Case Presentation:
We present a patient with massive cutaneous bleeding from a collateral site — Ihe caput medusa. A43‐year‐old man with history of alcoholic liver disease, Child‐Pugh class B, presented to the hospital with cutaneous bleeding. Examination revealed splenomegaly, nontender ascites and caput medusae. A 2‐cm umbilical hernia with brisk bleeding from The inferior margin was noted. The patient was resuscitated with intravenous fluids and blood. The bleeding site was sutured. Patient underwent a transjugular intrahepatic portosystemic shunt (TIPS) procedure. The dilated umbilical vein was the primary outflow for the portal vein with minimal anterograde flow to the liver. A transcatheter embolization of a recanalized umbilical vein was performed. Patient was discharged in a stable condition with a hemoglobin of 10.9 g/dL. 48 hours later he was discovered al home, unresponsive, in a pool of blood. Vital signs revealed BP of 101/50 mmHg. Physical examination revealed rebleeding from previous site. Repeat hemoglobin was 6.0 g/dL. Patient was resuscitated with fluids, 7 units of blood and fresh frozen plasma. CT scan revealed a large splenic varix leading tc the umbilicus. The splenic varix was embolized and hemorrhage controlled.
Discussion:
Increased portal pressure results in extensive collateral circulation. Caput medusae (Latin for “head of Medusa”) is the appearance of distended and engorged paraumbilical veins seen radiating across the abdomen. Cruveilhier‐Baumgarten syndrome results from recanalizalion of umbilical vein due to increased portal pressure. In 15%–29% of patients, collaterals Through The paraumbilical or recanalized umbilical veins connect into systemic veins. The majority of variceal hemorrhage is gastro‐esophageal in origin. Bleeding from a caput and umbilical veins are very rare. Only a few cases have been reported that resulted in massive external hemorrhage. The bleed usually is initiated by mechanical damage to the vessel wall. Once started, it can be brisk given the high pressure within the portal system. There are no established guidelines for treatment given the rarity of the condition. Gaining hemodynamic stability is the first step in management. Local measures to control bleeding such as direct pressure or suture ligation can be used to control the bleeding. Definitive therapy includes sclerosant injections, embolization of varices or feeding vein, portosystemic shunts surgery and TIPS procedures.
Conclusions:
Porto syslemic collaterals frequently develop in patients with cirrhosis. However, caput medusa bleeding is a rare primary manifestation of variceal hemorrhage. Supportive and definitive measures should be utilized to control bleeding. We report this case to increase general awareness of this condition.
Author Disclosure:
A. Cheema, none; K. Malhorta, none; M. Aiyer, none.