B64-03 A Race Against the Right Ventricle: Rapid Right Ventricular Failure From Pulmonary Leukostasis

Abstract Introduction Pulmonary leukostasis is an uncommon and catastrophic complication of acute myeloid leukemia (AML), typically occurring in the setting of hyperleukocytosis. Accumulation of blasts within the pulmonary microvasculature can cause severe impairment in gas exchange, pulmonary hypertension, and acute right ventricular (RV) failure. Early recognition and management is crucial, as respiratory compromise and hemodynamic collapse can occur rapidly despite supportive care. Case Description We present the case of a 69-year-old man admitted for management of newly diagnosed acute myeloid leukemia (AML). On hospital day two, he developed sudden dyspnea, chest discomfort and hypoxemia (SpO2 80% on room air, improving to 92% with 4 L oxygen via nasal cannula). Laboratory studies showed an elevated lactate of 4 mmol/L, troponin 800 ng/L (previously normal) and a rapidly rising white blood cell count of 112 × 109/L, up from 40 × 109/L within the last 20 hours. Electrocardiogram showed sinus tachycardia, and CT pulmonary angiography was negative for pulmonary embolism. Bedside point-of-care ultrasound (POCUS) demonstrated a new markedly dilated right ventricle compared to a previously normal transthoracic echocardiogram obtained two days earlier, with preserved left ventricular systolic function. Patient was transferred to the intensive care unit and managed with hydroxyurea 2000 mg, intravenous fluids, and allopurinol, with plans for emergent leukopheresis. Despite aggressive management, his respiratory distress worsened culminating in cardiopulmonary arrest with patient expiring despite multiple resuscitation attempts. Discussion and learning points Pulmonary leukostasis is estimated to affect approximately 3-5% of AML patients presenting with acute onset shortness of breath and hypoxia. Acute right heart failure is a rare manifestation described only in isolated case reports with disease progression reported over several days to weeks. The sudden leukocytic proliferation leads to microvascular obstruction within the pulmonary circulation, causing a rapid rise in pulmonary vascular resistance and the development of pulmonary hypertension. Faced with this abrupt increase in afterload, the right ventricle must generate higher pressures to maintain forward flow, resulting in acute right ventricular dilation, ischemia, and eventual failure. Our case adds to the limited body of literature describing pulmonary leukostasis as a possible direct cause of acute right heart failure highlighting the exceptionally rapid, in this case ufolding within hours, and fulminant progression of this process. Early imaging findings may be nonspecific, also emphasizing the utility of POCUS in urgent recognition of evolving right heart strain. This abstract is funded by: None