Tranexamic acid (TA) is a synthetic drug that inhibits fibrinolysis. It has been administered to decrease the use of blood products during cardiac surgery and orthotopic liver transplantation when infused in larger doses. A small-dose infusion of aprotinin causes a reduction in fibrinolysis and blood product requirement during orthotopic liver transplantation without apparent risk of intravascular thrombosis. This prospective study was designed to investigate whether a small-dose infusion of TA would be equally effective in reducing fibrinolysis and blood product transfusions during orthotopic liver transplantation. A double-blind, controlled study was undertaken to compare the efficacy of a small-dose TA infusion with that of a placebo. Thirty-two consecutive patients were randomized either to the TA group (n = 16), which received an intravenous infusion of 2 mg x kg(-1) x h(-1), or to the control group (n = 16), which received an identical volume of normal saline. Coagulation values were measured, a field rating was made by the surgeon, and a thromboelastogram was produced at four predetermined intervals throughout the case-before TA infusion was started, after portal vein ligation, 10 min after reperfusion, and at the end of surgery. Intraoperative transfusion requirements were recorded during the procedure and for the first 24 h postoperatively. A record was kept of any intraoperative epsilon-aminocaproic acid administered for uncontrolled fibrinolysis. The thromboelastogram clot lysis index was significant for lysis in the control group during both the anhepatic and the neohepatic phases (P < 0.01 and P < 0.05, respectively) when compared with the TA group. Fibrin degradation products were significantly increased (>20 microg/mL) in the control group at reperfusion (P < 0.03) and at the end of surgery (P < 0.01). D-dimers were also significantly increased (>1 mg/L) in the control group at the end of surgery (P < 0.04). Nine of the 16 control patients versus 3 of the 16 TA patients required epsilon-aminocaproic acid rescue for fibrinolysis. There were no other significant differences between groups. Transfusion requirements during surgery and for the first 24 h postoperatively did not differ significantly between the two groups. We conclude that the use of small-dose TA reduces fibrinolysis but not transfusion requirements during orthotopic liver transplantation.

A patient with end-stage liver disease as a result of ␣ 1 -antitripsin deficiency presented for orthotopic liver transplantation. The liver cirrhosis was complicated by portal hypertension and hepatopulmonary syndrome resulting in varicosities and severe hypoxia (room air oxygen saturation 69%). After transplantation, the hepatopulmonary syndrome improved but, over the next 14 months, the patient developed severe pulmonary hypertension. Six years posttransplantation, his room air oxygen saturation was 95% with pulmonary artery pressures of 109 mm Hg systolic and 26 mm Hg diastolic (mean 55 mm Hg) and a pulmonary vascular resistance 688 dynes·sec·cm. 5 Copyright 1998 by the American Association for the Study of Liver Diseases H epatopulmonary syndrome (HPS) and portopulmonary hypertension are the result of two very different pathophysiological states. Both are associated with liver cirrhosis and portal hypertension, but HPS develops as the result of vascular dilatations in the lung, whereas portopulmonary hypertension is the result of pulmonary arterial wall thickening resulting in an increased resistance to flow. 1,2 If severe, they are both associated with high mortality rates, and whether they reverse after orthotopic liver transplantation (OLT) is still subject to conflicting reports. [3][4][5][6][7] To add to this dilemma, we report on a patient who presented for OLT with severe hypoxia as a result of HPS, which ameliorated posttransplantation, but the patient went on to develop severe pulmonary hypertension despite long-term therapy with calcium channel blockers. Case ReportA 33-year-old man (weighing 80 kg) with end-stage liver disease secondary to ␣ 1 -antitrypsin deficiency was referred for OLT. At 7 years of age, he was found to have splenomegaly and was diagnosed with portal hypertension and cirrhosis of the liver. At 17 years of age, he underwent a partial splenectomy because of a traumatic injury and was also noted to have portal hypertension with varicosities, and a liver biopsy showed cirrhosis.On examination before transplantation, he was found to be severely short of breath and cyanotic with digital clubbing and multiple telangectasia. The chest radiograph was normal. Orthodeoxia was shown by an arterial oxygen pressure (PAO 2 ) breathing room air while supine of 69 mm Hg and 36 mm Hg when upright. The PAO 2 increased to 266 mm Hg in response to breathing 100% oxygen. Spirometry was normal except for a mild decrease in diffusion capacity for carbon monoxide (DLCO) ( Table 1). A right heart catheterization showed normal pulmonary artery pressures (PAPs) and a cardiac output of 12 L/min. (Table 2). A technetium-99 macroaggregate albumin perfusion lung scan confirmed intrapulmonary shunting with a shunt fraction calculated at 45%. A diagnosis of HPS was made. OLT was performed without complication. Two weeks postoperatively, breathing 50% oxygen, the supine oxygen saturation was 95%.Fourteen months posttransplantation, the oxygen saturation breathing room air had improved to 90%; however, an echocar...

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