A 54-year-old male with decompensated alcoholic cirrhosis presented after a syncopal event and ground-level fall. Initial examination noted a distended abdomen without overlying bruising. At admission, his hemoglobin was 6.3 g/dL from a baseline of 8-10 g/dL. A computed tomography scan of the abdomen was notable for “complex ascites” adjacent to his liver concerning for blood. On hospital day 2, his hemoglobin dropped further to 5.3 g/dL. On hospital day 3, a large-volume paracentesis was performed, and 12.8 liters of bloody ascites were removed. Four hours later, the patient was hypotensive with mean arterial pressures in the 30s to 40s mmHg. Vasopressors were initiated, and the patient was transferred to the medical intensive care unit. The patient underwent massive transfusion protocol with a total of 68 units of blood products. On hospital day 4, emergent exploratory laparotomy removed 10 liters of blood from the abdominal cavity and revealed a bleeding short gastric vessel, which was ligated. His postoperative course was complicated by multiple organ failure. Given his continued clinical decline, his family pursued comfort care. He died soon after withdrawal of life-supporting measures on hospital day 18.
Discussion
Hemorrhagic ascites is defined as ascitic fluid with a red blood cell count of 10,000 cells/µL or greater.1, 2Hemorrhagic ascites is not a benign finding and is associated with increased morbidity and mortality.1, 2 In cirrhosis, hemorrhagic ascites can be due to chronic or acute hemorrhage from a ruptured hepatocellular carcinoma lesion, leakage from the splanchnic vascular bed, or ruptured lymphatics or varices.3
Portal hypertension creates collateral circulation and varices that serve as functional anastomoses between portal and systemic circulation and are most commonly found in the esophagus or periumbilical area (caput medusa) or rectally.3 However, they can also form in the intra-abdominal or retroperitoneal spaces at junctures of the splanchnic bed.1, 2, 3, 4, 5, 6 Rupture of these intra-abdominal varices is a rare but life-threatening cause of hemorrhagic ascites. Incidence is difficult to estimate due to the associated high mortality and the need for bleeding vessel localization for diagnosis. A retrospective study estimated an incidence of 19%.1
Mortality from acute intra-abdominal variceal rupture is as high as 75%,1 with most patients dying from hemorrhagic shock.1, 2, 3, 4, 5, 6, 7 Acute rupture can present with abdominal pain, increasing abdominal girth, and signs of hypovolemic shock.2, 3 Although immediate care is supportive, definitive treatment requires an exploratory laparotomy to visualize the bleeding source for ligation.2, 3, 4 Angiography is a potential modality but localizes the source of bleed only about a third of the time.4, 6
It is important to recognize intra-abdominal variceal rupture early to avoid delaying therapy, as it has a high mortality rate despite treatment. Patients who are hemodynamically stable with bloody ascites via serial paracenteses may be at higher risk of hemorrhage than the typical patient with cirrhosis despite the chronicity of the bleed. Caution should be exercised in these patients when performing paracentesis, particularly if large-volume paracentesis is needed or in those with a history of recent trauma.
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-Helen H. Lin, MD, Adam M. Garber, MD
This article originally appeared in the October issue of The American Journal of Medicine.
