Coagulation function and placental pathology in neonates with placental abruption.

This study aimed to investigate the coagulation function and placental pathology in neonates with placental abruption (PA). A total of 60 neonates with PA and 60 neonates without PA were recruited. Neonates with PA were further subdivided into mild and severe groups. Neonates with PA had a higher incidence of anemia and hypovolemic shock (P<0.05), and were more likely to develop metabolic acidosis, asphyxia, intracranial hemorrhage, hypoxic-ischemic myocardial injury, hypoxic-ischemic encephalopathy, and disseminated intravascular coagulation (P<0.05). They also had longer hospital stay (P=0.033). At 6 h, the prothrombin time (PT), activated partial thromboplastin time (APTT), and D-dimer (D-D) were higher (P<0.05), but fibrinogen (FIB) was lower (P=0.000) in PA neonates than in controls. Significant differences were observed in tissue factor (TF), tissue factor pathway inhibitor (TFPI), and TF/TFPI among the mild PA group, whereas the severe PA and control groups were observed among different time points (P<0.05), and during time-group interaction (P<0.05). Thus, PA may cause coagulation dysfunction in neonates. The larger the separation area, the more evident the coagulation dysfunction was. TF and TFPI are involved in the pathogenesis of coagulation dysfunction in PA neonates and early heparin intervention is effective to imporve coagulation function and prognosis.