Does Cocaine Cause Bronchospasm?
Yes, cocaine can cause bronchospasm, particularly when smoked as crack cocaine, through direct local airway irritation rather than systemic effects. 1
Mechanism and Route-Dependent Effects
The bronchospastic effects of cocaine are primarily route-dependent:
Smoked cocaine (crack) causes significant bronchoconstriction through local airway irritation, with studies demonstrating a 25.4% decrease in specific airway conductance within 5 minutes of inhalation 1
Intravenous cocaine does not cause bronchospasm, as demonstrated in controlled studies where IV cocaine hydrochloride produced no significant changes in airway resistance, despite causing comparable systemic intoxication and cardiovascular effects 1
The mechanism appears to be direct thermal and chemical irritation of airways rather than cocaine's systemic sympathomimetic effects 1, 2
Clinical Manifestations
Cocaine-induced bronchospasm presents with:
Wheezing reported in 32% of habitual crack smokers 1
Acute hypoxic and hypercapnic respiratory failure that can mimic acute asthma exacerbation 3
Symptoms occurring minutes to hours after cocaine use, associated with all routes of administration but most severe with smoking 4
Nasal and bronchial epithelial thickening decreases with chronic use, along with increased mucus production 5
Differential Diagnosis Considerations
Cocaine-induced bronchospasm is a diagnosis of exclusion that should be considered when acute respiratory failure cannot be explained by:
- COPD or asthma exacerbation
- Anaphylaxis
- Exercise-induced bronchospasm
- Infection 3
Special Populations at Risk
Asthmatic patients face heightened risk, as:
- Lignocaine (used during procedures) may produce bronchoconstriction in asthmatic patients 4
- Asthmatic subjects should receive bronchodilator premedication before any airway procedures 4
- The combination of cocaine use and underlying asthma creates compounded risk for severe bronchospasm 1, 6
Management Approach
When encountering suspected cocaine-induced bronchospasm:
Avoid beta-blockers within 4-6 hours of cocaine exposure due to risk of unopposed alpha-stimulation and worsening coronary vasospasm 7, 8
First-line treatment includes benzodiazepines (lorazepam or diazepam) for managing associated tachycardia and hypertension 7
Nitroglycerin and calcium channel blockers (such as diltiazem 20 mg IV) are recommended for cardiovascular complications 7, 8
Standard bronchodilator therapy remains appropriate for the bronchospastic component
Chronic Pulmonary Effects
Beyond acute bronchospasm, chronic crack cocaine inhalation causes:
- Extensive histological changes throughout the respiratory tract including increased alveolar macrophage density and hemosiderin content 5
- Pulmonary artery vasoconstriction and increased wall thickness 5
- Diverse disorders including thermal airway injury, pulmonary edema, hemorrhage, and interstitial lung disease 2, 6