Coagulation Studies in Extremely Premature Infants

Abstract

SummaryEvidence of developmental evolution of coagulation can be seen when the studies of 10 thriving extremely premature (EPT) infants are compared to normal full-term (FT) infants. The prothrombin time, partial thromboplastin time, and thrombin time all became shorter with increasing gestational age. Fibrinogen levels and platelet counts appear to be comparable to term infant and adult levels. Fibrin degradation products (FDP) of 10 pg/ml or less were found in the thriving EPT infants. When compared to healthy fullterm infants, there is a definite gestational dependency of antithrombin 111 levels. Factors 11 and VII appear to be related to intrauterine maturation after the age of viability (24 wk), but factor VII-X complex does not. The contact factors XI, XII, high molecular weight kininogen (Fitzgerald factor), and prekallikrein (Fletcher factor) are all markedly decreased in thriving EPT infants. The mean factor V level is lower than that found in FT infants. This study confirms a gestational age dependency of factor VIlI activity. The ratio of factor VIlI antigen to factor VIlI clotting activity is increased (2.8 vs 1.01 in FT and adults). Thriving small for gestational age (SGA) infants had coagulation studies which were not statistically different from those of thriving EPT infants. The coagulation changes which occurred in severely ill EPT were mainly in the factors which decrease during intravascular coagulation (factors I, V, and VIII). The present study suggests that because of the high antigen to activity ratio seen in thriving EPT infants, a dysfunctional or fetal factor VlIl may have been produced. However, the further elevation of this ratio in the severely ill EPT infants is in keeping with a pathologic proteolysis or increased endothelial release of factor VIII antigen. SpeculationPrevention of and prompt therapeutic intervention for asphyxia, sepsis, hypovolemia, hypotension, hypothennia, hypoxia, and acidosis may prevent the occurrence of the coagulation changes seen in the severely ill EPT infants. A distinction between abnormal proteolysis versus production of dysfunctional proteins is essential before specific therapies can be designed.

The coagulation system of extremely preterm infants: influence of perinatal risk factors on coagulation

“…6,7 The number of included extremely preterm infants <28 weeks GA in both studies is small (n ¼ 10 (ref. 6); n ¼ 21 (ref.…”

Coagulation Parameters in Maternal and Cord Blood at Delivery

“…[1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16] The data, which represent the reference values for Saudi neonates, are compared in Table 2 with similar data from other ethnic populations.…”

“…Prolongation of the PTT in the neonate is attributed to a deficiency of the clotting factors operating in the intrinsic pathway of the clotting system . 7,11,[27][28][29] This in turn is due to immature synthetic capabilities of the liver rather than vitamin K deficiency. 1,3,13,28,29 Previous studies on the levels of factor VIII activities (factor VIII:C, vWFAg, and ristocetin cofactor) in the newborn have yielded widely contrasting results.…”

“…However, in sick neonates, especially those with severe respiratory disease or disseminated intravascular coagulation, antithrombin III levels were shown to drop precipitously below normal adult levels. 2,11,34,35 The relative deficiency in the various components of the hemostatic mechanism, established in this and many other studies, occurs in otherwise healthy symptom-free neonates. Therefore these alterations should be considered physiological or normal 5 since normal full and preterm infants display adequate hemostasis.…”

“…[1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16] Although this subject has interested many researchers in the last two decades, the numerous data available for healthy newborn infants are inconsistent and difficult to obtain and interpret. This is due to such factors as variable methods of blood collection and assay procedures, variable gestational age, birth weight and vitamin K status, wide ranges of clotting factor proteins, and small number of observations, which make it difficult to define true normal values or to draw valid comparisons between these data.…”