A 48-Year-Old With Cirrhosis and Sudden Abdominal Distension

The patient in this case was discovered to have hemorrhagic ascites on the basis of the findings from his paracentesis. Hemorrhagic ascites is found in approximately 5% of patients with cirrhosis.^[10] The grossly hemorrhagic fluid collected by paracentesis is not necessarily attributed to iatrogenic puncture of a dilated peritoneal vessel or the inferior epigastric artery. In fact, traumatic paracentesis is a rare cause of hemorrhagic ascites, particularly when the ascitic fluid HCT exceeds 5%. In case of uncertainty, repeating the paracentesis can be helpful.^[11]

The differential diagnosis of hemorrhagic ascites deserves mention. In patients with cirrhosis, hemoperitoneum most often results from structural lesions rather than from thrombocytopenia or coagulopathy.^[12] Cirrhotic patients with splenomegaly are at greater risk for intraperitoneal hemorrhage from blunt abdominal trauma, which may be occult in patients who are unable to provide a reliable history, such as those with encephalopathy or in an alcoholic stupor. Hemoperitoneum can also occur spontaneously in the absence of trauma. Rupture of a hepatocellular carcinoma is one of the most common causes of spontaneous hemoperitoneum in cirrhotic patients, occurring at a rate as high as 14.3%,^[13] and it is usually life threatening. In female patients without portal hypertension, ovarian cancer is the most common cause of hemorrhagic ascites.

Less common causes of hemorrhagic ascites include hemorrhagic pancreatitis, as well as peritonitis secondary to tuberculosis infection. In one third of patients with hemorrhagic ascites, no specific cause can be identified.^[10] CT scanning may be useful in narrowing the list of potential causes of hemorrhagic ascites, as a ruptured ovarian or hepatic tumor would be evident. Specifically, in a patient with cirrhosis, the absence of a mass lesion or traumatic injury makes a rupture of an ectopic varix most likely, even though this diagnosis is relatively uncommon.^[11]

Patients with ruptured intraperitoneal varices typically present with marked abdominal distention, with an increase in abdominal girth occurring more rapidly than the typical accumulation of nonhemorrhagic ascitic fluid. Patients usually report abdominal pain and may give a history of syncope or light-headedness. Most patients will have historical evidence of portal hypertension; however, a history of bleeding from esophageal varices is often absent. Vital signs may be notable for tachycardia and/or hypotension, among other signs and symptoms of shock. A physical examination may demonstrate stigmata of chronic liver disease, including scleral icterus, jaundice, palmar erythema, spider angiomata, or gynecomastia. Patients with intra-abdominal or retroperitoneal hemorrhage may display characteristic ecchymoses (Grey Turner's or Cullen's signs) from infiltration of blood into subcutaneous tissue. Signs and symptoms of hepatic encephalopathy, such as asterixis, may be evident on physical examination, as may the characteristic shifting dullness found on percussion of the abdomen.

Management begins with prompt and aggressive resuscitation of hemorrhagic shock. Multiple sites of large-bore intravenous access should be established, as the patient may require multiple units of blood products. While waiting for typing, cross-matching, and the arrival of blood and blood products, resuscitative efforts should include aggressive administration of intravenous fluids. Vital sign response and urine output should be monitored closely. In addition to packed red blood cells, patients often require FFP, cryoprecipitate, calcium, and platelets. Referral to a tertiary care center is indicated if the patient is hemodynamically stable enough to survive transfer. The role of vasoactive drugs, such as octreotide to control bleeding of ectopic varices, is unknown.^[14]

Definitive management of extraluminal variceal hemorrhage is challenging. Laparotomy can be both diagnostic and therapeutic, but it carries substantial mortality, mostly related to the patient's underlying liver disease but also resulting from abdominal decompression itself, which can lead to rapid exsanguination.^[15] The fluid within the peritoneal cavity keeps the intraperitoneal pressures raised enough to keep more blood from spilling out into the peritoneal cavity. As soon as that pressure is taken away, the low intraperitoneal pressures cause massive blood leakage, which can be rapidly fatal. In patients who are unlikely to survive surgery (Child-Pugh classes B and C), angiography with TIPS placement and/or embolization are possible alternatives. In many cases, the culprit varix cannot be identified on angiography, and embolization alone is associated with high rates of rebleeding, reformation of collaterals, and portomesenteric thrombosis.

Some case series have demonstrated better success in the management of ectopic variceal bleeding with a combination of embolization and TIPS placement.^[16,17] However, patients with Child-Pugh class C cirrhosis are at substantial risk for encephalopathy, progressive liver failure, and hepatorenal syndrome after TIPS placement. These risks must be weighed against the benefit of hemostatic control, particularly if the patient is not a liver transplant candidate.

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