Abstract Diffuse alveolar hemorrhage (DAH) is a relatively rare but life-threatening condition that requires a high clinical suspicion for diagnosis, followed by prompt investigation and treatment. DAH, frequently arising as a complication from a separate disease state, originates from the pulmonary microcirculation, involving the majority of the alveolar capillary surface. Patient is a 60-year-old male without prior lung disease who presented to the emergency department with chief complaint of shortness of breath for one week. He has a history of hypertension, depression and insomnia in addition to endorsing regular use of intra-nasal cocaine and tobacco use. Lab work revealed a hemoglobin of 5.2 g/dL without reports of hematemesis or melena. Initial CT chest without IV contrast demonstrated extensive ground-glass opacities with interstitial thickening and bronchiectasis. An arterial blood gas on 8L via non-rebreather mask showed pH 7.39, CO2 33, PO2 55. The patient was started on IV Vancomycin, Zosyn, Doxycycline and Bactrim as well as two units of red blood cells for his anemia. He was initially admitted to the step-down unit before necessitating increased oxygen support via high-flow nasal canula and transferred to the intensive care unit. On the second day of ICU admission, the patient had continued shortness of breath despite increasing oxygen support and the decision was made to proceed with diagnostic and therapeutic bronchoscopy. There were no abnormal secretions or endobronchial lesions visualized. Serial aliquots of 60cc of sterile normal saline were injected to the lateral segment of the right middle lobe which returned progressively bloodier samples, consistent with the diagnosis of DAH. The patient was started on methylprednisolone 1000mg daily for 3 days followed by an oral steroid taper at discharge. He was extubated to high-flow nasal canula two days after intubation. He was also started on oral sulfamethoxazole-trimethoprim 800-160mg tablets daily for PJP prophylaxis. Autoimmune laboratory work-up including ANA, p-ANCA, c-ANCA, anti-glomerular basement membrane antibody, cryoglobulins and complement levels were all normal. Bacterial culture, mycobacterial culture, PJP PCR and cytology from the right middle lobe BAL were all unremarkable. Given the negative autoimmune work-up, it was felt that the diffuse alveolar hemorrhage was secondary to cocaine abuse, a subset of DAH referred to as ‘Bland Alveolar Hemorrhage.’ This remains a rarer form of DAH which requires a high clinical suspicion followed by prompt diagnosis and treatment. This abstract is funded by: None
Carroll et al. (Fri,) studied this question.