Related Experiment Videos
Coagulation studies in extremely premature infants
Insights
Coagulation factors in extremely premature infants (EPT) show developmental changes with gestational age, differing from full-term infants. Severely ill EPT infants exhibit coagulation alterations linked to intravascular coagulation and potential factor VIII dysfunction.
Area of Science:
- Neonatal physiology
- Hemostasis and thrombosis
- Developmental biology
Background:
- Infant coagulation systems differ significantly from adults.
- Premature infants, especially extremely premature (EPT), present unique hemostatic challenges.
- Understanding these differences is crucial for managing bleeding and clotting risks.
Purpose of the Study:
- To investigate the developmental evolution of coagulation in thriving extremely premature (EPT) infants.
- To compare coagulation profiles of EPT infants with normal full-term (FT) infants.
- To identify specific coagulation factor alterations in EPT infants, including those who are severely ill.
Main Methods:
- Comparative analysis of coagulation studies in EPT and FT infants.
- Assessment of prothrombin time, partial thromboplastin time, thrombin time, fibrinogen, platelets, and fibrin degradation products.
- Evaluation of anti-thrombin III, factors II, VII, VII-X complex, XI, XII, high molecular weight kininogen, prekallikrein, factor V, and factor VIII activity and antigen levels.
Main Results:
- Coagulation times shortened with increasing gestational age in EPT infants.
- Fibrinogen and platelet levels were comparable to term infants and adults.
- Marked decreases in contact factors and factor V were observed in EPT infants.
- Gestational dependency of anti-thrombin III and factor VIII activity was confirmed, with an elevated factor VIII antigen to activity ratio in EPT infants.
- Severely ill EPT infants showed changes in factors I, V, and VIII, consistent with intravascular coagulation.
Conclusions:
- Coagulation in EPT infants demonstrates significant gestational age dependency.
- A dysfunctional or fetal factor VIII may be produced in thriving EPT infants, indicated by the high antigen to activity ratio.
- Severely ill EPT infants exhibit pathological proteolysis or increased endothelial release of factor VIII antigen, further elevating this ratio.
Abstract:
Evidence 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 micrograms/ml or less were found in the thriving EPT infants. When compared to healthy full-term infants, there is a definite gestational dependency of anti-thrombin III levels. Factors II 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 VIII activity. The ratio of factor VIII antigen to factor VIII 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 VIII 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.