Altered Platelet Function in Newborns

Abstract

Extract: Studies 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 gesta-tional 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.

Speculation: Transient physiologic alterations have been described in many components of the newborn's blood, i.e., decreased plasma coagulation factors, red cell enzyme changes, low immunoglobulins, and an altered kinin system. It is not surprising, therefore, to find a transient platelet functional deficiency as well. Indeed, this hypofunction may be a defense against intravascular coagulation at a time when the infant's blood may be hypercoagulable and susceptible to increased thrombotic tendencies. Whether this platelet functional alteration could aggravate or be related to the cause of hemorrhage in severely ill infants remains to be shown.

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