What Is Crack Lung? Symptoms, Causes, and Treatment

“Crack lung” describes an acute pulmonary syndrome caused by inhaling vaporized crack cocaine. This condition is a sudden and severe lung injury that typically manifests within minutes to 48 hours following drug use. Formally known as Acute Cocaine-Induced Pulmonary Injury, it reflects direct damage to the respiratory system. Crack lung represents a potentially life-threatening medical emergency that can lead to complications, including respiratory failure, necessitating immediate medical intervention.

Clinical Definition and Mechanisms of Injury

Crack lung is medically characterized as an acute syndrome of diffuse alveolar damage and hemorrhagic alveolitis. This involves widespread injury to the tiny air sacs in the lungs and surrounding tissue, beginning the moment the vaporized cocaine is inhaled.

A significant mechanism is thermal injury caused by the heat of the inhaled vapor, as crack cocaine vaporizes at approximately 187°C. This high temperature directly damages the delicate lining of the airways and alveoli. The chemical nature of the cocaine compound and its cutting agents are also directly toxic to lung cells, triggering a profound inflammatory response.

The inflammation leads to diffuse alveolar damage (DAD) and hemorrhagic alveolitis (bleeding into the air spaces). This damage increases the permeability of the alveolar-capillary membrane, causing fluid to leak into the lungs and resulting in pulmonary edema. An immunological reaction, known as pulmonary eosinophilia, may also occur, marked by an abnormal accumulation of eosinophils in the lung tissue.

Recognizing the Acute Symptoms

The clinical presentation of crack lung is acute, occurring shortly after crack cocaine inhalation. Patients experience the sudden onset of dyspnea, or shortness of breath, which can progress rapidly. This respiratory distress is frequently accompanied by acute, pleuritic chest pain, often described as a burning sensation.

A characteristic symptom is a persistent cough that may produce unusual sputum. This can include hemoptysis (coughing up blood) or black, carbonaceous sputum, a residue from drug combustion. Patients may also present with a fever and low oxygen saturation (hypoxia), reflecting impaired gas exchange in the damaged lungs.

The forceful inhalation maneuvers employed to maximize the drug’s effect can lead to barotrauma. This trauma causes air to leak from the damaged lung tissue into the surrounding chest cavity or mediastinum, resulting in conditions like pneumomediastinum or pneumothorax. The presence of these specific symptoms, especially with recent crack cocaine use, immediately raises suspicion for the syndrome.

Medical Management and Recovery

Diagnosis relies on establishing a temporal relationship between symptom onset and crack cocaine inhalation, ideally within a 48-hour window. Medical evaluation begins by excluding infectious causes, such as pneumonia, which presents with similar symptoms like fever and cough. Diagnostic imaging is a significant component, with chest X-rays often revealing diffuse pulmonary infiltrates, which appear as cloudiness in both lungs.

A computed tomography (CT) scan may provide more detail, frequently showing widespread patchy infiltrates or ground-glass opacities throughout the lung fields. The primary approach to treatment is supportive care, focusing on maintaining adequate oxygenation. Supplemental oxygen is administered to correct hypoxia, and severe respiratory failure may require non-invasive or invasive mechanical ventilation. Bronchodilators may also be used to manage any associated bronchospasm.

Corticosteroids are commonly used to manage the intense inflammatory component of the syndrome. This treatment is particularly considered when a lung biopsy or bronchoalveolar lavage suggests eosinophilic pneumonia, an immune-mediated reaction often seen in crack lung. Provided the patient survives the acute phase and abstains from further use, the prognosis is generally favorable. Symptoms and hypoxemia typically resolve rapidly, often within days to a few weeks, and radiographic findings commonly show marked improvement within 48 hours of treatment initiation.