Fibrinolytic Activity, Thrombin Inhibitor and Kinetics of Clot Formation in Premature Infants with Respiratory Distress Syndrome

Kaulla, K. N. von; Kaulla, E. von; Butterfield, Joseph H.

doi:10.1111/j.1651-2227.1965.tb06423.x

Cited by 7 publications

(2 citation statements)

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“…The normal adhesiveness of platelets to glass that we obtained could be related to the high hematocrit seen in the newborn [9]. The hypercoagulability of newborn blood (short r+k, increased ma on the TEG), which is only inferentially related to platelet function, has been previously reported by VON KAULLA and BUTTERFIELD [22], and MARKARIAN et al [15]. HILGARTNER [10] also has found impaired clot retraction in the newborn as well as impaired platelet factor 3 release and ADP platelet aggregation.…”

Section: Discussionsupporting

confidence: 50%

Altered Platelet Function in Newborns

Mull¹,

Hathaway²

1970

Pediatr Res

135

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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.

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