Abstract
Neonatal sepsis is considered critical for a significant increase in neonatal morbidity and mortality among hospitalized neonates. Neonatal sepsis, in most cases, coexists with coagulopathy, which can prove to be life-threatening. Complex molecular and cellular systems are involved in the cross-talk between inflammation and hemostasis during sepsis. Disturbances in the regulating systems of the vascular endothelium, and platelet–endothelial and platelet–neutrophil interactions play a pivotal role in both inflammation and coagulation. This complex process is poorly understood in neonates. In addition to the developmental maturation of hemostasis and the immune response in neonatal sepsis, a cellular model of hemostasis during sepsis should be taken into account. This review focused on the molecular and cellular mechanisms underlying inflammation and hemostasis during neonatal sepsis, taking the developmental immune response and developmental hemostasis into account in order to provide future diagnostic approaches to be applied in everyday clinical settings. Regarding the diagnostic modalities, we briefly provide the limitations of the currently used conventional coagulation assays, focusing on viscoelastic tests and platelet flow cytometry.
Highlights
Neonatal sepsis is the third most common cause of newborn mortality [1]
This review focuses on the molecular and cellular mechanisms underlying inflammation and hemostasis during neonatal sepsis, presents the main developmental differences between neonatal and adult hemostasis and platelet function, briefly reviews the currently available hemostatic tests in neonates and their limitations, and provides future diagnostic approaches to be applied in everyday clinical settings
Neonatal sepsis coexists with coagulopathy, which ranges from mild coagulation disorders and hypercoagulability with little or no clinical impact to severe hypocoagulability as detected in septic shock and bleeding in DIC
Summary
Neonatal sepsis is the third most common cause of newborn mortality [1]. To date, the reported fatalities from neonatal sepsis have reached a rate of 2% in full-term infants and. Sepsis is frequently related to coagulation disorders and presents with varied severity In sepsis, both hemostasis and the immune system are activated, sharing common pathways that respond to cellular–endothelium interactions, eventually resulting in microvascular thrombosis. Both hemostasis and the immune system are activated, sharing common pathways that respond to cellular–endothelium interactions, eventually resulting in microvascular thrombosis This complex process of thrombosis formation is poorly understood in adults and not at all in neonates [6,7]. Neonatal sepsis can present as mildly prolonged coagulation times and mild thrombocytopenia It is often accompanied by significant and sometimes life-threatening coagulopathy, as well as by disseminated intravascular coagulopathy and thromboembolic events that impair organ function and fulminant bleeding that require prompt and appropriate intervention [8,9,10]. We considered the viscoelastic tests and platelet flow cytometry
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