Tristan J. Huie and Charles A. Read
The lungs are particularly vulnerable to medical complications in drug abuse because the most common routes of administration are inhalation and intravenous (IV) injection. Drug abuse may cause infectious and noninfectious lung disorders (Table 31-1). Knowledge of the epidemiology and typical presentation may facilitate timely diagnosis and appropriate treatment.
Illicit drug users are susceptible to numerous infections that arise because the host’s immune defenses are suppressed or bypassed. The increased prevalence of HIV infection among drug abusers leads to infectious and noninfectious complications, including community-acquired bacterial pneumonia, pneumocystis pneumonia, tuberculosis, and Kaposi sarcoma (see Chapter 61). In addition to the immune suppression that occurs with HIV infection, the drug user’s immune system may be suppressed by the direct effects of the drug itself. Studies in cocaine and marijuana users demonstrate impaired function of alveolar macrophages. Alveolar macrophages exposed to marijuana smoke have reduced phagocytic, bactericidal, and fungicidal activity. Marijuana exposure results in decreased expression of proinflammatory cytokines, such as tumor necrosis factor (TNF)-α and interleukin (IL)-6. T-cell proliferation is shifted from T helper 1 (TH1) cells that are responsible for cell-mediated immunity to T helper 2 (TH2) cells that mediate allergy and atopy. This shift may cause an increased risk of infection and malignancy in marijuana users. Macrophages exposed to crack cocaine are less able to kill bacteria or tumor cells, possibly because of decreased production of reactive oxidant species. Marijuana and cocaine smoking also harm the lungs’ primary defenses by replacing ciliated epithelium with nonciliated mucus-secreting cells or metaplastic squamous epithelium. These findings help explain the enhanced susceptibility to infections observed in drug addicts.
Pulmonary Complications of Illicit Drug Use |
Infectious |
Aspiration pneumonia |
Septic emboli |
Bacterial pneumonia |
Acute bronchitis |
Tuberculosis |
Fungal pneumonia |
Noninfectious |
Vascular complications |
Noncardiogenic pulmonary edema |
Pulmonary hemorrhage |
Pulmonary hypertension |
Interstitial lung disease |
Granulomatous lung disease |
Talcosis |
Organizing pneumonia (BOOP) |
Airway complications |
Upper airway injury |
Bronchospasm/asthma |
Chronic bronchitis |
Bullous disease |
Bronchiectasis |
Pleural complications |
Pneumothorax/pneumomediastinum |
Pleural effusions/empyema |
Respiratory failure |
Cancer of upper and lower airway |
Aspiration into the lower respiratory tract commonly occurs after the use of many illicit drugs. Pneumonia complicates heroin overdose in up to half of cases. Sedative overdose depresses consciousness, diminishes protective airway reflexes, and increases the risk for aspiration of oropharyngeal or gastric contents. The initial inflammatory response can result in significant alveolar edema. Patients present with fever, tachypnea, and hypoxia. Radiographs may be normal or may show localized or bilateral diffuse infiltrates, depending on the volume of aspiration and the severity of the inflammatory response. Treatment is generally supportive. The use of antibiotics is controversial, but if used should be directed against the oropharyngeal flora.
Septic pulmonary emboli commonly occur in injection drug users and may occur in up to one quarter of hospitalized drug addicts with pulmonary complaints. Emboli originate from endocarditis, typically of the tricuspid valve, or from thrombophlebitis at the injection site. Presenting symptoms typically include pleuritic chest pain, hemoptysis, and fever. Physical examination in the case of thrombophlebitis reveals erythema, induration, and warmth at the injection site. A palpable cord may be present. In contrast, tricuspid valve endocarditis is often difficult to detect on examination. Tricuspid murmurs are usually soft, and the peripheral stigmata of endocarditis are not present with right-sided lesions. Typical radiographic manifestations include diffuse infiltrates or peripheral nodules, which may cavitate. Sequentially appearing nodules suggest endocarditis. Pleural effusions may occur; hilar and mediastinal lymphadenopathy is rarely seen. Blood cultures are usually positive. Staphylococcus aureus causes 80% of cases; Gram-negative bacteria and Candida are rarer causes. Complications include lung abscess, empyema, and bronchopleural fistula. Appropriate antimicrobial therapy should be continued for 4 to 6 weeks and is typically effective if compliance is achieved.
Community-acquired pneumonia occurs with increased frequency in drug abusers. There is a 10-fold increased risk of pneumococcal pneumonia in illicit drug users compared to nonusers. The presentation, course of illness, and response to treatment are similar in drug-using and nonusing populations. The usual community-acquired organisms are most common in drug users; however, aspiration is also associated with anaerobes (particularly in the setting of poor dentition), and intravenous drug use is associated with Gram-negative bacilli and S. aureus. Drug use increases the risk of methicillin-resistant S. aureus infection.
Acute bronchitis develops at an increased frequency in marijuana users. This increased incidence may result in part from the respiratory irritants in marijuana smoke. Although not well studied, other inhaled drugs may also predispose to acute bronchitis. The treatment of acute bronchitis in drug users is similar to that in nonusers.
Pulmonary tuberculosis occurs more frequently in drug users and appears to be related to lower socioeconomic status and the decreased immunity and higher rate of reactivation in this population. Clinically and radiographically, tuberculosis in drug users is indistinguishable from that of nonusers and should be treated with the standard multidrug antimycobacterial regimen. However, directly observed therapy is advisable in drug addicts to ensure compliance and avoid development of resistance.
Fungal pulmonary infections have been linked to illicit drug use. Invasive aspergillosis has been reported in immunocompromised patients who have smoked marijuana contaminated with the fungus. Cases have been described in patients with advanced HIV, chronic granulomatous disease, after bone marrow transplant, and in patients with lung cancer treated with chemotherapy. Aspergillus-laden marijuana has been implicated in allergic bronchopulmonary aspergillosis. Lobar candidal pneumonia and systemic candidiasis resulting in the acute respiratory distress syndrome (ARDS) have been reported in heroin users. A purported source of candidal infection in this population is the lemon used to acidify the heroin fix. Although severe fungal infections are rare, drug abusers have a high prevalence of serum precipitins against these fungi, suggesting widespread fungal contamination of illicit drugs. Treatment should focus on standard aggressive antifungal therapy.
Illicit substance abuse is also responsible for numerous noninfectious lung disorders that may occur within the pulmonary vasculature, interstitium, airways, or pleura.
Noncardiogenic pulmonary edema is perhaps the most frequent fatal complication of illicit drug abuse. A large number of drugs, including narcotics, cocaine, amphetamines, sedatives, tranquilizers, and hydrocarbons, can acutely produce pulmonary edema. Heroin is a particularly common offender. In one large series, 18% of those with heroin-induced pulmonary edema died. Pulmonary edema has been documented in both the first-time user and the experienced addict; it can occur immediately or up to 24 hours after use. Patients typically are stuporous or comatose, with fever, cyanosis, and crackles. Constricted pupils suggest opiate intoxication. Chest films classically demonstrate fluffy, bilateral alveolar infiltrates without cardiomegaly. The pathophysiology appears to differ depending on the drug involved, but increased permeability is suggested by studies that demonstrate equivalent protein concentrations in the alveolar fluid and serum. Treatment is generally supportive with supplemental oxygen and mechanical ventilation as needed. Naloxone should be considered in opiate-induced edema to reverse respiratory depression. Typically, the edema resolves within 24 to 72 hours, but it can take several weeks until the lung volumes, compliance, and diffusing capacity normalize. This suggests a component of acute lung injury has occurred in these cases.
Crack lung