A 43-year-old female presented to the emergency department for a first episode of sudden onset shortness of breath and several episodes of hemoptysis. The patient did not have any chest pain, cough, fever, weight loss, hematemesis, hematochezia, or hematuria. The patient did not have any history of exposure to toxic substances, smoking, or alcohol.
Her past medical history was remarkable for hypertension diagnosed five years back. The patient was on medical treatment (Valsartan/Amlodipine 160mg/10mg tablet), but she had discontinued her medication for the last two months. In addition, she had a history of uncontrolled diabetes mellitus type 2.
On physical examination, the patient was tachypneic (respiratory rate 30 per minute) with low oxygen saturation SPO2 90% on room air that improved with oxygen supplementation by 3 L/min nasal cannula to 99%, hypertensive (blood pressure=224/143, tachycardiac (heart rate 105 per minute) and normal temperature. On auscultation, chest is clear, no wheezes or crackles, and normal s1 and s2 without any added sounds or murmurs.
Laboratory blood tests were all within the normal range. Notably, her hemoglobin dropped from 14.7 to 13.6 g/dL and her hematocrit dropped from 43.1% to 40.6%. White blood cells WBC= 8x103/microliter. Procalcitonin=0.05 ng/mL. Normal coagulation studies (INR=0.9, Aptt=26.4 seconds). Renal function tests were within the normal range (urea 5.8 mmol/L, creatinine 83 mumol/L), Na 138 mmol/L, K=4 mmol/L. Chest x-ray (Figure 1) showed prominent broncho-vascular markings with focal infiltrates in the right middle zone and cardiomegaly.
CT chest with contrast (Figure 2) (pulmonary angiography protocol) showed diffuse fluffy ground glass opacities bilaterally involving the right upper and middle lobes, which suggest alveolar hemorrhage or edema with no evidence of pulmonary embolism.
Echocardiography showed mildly reduced left ventricular systolic function with a calculated ejection fraction of 47%, grade 1 diastolic dysfunction, and normal left atrial pressure. There was mild concentric left ventricular hypertrophy. COVID-19 PCR, acid-fast bacilli smear, tuberculosis PCR and immunology workup were all negative.
During bronchoscopy, mucosa was looking normal without active bleeding; however, sequential lavage taken from the right upper lobe was hemorrhagic, worsening and not clearing. Bronchial wash and bronchial alveolar lavage consisted of reddish and turbid fluid. Microscopy was negative for malignancy and granuloma. Bronchoscopy showed 26% lymphocytes with positive hemosiderin-laden macrophages.
Within a few hours, blood pressure was controlled with three boluses of intravenous labetalol 20mg and Valsartan/Amlodipine 160mg/10mg tablet. Hemoptysis stopped. Shortness of breath improved, and oxygen requirements gradually decreased (blood oxygen saturation 98% on room air). No other drugs were needed. The patient was discharged home after 48 hours on Valsartan/Amlodipine 160mg/10mg tablet. Based on the clinical presentation, imaging, bronchoscopy findings and laboratory blood tests, the patient was diagnosed with DAH as a complication of severe hypertension.