![]() Hyperfibrinolytic activity in hospitalized cirrhotic patients in a referral liver unit. 2004 15:67-72.Ģ. u KQ, Yu AS, Tiyyagura L, Redeker AG, Reynolds TB. Coagulation and fibrinolysis in individuals with advanced liver disease. Prompt diagnosis of hyperfibrinolysis in cirrhotic patients and early administration of EACA may provide an effective management for life-threatening bleeding.ġ. anthiel DH, George M, Mindikoglu AL, Baluch MH, Dhillion S. Specific tests, as discussed above, assessing plasminogen activation and clot-lysis are required to correctly diagnose hyperfibrinolysis and differentiate it from other causes of bleeding, including disseminated intravascular coagulation. Hyperfibrinolysis in cirrhotic patients correlates with the Child-Pugh classification, but it is often difficult to identify. It works as a serine-protease inhibiting plasmin and kallikrein. 5 Aprotinin is another drug commonly used in hyperfibrinolysis after liver transplantation. EACA is effective and safe in treating patients with accelerated fibrinolysis who develop bleeding. EACA is a synthetic derivative of the amino acid lysine that binds reversibly to the lysine-binding site of plasminogen and blocks the binding of fibrin. Treatment of hyperfibrinolysis is supportive and includes transfusion of packed red blood cells and therapies that inhibit plasminogen activation and fibrin breakdown. ![]() 1,3 Hyperfibrinolysis in cirrhotic patients usually causes mucocutaneous bleeding, but it can also cause gastrointestinal bleeding. In patients with cirrhosis, the fibrinolytic pathway is activated by an increased endothelial release of tissue plasminogen activator (t-PA), decreased hepatic clearance of t-PA, decreased thrombin activatable fibrinolysis inhibitor, and decreased synthesis of alpha-2 antiplasmin and plasminogen activator inhibitor. The patient’s hemoglobin level remained stable at 9.2 mg/dL. This treatment resulted in resolution of bleeding. An oral loading dose of 150 mg/kg was followed by a dose of 1 g given during 4 hours in 2 separate doses, in addition to 2 more units of packed red blood cells. ![]() The patient was treated with epsilon-aminocaproic acid (EACA). A repeat test of hemoglobin showed that the level was 7 g/dL. 2 The patient received 4 units of packed red blood cells and 4 units of fresh frozen plasma in a 6-hour period. A computed tomography scan of the neck showed a large intramuscular, subcutaneous hematoma.Īn acute drop in hemoglobin caused by intramuscular bleeding due to hyperfibrinolysis was diagnosed, based on the decreased alpha-2 antiplasmin and euglobulin lysis time and normal measures of factor VIII and activated partial thromboplastin time. Euglobulin lysis time is a modified plasma clot lysis time and measures increased plasminogen activation. The euglobulin lysis time was 60 seconds (normal, >180 seconds). Alpha-2 antiplasmin was low at 20% (normal range, 80–120%). The serum fibrinogen level was low, at 104 mg/dL (normal range, 175–400 mg/dL), and antithrombin III was low at 24% (normal range, 80–120%). ![]() All liver-dependent coagulation factors were low (Table 1). Laboratory testing showed that hemoglobin was 6.5 g/dL, platelet count was 110,000/mm 3, prothrombin time was 16.3 seconds, international normalized ratio was 1.6, and partial thromboplastin time was 40 seconds. His Child-Pugh classification was category B, with a score of 8. There was a large, tender hematoma involving the neck and the back with extension into the flanks. The physical examination showed severe pallor, conjunctival icterus, and splenomegaly. He had not experienced any physical trauma and was not receiving antiplatelet agents or anticoagulants. We present a case of a cirrhotic patient with extensive spontaneous ecchymosis and an acute drop in hemoglobin level, which were due to primary hyperfibrinolysis.Ī 65-year-old man with alcoholic cirrhosis presented with extensive bruises on his back. 1 Hyperfibrinolysis in cirrhotic patients is the result of excess fibrin breakdown leading to defective hemostasis. Nair, MD, Department of Pulmonary and Critical Care, Winthrop University Hospital, 222 Station Plaza, Suite 400, Mineola, NY 11501 Phone: 51 Fax: 51 E-mail: coagulopathy in advanced hepatic disease is characterized by coagulation factor deficiencies as well as accelerated fibrinolysis. 1Department of Internal Medicine 2Division of Gastroenterology 3Division of Hematology-Oncology, William Beaumont Hospital, Royal Oak, MichiganĪddress correspondence to: Girish B.
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