicates severe sodium channel blockade 1
- Seizures - Particularly if prolonged or recurrent 3
- Chest pain with ECG changes - May indicate cocaine-induced myocardial ischemia 1
Pitfalls and Caveats
- Standard cardiac diagnostic tools like ECG and cardiac markers may be less accurate in cocaine users with chest pain 2
- Cocaine toxicity should be suspected in younger patients presenting with chest pain or cardiovascular symptoms without traditional risk factors 1, 2
- The combination of cocaine with alcohol or cigarettes can intensify cardiovascular effects 1
- Patients may present with multi-system involvement requiring simultaneous management of cardiovascular, neurological, and other manifestations 4, 5