PubMed · 14812425
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UNEXPLAINED bleeding.. https://pubmed.ncbi.nlm.nih.gov/14812425/
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Caput medusa is a frequent incidental finding in patients with portal hypertension that usually represents paraumbilical vein portosystemic collateral vessels draining into body wall systemic veins. A symptomatic caput medusa was seen in a morbidly obese patient after an umbilical hernia repair, which was fed not by the left portal vein but by the left gastroepiploic vein, in a recurrent adhesed umbilical hernia that likely contained herniated omentum. Refractory hemorrhage from this caput medusa was successfully treated by transjugular intrahepatic portosystemic shunt creation and balloon-occluded variceal sclerosis.
Von Willebrand factor (VWF) behaves as an extracellular adapter molecule, linking platelets to the extracellular matrix at sites of vascular injury. These interactions are crucial for hemostasis. Too little platelet adhesion causes bleeding that is typical of von Willebrand disease, whereas too much platelet adhesion may cause thrombotic thrombocytopenic purpura. Mutations in VWF or platelet glycoprotein Ib can either reduce or increase the affinity of platelet binding. Paradoxically, affinity changes in either direction cause bleeding. Crystallographic studies now suggest molecular explanations for all of these phenotypes. Clinical investigations of von Willebrand disease type 1 are defining the relationship between plasma VWF level and the risk of bleeding or thrombosis. Emerging data suggest that VWF level is a useful biomarker for the risk of either bleeding or thrombosis and could be incorporated into a comprehensive approach to treat or prevent these adverse events.