Abstract: PUB050
Spontaneous Tumor Hemorrhage: A Case of AKI
Session Information
Category: Acute Kidney Injury
- 102 AKI: Clinical, Outcomes, and Trials
Authors
- Kaur, Ramandeep, Dartmouth Health, Lebanon, New Hampshire, United States
- Truglio, Thomas S., Dartmouth Hitchcock Medical Center, Lebanon, New Hampshire, United States
- Remillard, Brian D., Dartmouth Hitchcock Medical Center, Lebanon, New Hampshire, United States
- Block, Clay A., Dartmouth Hitchcock Medical Center, Lebanon, New Hampshire, United States
Introduction
We present a case of spontaneous hemorrhage in a yolk sac tumor resulting in hemorrhagic ascites causing intra-abdominal hypertension, hydronephrosis and acute kidney injury (AKI).
Case Description
A 22-year-old man with previous medical history of asthma presented with abdominal distention and loss of appetite for 3 weeks. The serum creatinine (SCr) at presentation was 0.8 mg/dL (reference range 0.8-1.5 mg/dL) and hemoglobin (Hgb) 7.8 g/dL (reference range - 13.7 -16.5 g/dL). Computed tomographic (CT) imaging demonstrated multiple lesions in the liver, omental and paralumbar masses, a retroperitoneal (RP) hematoma and ascites. Alpha fetoprotein was 18,158 ng/mL (reference range - < 8.3 ng/mL). Biopsy of a liver lesion identified non-seminomatous yolk sac tumor. Chemotherapy with bleomycin, etoposide and cisplatin was initiated, but abdominal distention progressed. By day 5, Hgb had fallen to 5.7 g/dL. SCr rose to 2.4 mg/dL. The worsening ascites was refractory to diuretics. Tumor lysis syndrome was excluded on the basis of normal uric acid and potassium. Ultrasound-guided paracentesis demonstrated intraabdominal hypertension (IAH) with direct pressure measurement of 20 mmHg; mild right-sided hydronephrosis was also observed. The hematocrit of the ascitic fluid was 26.8% suggesting hemorrhagic ascites. CT angiography and the tagged red blood cell scintigraphy failed to identify an actively bleeding vessel. Tumor neovascularity in the large omental and paralumbar mass fed by the right and left gastroepiploic arteries and lumbar arteries without an active extravasation was noted. IAH was resolved with recurrent large volume paracentesis leading to normalization of kidney function. Multiple red blood cell transfusions stabilized the hemoglobin.
Discussion
Spontaneous hemorrhage in yolk sac tumor as a cause of hemorrhagic ascites resulting in IAH and AKI is not well studied, but incidence of 15% in hepatocellular carcinoma has been reported. The etiology likely involves rapid tumor growth and spontaneous and/or chemotherapy related necrosis. Our patient had bleeding prior to the presentation since he came with RP hematoma; suggesting spontaneous necrosis had occurred. IAH results in high renal vein and parenchymal pressure, thereby reducing renal perfusion pressure. Ascites, particularly with IAH, can cause hydronephrosis and AKI.