A 26-year-old previously healthy woman comes to the emergency department in the early morning with rapid-onset shortness of breath. She attended a rave last night and reports "smoking a bunch of things." Temperature is 37.2 C (99 F), blood pressure is 162/94 mm Hg, pulse is 113/min, and respirations are 32/min. Oxygen saturation is 89% on 4 L/min of oxygen by nasal cannula. The patient appears disheveled and restless but is able to follow commands. The pupils are dilated and equally reactive. Cardiovascular examination demonstrates tachycardia but no other abnormalities. Inspiratory crackles are present on pulmonary auscultation. Superficial burns are present on her fingertips. ECG and B-type natriuretic peptide and troponin-I levels are normal. Chest x-ray shows a normal cardiomediastinal silhouette and diffuse bilateral airspace opacities. What is the most likely process underlying this patient's current respiratory condition?
Diffuse alveolar hemorrhage | |
Etiology & pathogenesis |
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Clinical presentation & diagnosis |
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Management |
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ANCA = antineutrophil cytoplasmic antibody; ARDS = acute respiratory distress syndrome; CXR = chest x-ray; SLE = systemic lupus erythematosus. | |
Rapid onset of hypoxemia with diffuse, bilateral alveolar opacities typically reflects fluid, cells, or blood. This patient's history of recreational drug use, paired with a sympathomimetic toxidrome and fingertip burns, raises concern for acute inhalational cocaine-induced lung toxicity ("crack lung"), causing diffuse alveolar hemorrhage (DAH; blood).
Cocaine can be insufflated (snorted) or inhaled. Central stimulation of sympathetic outflow causes hypertension, tachycardia, and mydriasis. Burns occur due to handling of hot pipes (while nociception is blunted) and are a specific indicator of inhalant abuse. When inhaled, cocaine undermines the blood-alveolar barrier via thermal damage (scorching hot smoke), ischemia-reperfusion injury (intense pulmonary vasospasm), and direct cellular toxicity. This can result in DAH, a form of widespread alveolar capillary bleeding.
Respiratory symptoms begin within 48 hours of smoking cocaine. A clinical diagnosis is made based on diffuse pulmonary opacities and suspected recent inhaled cocaine exposure or positive urine drug screen. Because the bleeding occurs deep in the lungs, hemoptysis may be absent in half of the patients. Although not usually needed, bronchoscopy with serial lavage shows sequentially bloody vials, differentiating DAH (blood from alveoli) from nonalveolar sources (eg, aspirated blood).
(Choice A) Bronchospasm (eg, irritant-induced asthma) can cause acute respiratory distress and hypoxemia. However, it would be accompanied by wheezing on examination and hyperinflation (rather than diffuse opacities) on chest x-ray.
(Choice B) Cardiogenic pulmonary edema (eg, cocaine-induced left ventricular ischemia) can also cause bilateral infiltrates (fluid). However, this patient has normal cardiac and mediastinal contours and no evidence of myocardial injury (normal ECG and negative troponin-I) or stretch (no volume overload, normal B-type natriuretic peptide).
(Choice D) Pulmonary fibrosis (eg, idiopathic or drug-induced [nitrofurantoin, methotrexate]) can cause dyspnea and inspiratory crackles on examination. Idiopathic pulmonary fibrosis reflects gradual parenchymal lung scarring, so patients are usually diagnosed at an advanced age and typically have insidiously progressive (rather than acute onset) dyspnea. Because the disease involves increased matrix deposition, chest imaging shows interstitial thickening rather than airspace opacification.
(Choice E) Venous thromboembolism (eg, cocaine-induced hypercoagulability) presents with clear lungs, clear airfields on chest x-ray, and evidence of right ventricular strain (eg, right bundle-branch block, elevated myocardial biomarkers such as troponin-I and B-type natriuretic peptide). Anticoagulation is generally contraindicated during active DAH.
Educational objective:
Cocaine can induce acute lung toxicity in the form of diffuse alveolar hemorrhage (DAH). DAH presents with rapid onset of dyspnea; diffuse, bilateral airspace opacities; and hypoxemia soon after inhaled cocaine exposure.