Clinical Features of Cocaine Toxicity
Introduction to 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, 2
Cardiovascular Manifestations
- Tachycardia results from postsynaptic β-adrenergic receptor agonism due to catecholamine reuptake inhibition 1
- Hypertension is 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, can occur 1, 3
- Coronary vasospasm can be caused by even small intranasal doses, which may be more pronounced in patients with preexisting coronary artery disease 4, 5
- Acute coronary syndrome is the most frequent cocaine-related reason for hospitalization in adults 6
- Myocardial ischemia/infarction results from increased oxygen demand, decreased supply via vasoconstriction, and thrombosis 5
Neurological Manifestations
- Seizures can occur due to CNS stimulation and lowered seizure threshold 1
- Altered mental status, ranging from agitation to psychosis, can be present 1
- Increased psychomotor activity is a hallmark of sympathomimetic toxidrome 1
Other Clinical Features
- Hyperthermia can be rapidly life-threatening and requires aggressive management 1, 3
- Diaphoresis is part of the sympathomimetic toxidrome 1
Electrocardiographic Changes
- QRS prolongation is due to sodium channel blockade during phase 0 of the cardiac action potential 1, 3
- QT interval prolongation is from blockade of cardiac potassium channels 1
- Brugada pattern has been reported in severe cocaine toxicity 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 5
- Elevated inflammatory markers, including C-reactive protein, von Willebrand factor, and fibrinogen, can be present 5
High-Risk Features
- Hyperthermia is associated with increased toxicity and mortality 6
- Wide-complex tachycardia indicates severe sodium channel blockade 1, 3
- Chest pain with ECG changes may indicate cocaine-induced myocardial ischemia 4, 5