High-Risk Pregnancies and Their Impact on Neonatal Primary Hemostasis

Abstract

Primary hemostasis, similar to other systems in the adjusting and transitioning neonate, undergoes developmental adaptations in the first days of life. Although platelets of neonates do not differ quantitatively compared with those of adults, they functionally present with major differences, thus supporting the theory of a “hypofunctional” phenotype that is counterbalanced by high hematocrit and more potent von Willebrand factor multimers. No clinical effect of bleeding tendency has hence been established so far for healthy term neonates. However, discrepancies in functionality have been noted, associated with gestational age, with more pronounced platelet hyporesponsiveness in preterm neonates. Multiple methods of in vitro platelet function evaluation such as PFA-100/200, platelet aggregometry, flow cytometry, and cone and platelet analyzer have been used for assessment of neonatal primary hemostasis. Several pregnancies are characterized as “high-risk” when risk factors preexist in maternal history or evolve during pregnancy. These pregnancies require specialized observation as they may have unpredictable outcome. High-risk pregnancies include clinical entities such as preeclampsia, pregnancy-induced smoking during pregnancy, gestational diabetes mellitus (GDM), autoimmune diseases, and other maternal hematological conditions. In some cases, like systemic lupus erythematosus, antiphospholipid antibody syndrome, and maternal immunologically based thrombocytopenia, neonatal thrombocytopenia is regarded as a prominent hemostasis defect, while in others, like pregnancy-induced hypertension and preeclampsia, both quantitative and qualitative disorders of neonatal platelets have been reported. In other pathologies, like GDM, neonatal primary hemostasis remains vastly unexplored, which raises the need for further investigation. The extent to which primary hemostasis is affected in neonates of high-risk pregnancies is the main objective of this narrative review.

Gestational Diabetes Melitus and Cord Blood Platelet Function Studied via the PFA-100 System

“…All of these are responsible for the higher mortality and morbidity rates observed in these neonates, which are directly proportional to the maternal glycemic control [ 7 ]. High-risk pregnancies, including those complicated with preeclampsia, GDM and autoimmune diseases, have been linked to quantitative changes and in some cases qualitative changes in hemostasis, and especially in platelet function [ 8 ]. Hematological indices in these pregnancies have been explored to a substantially higher extent in the mother, leaving several unanswered questions as to how neonatal platelets respond to vascular and metabolic changes [ 9 , 10 ].…”

Assessment of Hemostatic Profile in Neonates with Intrauterine Growth Restriction: A Systematic Review of Literature

“…[3][4][5] Mounting evidence has recently shown that IUGR neonates have substantial hematologic and coagulation dysfunction, including neutropenia, polycythemia, thrombocytopenia, and prolongation of standard coagulation tests. [9][10][11][12] Chronic hypoxia leading to elevated erythropoietin levels and subsequent alterations in the hematopoiesis process in favor of erythroid progenitor cells, resulting in downregulation of megakaryocytopoiesis, may be the mechanism responsible for thrombocytopenia in IUGR infants. 9 Moreover, hepatic impaired blood supply may aggravate coagulopathy due to compromised synthesis of clotting factors.…”

Editorial Compilation VIII

“…The "neonate" theme continues with the contribution from Politou et al, on high-risk pregnancies and their impact on neonatal primary hemostasis. 9 Primary hemostasis, similar to other systems in the adjusting and transitioning neonate, undergoes developmental adaptations in the first days of life. Although platelets of neonates do not differ quantitatively compared with those of adults, they functionally present with major differences, thus supporting the theory of a The issue changes focus with the next contribution from Larsen et al, who explore the benefits and harm of treatment with P2Y12-inhibitors beyond 12 months, in patients with coronary artery disease (CAD).…”