ABSTRACT
Alterations in the cerebral blood flow in the neonate can be assessed by Duplex Doppler. Stressed neonates may be liable to cerebral thrombosis owing to disturbed procoagulant balance between reactive fibrinolysis and antifibrinolysis. This study assessed some plasma hemostatic markers in correlation with cerebral hemodynamics in a group of stressed FT neonates. To investigate possible relation of both measurements to the type of the offending risk factor and to the severity of neurologic presentation. In this study, plasma level of D-dimer, a marker of fibrin formation and reactive fibrinolysis, and plasminogen activator inhibitor-1 [PAI-1], a marker of anti-fibrinolysis were assessed in 62 FT neonates. Of these, 52 were perinatally distressed, having neurological manifestations in the immediate post-natal period and 10 were healthy FT neonates who served as control. Studied neonates were clinically assessed at birth by Apgar score, resuscitated as required, sampled for ABG and CRP, and subjected to full clinical evaluation. Stressed neonates were categoriesed according to the type of perinatal insult into: One risk factor group; namely perinatal asphyxia [group A] and intrapartum trauma [group B], Two risk factor group; comprising group C, that included the above two risks, groups D and E that included any of the above two risks with superadded early postnatal sepsis. They were eventually classified by neurological criteria according to early postnatal encephalopathy score [ES] into minimum ES and maximum ES groups. Re-sampling followed for ABG and laboratory investigations that included CBC, platelet count, PT, PTT, D-dimer and PAI-1 assay by enzyme linked immunosorbant assay [ELISA]. Within 24 hours of birth, middle cerebral artery blood flow velocity was assessed and resistive index [RI] was measured using Duplex Doppler sonography. The mean values of RI, plasma D dimer and PAI-1 were significantly higher than control in all stressed neonates and in each high risk group. Reduced cerebral blood flow in asphyxiated neonates was mainly aggravated by birth trauma. Traumatised neonates had significantly higher mean plasma D-dimer and PAI-1 as compared to neonates with perinatal asphyxia. Development of postnatal sepsis significantly raised plasma level of PAI-1 in asphyxiated neonates. RI was more predictive of severity of encephalopathy than either hemostatic markers. Cerebral ischemia was significantly associated with instrumental delivery, premature rupture of membranes [PROM] while no significant association existed with either fetal bradycardia, liquor stained meconium, emergency CS, degree of hypoxemia or hypocarbia. A significant positive correlation existed between values of RI and each of plasma levels of D-dimer and PAI-1 in all stressed neonates. Conclusions: On the first day of life, cerebral blood flow is reduced and some plasma prothrombotic markers are elevated in FT neonates subjected to trauma or asphyxia at birth. Cerebral ischemia in severely stressed FT neonates may pave the way to future cerebrovascular thrombosis. It follows that early screening by cerebral Duplex Doppler is crucial for high risk FT neonates especially following exposure to intrapartum trauma