SummarySynthetic colloids have been implicated as a cause of coagulopathy when administered in large quantities. The effect of profound haemodilution (50%) on coagulation profile was measured in vitro by thromboelastography. Blood samples were taken from 11 ASA grade 1 patients prior to induction of anaesthesia for elective surgery. Each sample was simultaneously tested in four different preparations: undiluted blood (control sample); blood diluted with hydroxyethyl starch 6%; blood diluted with modified fluid gelatin 4%; blood diluted with dextran 40 10%. There was a significant decrease in reaction time in the preparations treated with hydroxyethyl starch 6% and modified fluid gelatin 4%, reflecting activation of initial fibrin formation. A significant increase in clot formation time was noted in the hydroxyethyl starch 6%-treated preparations. There was also a significant decrease in clot formation rate and maximum amplitude in the hydroxyethyl starch 6% group. Clot formation time, clot formation rate and maximum amplitude did not change in the modified fluid gelatin 4% group. Profound haemodilution with dextran 40 10% exerted extreme effects on the measured variables, very often resulting in a straight line on the thromboelastography profile. To avoid the risks associated with transfusion of homologous blood products and to limit the high cost of albumin solutions, artificial colloid solutions represent an alternative for intra-operative blood loss replacement [1]. However, synthetic colloids have been implicated as a cause of coagulopathy when administered in large quantities [1]. Although profound normovolaemic haemodilution (50% of circulating blood volume or haematocrit less than 20%) is not part of most blood-sparing strategies, clinical interest in maximising peri-operative blood conservation may involve normovolaemic haemodilution beyond currently accepted end points [2]. However, what effect this might have on coagulation is unclear as most studies examine only the effects of moderate quantities of artificial colloids [3,4].In this study, we measured the degree of impairment of the coagulation process when whole blood is diluted in vitro with large quantities (50% dilution) of hydroxyethyl starch 6%, modified fluid gelatin 4% and dextran 40 10%. Thromboelastography (TEG) records the dynamics of whole blood coagulation, including the interaction of cellular elements (red blood cells, platelets), coagulation factors and calcium [5,6] and was used to give overall evaluation of the clotting process. Methods

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Pulmonary hypertension is a recognized but unusual complication of liver disease. It can complicate the perioperative course of liver transplantation. Mild to moderate pulmonary hypertension is generally well tolerated during the procedure and does not appear to contribute to mortality. Since the pulmonary vascular disease may progress rapidly, it may have advanced to the point of irreversibility at the time of surgery. So, patients with known moderate pulmonary hypertension should have pulmonary arterial catheterisation immediately prior to transplantation. If pulmonary artery hypertension has become severe, then a preoperative trial of vasodilators is warranted. If this fails, the procedure should be cancelled. We present a patient with alcoholic liver cirrhosis in whom a rapidly progressive pulmonary hypertension made liver transplantation impossible.

The interaction of aprotinin with normal coagulation was studied in blood samples obtained from 10 healthy subjects. Each sample was simultaneously tested in four different preparations: NaCl-treated blood: 0.03 mL 0.9% NaCl in 0.33 mL blood; aprotinin treated blood: 0.33 mL blood+aprotinin in 0.03 mL in aliquots to obtain a final blood concentration of respectively 50 KIU mL-1; 100 KIU mL-1 and 200 KIU mL-1. The coagulation process was analysed by thromboelastography. R-time, reflecting intrinsic coagulation, increased in a dose dependent manner between NaCl-treated and aprotinin-treated blood. These findings suggest a dose dependent impairment of intrinsic coagulation by aprotinin.

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