What does this research mean for the field?

Cocaine-induced diffuse alveolar hemorrhage can mimic autoimmune vasculitis and cause critical respiratory failure, requiring early bronchoscopy and supportive care for successful management. Novelty: ClaimNovelty.INCREMENTAL. Consensus alignment: ConsensusAlignment.NEUTRAL.

What question did this study set out to answer?

This case aims to demonstrate the diagnostic challenges of diffuse alveolar hemorrhage in the context of polysubstance abuse.

May 20, 2026

A52-03 Toxic Alveolar Hemorrhage Mimicking Autoimmune Vasculitis: A Case of Critical Respiratory Failure in a Cocaine User

Key Points

This case aims to demonstrate the diagnostic challenges of diffuse alveolar hemorrhage in the context of polysubstance abuse.
Presented case of a 52-year-old female with history of COPD and autoimmune features.
Performed bronchoscopy with bronchoalveolar lavage to confirm diffuse alveolar hemorrhage.
Managed with supportive ventilation and immunosuppressive therapy was deferred.
Patient developed severe hypoxia and pulseless electrical activity, requiring CPR and intubation.
Bronchoscopy confirmed DAH with progressively bloody return; infectious workup was negative.
Successfully extubated on day 3 and discharged to rehabilitation on supplemental oxygen.

Abstract

Abstract Introduction Diffuse alveolar hemorrhage (DAH) is a life-threatening pulmonary emergency characterized by intra-alveolar bleeding and hypoxemic respiratory failure. Etiologies range from autoimmune vasculitis to coagulopathy and inhalational toxins such as cocaine. We present a case of DAH with hypoxic cardiac arrest in a patient with polysubstance use and overlapping autoimmune features. Case Description A 52-year-old female with a history of COPD/asthma, cutaneous lupus erythematosus, von Willebrand disease, and prior Humira use for Crohn’s disease presented with substernal chest pain, hemoptysis, and progressive dyspnea. In the emergency department, she developed severe hypoxia refractory to non-rebreather oxygen, culminating in a pulseless electrical activity (PEA) arrest. She was resuscitated after one round of CPR and received DDAVP due to concern for underlying coagulopathy. She was emergently intubated and admitted to the ICU. Imaging revealed diffuse bilateral interstitial infiltrates, and post-intubation ABG demonstrated acute hypoxic hypercapnic respiratory failure. Empiric treatment included methylprednisolone, diuretics, and broad-spectrum antibiotics. Bronchoscopy with bronchoalveolar lavage confirmed DAH, with serial aliquots showing progressively bloody return. Infectious workup was negative. Autoimmune serologies revealed a positive ANA (1:160) and smooth muscle antibody, but other markers, including ANCA and anti-GBM, were unremarkable. A urine drug screen was positive for cocaine, fentanyl, THC, and benzodiazepines. Rheumatology deferred further immunosuppression given clinical improvement and suspicion for a toxic etiology. She was managed with lung-protective ventilation and prone positioning for ARDS and was successfully extubated on day 3 of hospitalization. She remained hemodynamically stable and was discharged to inpatient rehabilitation on supplemental oxygen. Discussion This case illustrates severe DAH with cardiopulmonary arrest in the context of polysubstance use and overlapping autoimmune markers. This case highlights the diagnostic complexity of cocaine-induced DAH and the importance of early bronchoscopy, multidisciplinary care, and supportive management, while reinforcing that toxic-induced alveolar hemorrhage must remain high on the differential to guide prompt and effective intervention. This abstract is funded by: None

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