B52-17 When the Heart Is Not to Blame: Myeloma Masquerading as Heart Failure-Related Ascites

Introduction Multiple myeloma is a malignant plasma cell disorder typically characterized by hypercalcemia, renal failure, anemia, and lytic bone lesions. However, it can present with atypical manifestations, making diagnosis challenging. We report a rare case of multiple myeloma presenting predominantly with recurrent, refractory ascites, in the absence of skeletal involvement or hypercalcemia. Case Discussion A 50-year-old male with a complex medical history including hypertension, heart failure with preserved ejection fraction (HFpEF), coronary artery disease, chronic kidney disease, type 2 diabetes mellitus, and chronic anemia presented to our institution following a mechanical fall. He reported progressive fatigue, lower extremity neuropathy, and worsening abdominal distention for 2 months. Interestingly, the patient had been undergoing regular therapeutic paracentesis for ascites over the past two years, which had been attributed to HFpEF. Cardiac workup revealed mild diastolic dysfunction with a preserved ejection fraction, and a non-obstructive coronary artery disease. He reported that the recurrence of the ascites became more often, now requiring weekly paracentesis. However, no diagnostic analysis had been performed on the ascitic fluid. On examination, the patient exhibited signs of fluid overload including periorbital, scrotal, and bilateral lower extremity edema, with a markedly distended abdomen demonstrating shifting dullness. Imaging confirmed large-volume ascites and a moderate left-sided pleural effusion. Skeletal survey showed no osteolytic lesions. Laboratory investigations were significant for normocytic, normochromic anemia, worsening renal function, and a monoclonal spike on serum protein electrophoresis (M spike 18 mg/dL). Immunofixation revealed IgG kappa monoclonal protein, with a markedly elevated kappa/lambda ratio (14.45). A bone marrow biopsy demonstrated 20% clonal plasma cells, and FISH analysis was positive for trisomy 11, consistent with multiple myeloma. Unfortunately, before treatment could begin, the patient developed renal and respiratory failure and expired from a fatal arrhythmia. Discussion This case underscores the importance of considering plasma cell dyscrasias in patients presenting with unexplained, recurrent ascites, particularly when conventional etiologies such as liver cirrhosis or heart failure are insufficient to explain the clinical picture. The absence of classical bone lesions and the presence of renal impairment, neuropathy, and anemia should prompt further hematologic evaluation. Conclusion Early recognition and diagnosis of atypical presentations are crucial for timely initiation of therapy and improved patient outcomes. Our case highlights the necessity of a broad differential and the value of diagnostic paracentesis in evaluating refractory ascites. This abstract is funded by: None