Abstract Diffuse alveolar hemorrhage (DAH) is a life-threatening condition characterized by bleeding into the alveolar spaces due to injury of the pulmonary microvasculature. It can be classified as non-bland or bland based on the presence or absence of inflammation. Non-bland DAH arises from immune-mediated or inflammatory processes such as vasculitis, autoimmune disease, or connective tissue disorders, whereas bland DAH occurs without significant inflammation and is typically associated with cardiac disease, coagulopathy, or drug-induced injury. Clinically, DAH presents with acute or rapidly progressive respiratory compromise, often within seven days of symptom onset. Diagnosis requires correlation of clinical, radiologic, and pathologic findings, with sequential bronchoalveolar lavage (BAL) showing progressively bloodier aliquots serving as the diagnostic hallmark. Treatment is directed by the underlying etiology, with high-dose corticosteroids and immunosuppressive therapy reserved for inflammatory causes and supportive management for non-inflammatory etiologies. Case A 41-year-old male with type II diabetes, obstructive sleep apnea, and morbid obesity presented with one month of worsening dyspnea and dry cough. He had been evaluated several times in urgent care and emergency settings, receiving levofloxacin and two short courses of corticosteroids. Each course led to transient improvement, but symptoms recurred immediately after discontinuation. Two prior CT scans had shown mosaic attenuation. On admission, he required 3 L/min oxygen by nasal cannula. His only notable exposure was inhaling flame-retardant powder from a fire extinguisher two weeks before symptom onset. High-resolution CT of the chest demonstrated cystic changes with mosaic attenuation and expiratory air trapping, consistent with small-airway involvement. Given the recurrent, steroid-responsive course and inhalational exposure, bronchoscopy with BAL was performed. Sequential aliquots revealed progressively bloodier lavage fluid, confirming the diagnosis of DAH. The patient was started on pulse-dose methylprednisolone followed by a structured three-month taper, resulting in rapid symptomatic and radiographic improvement. He was discharged on room air. Significant Decision-Making This case required careful differentiation between inflammatory and non-inflammatory DAH. The patient’s steroid responsiveness and imaging suggested an inflammatory process, yet his exposure history pointed toward toxin-induced lung injury rather than autoimmune vasculitis. Confirmatory BAL findings supported this conclusion and justified corticosteroid therapy without broader immunosuppression. The prompt recognition of inhalational DAH and targeted steroid treatment led to complete recovery. This case underscores the diagnostic challenge in distinguishing bland from non-bland DAH and highlights the importance of detailed exposure history and early bronchoscopy in guiding management when the diagnosis is uncertain. This abstract is funded by: None
Nimmagadda et al. (Fri,) studied this question.