Exposure to cardiopulmonary bypass (CPB) is associated with postoperative coagulopathy and hemorrhage. Recent literature indicates that heparin rebound occurs almost universally following cardiac surgery. We conducted this pilot study to evaluate if the presence of residual circulating heparin following cardiac surgery can be diagnosed by elevation of activated partial thromboplastin time (APTT).

Purpose Exposure to cardiopulmonary bypass (CPB) is associated with postoperative coagulopathy and hemorrhage. Recent literature indicates that heparin rebound occurs almost universally following cardiac surgery. We conducted this pilot study to evaluate if the presence of residual circulating heparin following cardiac surgery can be diagnosed by elevation of activated partial thromboplastin time (APTT).

Twenty five of 106 preterm infants of 34 weeks' gestation or less developed intraventricular haemorrhage within the first 48 hours of life. A comparison of infants with and without intraventricular haemorrhage showed no significant differences in their haemostatic parameters at birth. At age 48 hours the group with intraventricular haemorrhage showed a prolonged activated partial thromboplastin time and reduced factor II, VII, and X activity. There was a significant correlation between the severity of intraventricular haemorrhage and the degree of haemostasis abnormality both in cord blood and in blood obtained at age 48 hours. Those infants sustaining grade IV intraventricular haemorrhage had a significantly prolonged activated partial thromboplastin time, reduced factor II, VII, and X activity; and a decreased fibrinogen concentration at birth. At age 48 hours these defects were accompanied by reduced platelet counts and an increased megathrombocyte index. Although intraventricular haemorrhage is multifactorial, we postulate that correction of haemostasis abnormalities at birth may prevent progression to more severe grades of haemorrhage.

Coagulation studies were performed in a well-defined inborn population of preterm neonates in cord blood and arterial blood obtained at age 48 h. Eighty infants fulfilled all the inclusion criteria. Our results show an increase in the hepatic vitamin K1 dependent and independent factors with postnatal age. The APTT became shorter, the factor II-VII-X, α2-antiplasmin, plasminogen activities and fibrinogen level rose with increasing postnatal age. We found no change in the platelet parameters measured with postnatal age except that the megathrombocyte index was increased at age 48 h in infants < 29 weeks gestation. There was little change with gestational age of any factors except the vitamin K1 dependent factors. Factor II-VII-X activity rose and the APTT became shorter with increasing gestational age. Many of the haemostasis results did not fall within the normal adult range. We discuss the significance of ‘abnormal’ and ‘normal’ results in preterm infants.