Circulating Anticoagulants in the Newborn: Relation to Hypercoagulability and the Idiopathic Respiratory Distress Syndrome

Extract: Cord blood from 106 high risk and 68 normal deliveries was studied for hypercoagulability and levels of the circulating anticoagulants, antithrombin III (AT-III) and antiactivated factor X (anti-Xa). Table I shows that normal, term, appropriate for gestational age (AGA) infants showed a deficiency at AT-III when compared with normal children and adults (P < 0.001). Preterm (Pr) AGA infants had a lower level of AT-III than term (T) AGA infants (P < 0.001). The lowest levels of AT-III were seen in infants who developed idiopathic respiratory distress syndrome (IRDS); 66% of all infants with an AT-III time of 18 sec or less (mean ± sem AT-III value for T-AGA infants, 37 ± 2.8) developed IRDS. All except three of the infants (Fig. 1) with IRDS and/or low AT-III levels were offspring of mothers in the high risk category of premature labor or third trimester bleeding. When the thrombelastogram was used as a measurement of whole blood coagulability, T-AGA infants showed hypercoagulability when compared with adults and children (P = 0.025). The infants with the most hypercoagulability were offspring of the groups of severe erythroblastosis fetalis, third trimester bleeders, and premature labor.As seen in Table I and Figure 2, anti-Xa activity is slightly lower in the Pr-AGA group than in adults (P < 0.01), but the level of anti-Xa does not correlate well with the development of IRDS.Speculation: The susceptibility of the ill newborn infant to thrombotic, hemorrhagic, and necrotic pathologic lesions may be related to a deficiency of a potent, naturally occurring anticoagulant, antithrombin III. This AT-III, like α-1-antitrypsin, is a proteinase inhibitor. Both of these substances are severely deficient in infants with IRDS. The therapeutic implications of replacement of these proteins in groups of infants at risk to develop IRDS and hemorrhagic-thrombotic lesions remains to be explored.