Altered Platelet Function in Newborns

Abstract

ExtractStudies of platelet function were performed on venous blood specimens from 64 newborn infants within 0-48 h after birth. Fifty-two of the infants studied were normal, full-term average for gestational age (AGA) infants, three were normal, premature AGA infants, seven were premature AGA infants with the respiratory distress syndrome (RDS), and two were premature AGA infants who had repeated apneic periods. Although it was not possible to study all variables of platelet function in each of the groups, those studies that were performed showed no differences in the results based on the group to which an individual infant belonged.Compared with 24 normal adult controls, the infants showed impaired platelet aggregation in the presence of ADP, collagen, and thrombin. The mean time required for maximal platelet aggregation with ADP, collagen, and thrombin for the adults was 120, 230, and 74 sec, respectively, compared with values of 160, 443, and 158 sec for the infants (table II, figs. 2, 3, and 4). The percentage total platelet aggregation with ADP, collagen, and thrombin for the adults was 79, 91, and 74 % compared with 47, 73, and 47%, respectively, for the infants (table II, figs. 2, 3,.and 4). Infant whole blood and platelet-rich plasma clot retraction were markedly defective compared with normal adults (table I). In addition, platelet factor 3 release in 10 normal infants, as measured by the modified Stypven time, was decreased when compared with 10 values for normal adults ( fig. 5). Other variables of platelet function (bleeding times, native blood platelet adhesiveness, petechiometer tests) studied in newborn infants were normal (table I). Thrombelastograms were compatible with hypercoagulability of the blood (table I). None of the infants studied had clinical evidence of a bleeding tendency.In vitro mixing experiments suggested that the impaired ADP platelet aggregation was due neither to the presence of plasma ADP inhibitors, a refractory state due to increased circulating levels of ADP, anticoagulants, nor to a selected population of platelets. Physiologic alterations of infant platelets are similar to platelet functional changes observed in thrombasthenia.

Immunologic Studies of Prothrombin in Newborns

“…Tests of primary hemostasis taken during the newborn period show a diminished platelet aggregation, in spite of normal adhesion or retention of platelets (14,17). Some coagulation factors, especially those factors of the prothrombin complex, are significantly decreased (7,9,16).…”

Deficient Collagen-Induced Activation in the Newborn Platelet

“…The abnormalities of neonatal platelet function are less completely understood. In the mid-1970s, differences in the in vitro responses of cord and newborn platelets compared to those from older subjects were identified (3)(4)(5)(6). These abnormalities include a decreased aggregation response to certain agonists including ADP, epinephrine and collagen (3, 4), and decreased secretion of dense granule contents (5,6).…”

Deficiency of Plasma PGI2-Like Regenerating Activity in Neonatal Plasma. Reversal by Vitamin E In Vitro

“…Hrodek (7,8) observed a reduction in platelet factor 3 activity and availability and decreased platelet adhesiveness. The platelets of the newborn infant also demonstrate impaired aggregation to the physiologic agents adenosine diphosphate, epinephrine, collagen, and thrombin (2,7,8,15). Impaired release of nonmetabolic platelet adenine nucleotides (3) and decreased platelet prostaglandin endoperoxide formation.…”

“…Fluid phase coagulation factors are either normal (I, V, and VIII) or decreased (11, VII, IX, X, XI, and XII), and platelet function is well recognized to be impaired such that the hypercoagulable state cannot be ascribed to these changes (2,6,7,8,15). A deficiency of antithrombin 111, the most important of the zymogen inhibitors, is present in the nesnate (10).…”