What is the management approach for a cocaine overdose?

Management of Cocaine Overdose

Follow standard BLS and ACLS protocols for cardiac arrest, while using benzodiazepines as first-line therapy for hypertension, tachycardia, and agitation in non-arrest patients, adding nitroglycerin or calcium channel blockers for chest pain or persistent cardiovascular instability. 1

Immediate Resuscitation and Stabilization

Cardiac Arrest Management

• Apply standard BLS and ACLS algorithms without modification for cocaine-induced cardiac arrest, as this approach has demonstrated 55% neurologically intact survival in case series 1
• Specific antidotes are reserved for the post-resuscitation phase if severe cardiotoxicity or neurotoxicity persists 1

Seizure Control

• Administer benzodiazepines (diazepam or lorazepam) immediately for seizures, as seizure activity is a major determinant of lethality and drives metabolic acidosis 2
• Control of seizures takes priority over other interventions, as uncontrolled seizures lead to respiratory and metabolic acidosis, which worsens cardiac dysrhythmias 2

Airway and Ventilation

• Secure the airway and provide aggressive ventilation to correct acidosis, which can normalize cardiac rhythm and function 2
• Hyperthermia requires aggressive cooling measures as it is rapidly life-threatening and associated with increased mortality 3

Cardiovascular Toxicity Management

First-Line Pharmacologic Therapy

• Administer benzodiazepines (lorazepam or diazepam) as first-line treatment for hypertension, tachycardia, and agitation (Class IIa recommendation) 1, 4
• Add sublingual or IV nitroglycerin for chest pain or persistent hypertension 1, 4
• Calcium channel blockers (diltiazem 20 mg IV or verapamil) can be used for persistent cardiovascular instability 1, 4
• Morphine may be added for chest discomfort (Class IIa recommendation) 1

Critical Medication Contraindications

• Avoid pure beta-blockers in acute cocaine intoxication due to risk of unopposed alpha-adrenergic stimulation causing coronary vasospasm 4, 5
• Combined alpha/beta blockers (like labetalol) should generally be avoided in the acute setting, though may be reasonable in select circumstances only after vasodilator administration (Class IIb recommendation) 4

Wide-Complex Tachycardia

• For wide-complex tachycardia with QRS >120 ms, administer sodium bicarbonate 1 mEq/kg (1 mL/kg of 8.4% solution) IV bolus, repeated as needed until hemodynamic stability is restored and QRS narrows to <120 ms 1
• This approach is extrapolated from evidence in treating other sodium channel blockers (flecainide, tricyclic antidepressants), as cocaine acts as a Vaughan-Williams class Ic antiarrhythmic in severe overdose 1
• Lidocaine has no proven role in cocaine-induced wide-complex tachycardia 1

Acute Coronary Syndrome Management

Risk Stratification

• Obtain immediate 12-lead ECG to identify ST-segment elevation, which fundamentally changes management 4
• High-risk features requiring monitored admission include: ST-elevation or depression ≥1 mm, elevated cardiac markers, recurrent chest pain, or hemodynamic instability 4, 5
• Troponin I and T are preferred biomarkers over CK-MB, as CK can be elevated from skeletal muscle activity and rhabdomyolysis without myocardial infarction 5

Revascularization Strategy

• For ST-elevation MI, proceed immediately to PCI rather than fibrinolytic therapy, as cocaine users frequently have contraindications to thrombolytics 4, 5
• If no response to vasodilators in ST-elevation, proceed immediately to coronary angiography if available (Class IIa recommendation) 4
• Use bare-metal stents rather than drug-eluting stents due to shorter required duration of dual antiplatelet therapy, as cocaine users are unreliable with prolonged adherence and face high risk of in-stent thrombosis 4, 5
• Administer aspirin as part of standard acute coronary syndrome management 4

Monitoring and Complications

Multi-System Assessment

• Screen for life-threatening complications beyond MI: aortic dissection, coronary artery dissection, myocarditis, and cardiomyopathy (Class I recommendation) 4
• Monitor for rhabdomyolysis and acute kidney injury, which may occur with or without rhabdomyolysis due to direct renal toxicity, vasoconstriction-induced ischemia, and cellular damage 6, 7
• Serial vital sign assessment is crucial in patients with cardiovascular complications 4

Observation Unit Criteria

• Low to intermediate-risk patients without high-risk features can be safely managed in a chest pain observation unit for 9-12 hours with clinical and ECG monitoring plus repeat troponin measurements 5
• Only 0.7% to 6% of patients with cocaine-associated chest pain actually have myocardial infarction 5

Important Clinical Pitfalls

• Carefully dose medications to avoid hypotension after cocaine metabolism, as cocaine's effects are transient 1
• Young patients often have benign early repolarization mimicking ST-elevation, so only a small percentage with J-point elevation are actually having MI 4
• Cocaine causes accelerated coronary atherosclerosis, so suspect toxicity in younger patients with chest pain lacking traditional risk factors 3
• The combination of cocaine with alcohol or cigarettes intensifies cardiovascular effects 3
• Prompt consultation with a medical toxicologist is strongly recommended for severe cases 1