Abstract 4361909: A Blood(y) Pressure Crisis: Diffuse Alveolar Hemorrhage as a Rare Manifestation of Severely Uncontrolled Hypertension

Introduction: Diffuse alveolar hemorrhage (DAH) is characterized by hemoptysis, anemia, and diffuse pulmonary infiltrates due to alveolar bleeding. Common causes include vasculitides, coagulopathy, infections, and valvular heart disease. DAH secondary to severe hypertension is extremely rare. We present a case of DAH in a patient with poorly controlled hypertension. Case Description: A 58-year-old man with diabetes and poorly controlled hypertension presented with three days of hemoptysis. He denied other episodes of overt bleeding, chest pain, arthralgias, weight loss, or fever. He had a prior history of treated latent tuberculosis. He traveled to Las Vegas and noted a blow of moldy dust which he recalled as the only significant recent exposure. On arrival, BP was elevated at 206/131 mm Hg, but he was otherwise hemodynamically stable. Troponin was mildly elevated but later normalized. CBC and BMP were unremarkable. Inflammatory markers were minimally elevated (CRP: 3 mg/L, ESR: 10 mm/hr). CT chest showed diffuse bilateral ground-glass opacities. Bronchoscopy with BAL revealed friable mucosa and progressively bloody aliquots, confirming DAH. There was no evidence of malignancy or infection from BAL analysis. Extensive workup for DAH, including ANA, ANCA, cryoglobulins, anti-GBM, QuantiFERON, AFB smears and cultures, Leptospira, Legionella, Strongyloides, fungal, and bacterial cultures, was negative. TTE demonstrated normal EF and moderate LV hypertrophy; there was no valvular abnormality. With no alternate etiology, severely uncontrolled hypertension was deemed the most likely cause of DAH, supported by a few published case reports. The patient was started on nifedipine 60 mg and losartan 50 mg daily. With improved blood pressure for the remainder of his hospital stay, hemoptysis gradually resolved. At the post-hospital visit, he remained asymptomatic with good blood pressure control and complete resolution of lung opacities on imaging. Conclusion: Severe hypertension can cause end-organ damage, affecting the heart, brain, and kidneys; however, DAH is a poorly recognized complication. Proposed mechanisms include alveolar capillary stress failure, microvascular endothelial injury, and pulmonary venous hypertension. While DAH is a rare presentation of severe hypertension with very few cases reported in the literature, our case highlights this unique complication and the importance of strict blood pressure control in its management.