The Acute Blood Loss Anemia Mystery

Abstract

Presentation and outcomes related to hepatocellular carcinoma (HCC) tumor rupture vary greatly. We present a unique case of spontaneous rupture of HCC. A 64 year-old male with history of HCV cirrhosis, ascites, portosystemic encephalopathy, esophageal varices, presented with worsening weakness, lethargy, and gait instability. On presentation, he was alert and oriented with dry mucous membranes, scleral icterus, a mildly distended non-tender abdomen, trace bilateral lower extremity edema, without asterixis. The patient was hemodynamically stable and labs showed hemoglobin (hb) 12.0 g/dL, platelet 47 k/uL, INR 1.6, and ammonia 148 umol/L. Treatment was initiated with fluids and lactulose for volume depletion and grade I hepatic encephalopathy (HE). An IR-guided diagnostic paracentesis was negative for SBP. Few days later, the patient developed hypotension with a drop in Hb to 6.5 g/dL without overt GI bleeding. After transfusion, an EGD showed portal hypertensive gastropathy, and three columns of non-bleeding grade II varices that were prophylactically banded. Five days later, patient again became hypotensive with worsening HE, hyperkalemia, elevated creatinine and severe anemia (hb 4.7 g/dL), still without overt evidence of GI bleeding. Urgent diagnostic ultrasound guided paracentesis was consistent with hemoperitoneum. Emergent CTA (Figures 2, 3) revealed a 3.1 x 3.7cm exophytic lesion in the right hepatic lobe, with high density within, suggesting spontaneous rupture of HCC with active extravasation and intra-peritoneal hemorrhage. IR obtained hemostasis with gelfoam embolization of the right hepatic branches. Transplant hepatology service deemed the patient not to be a candidate due to risk of HCC seeding from ruptured tumor. HCC related mortality is commonly due to tumor progression and liver failure. The overall risk of spontaneous HCC tumor rupture is relatively low (3-30%), but with very high mortality risk (20-70%). Risk factors for rupture include hypertension, cirrhosis, portal hypertension, portal vein thrombosis and tumor location, size, and degree of extra-hepatic protrusion. Improved survival rates can be seen after embolization and radical resection. The patient's history, presentation, and recurrent acute unexplained anemia with overt GI bleed put him at high risk of tumor rupture. This case highlights the progression of HCC leading to hemorrhagic shock from a ruptured exophytic lesion in the setting of decompensated cirrhosis.2291_B Figure 2. CTA, arterial phase, with arrow pointing to exophytic liver lesion now measuring 3.1 x 3.7 cm compared to prior CT. There is high density within it equaled to the density within the hepatic vessels suggesting spontaneous rupture of hepatocellular carcinoma with active extravasation.2291_C Figure 3. CTA, Portovenous phase, arrow points to liver lesion.2291_A Figure 1. CT imaging 2-months prior to presentation with cirrhotic and shrunken liver. Arrow points to stable 2.3 cm exophytic mass arising from the lateral right hepatic lobe. There are small hypodense foci throughout the liver, too small to access.