Placenta · 2012
Patterns of placental pathology in preterm infants with a periventricular haemorrhagic infarction: association with time of onset and clinical presentation.
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Harteman J C, Nikkels P G J, Kwee A, Groenendaal F, de Vries L S
Аннотация
BACKGROUND: A periventricular haemorrhagic infarction (PVHI) is a complication of preterm birth with serious consequences. While various risk factors are recognized, little is known about the role of the placenta in the pathogenetic pathway of this type of white matter injury.
AIM: To evaluate prenatal, maternal and neonatal risk factors and describe placental pathology in infants with typical and atypical timing and presentation of PVHI.
METHODS: PVHI was defined as typical when the onset was within 6-96 h after birth in the context of established risk factors. PVHI was determined to be atypical when presumed antenatal (<6 h after birth) OR late in the postpartum course (>96 h). Maternal, prenatal and neonatal risk factors were collected retrospectively from patient charts. Microscopic placental pathology was described in 38/45 (84%) preterm infants (GA <34 wks) with a typical PVHI and 14/19 (74%) with an atypical presentation of PVHI.
RESULTS: Using univariate analysis clinical factors significantly associated with a typical PVHI were mechanical ventilation (p = 0.00), while fetal heart rate abnormalities (p = 0.00), a planned caesarean section (p = 0.00) and hypertensive disorders (p = 0.01) were associated with an atypical PVHI. Placental pathology was different between the typical vs atypical group with respect to chorioamnionitis (p = 0.04), funisitis (p = 0.05), fetal thrombosis (p = 0.01) and placental infarction (p = 0.00).
CONCLUSION: Chorioamnionitis and funisitis were significantly more common in infants with a typical PVHI. Fetal thrombosis and placental infarction were significantly more often associated with an atypical PVHI. Placental pathology in infants with PVHI reflects underlying disease processes and clinical conditions which may interact with the pathogenic mechanism of PVHI.
AIM: To evaluate prenatal, maternal and neonatal risk factors and describe placental pathology in infants with typical and atypical timing and presentation of PVHI.
METHODS: PVHI was defined as typical when the onset was within 6-96 h after birth in the context of established risk factors. PVHI was determined to be atypical when presumed antenatal (<6 h after birth) OR late in the postpartum course (>96 h). Maternal, prenatal and neonatal risk factors were collected retrospectively from patient charts. Microscopic placental pathology was described in 38/45 (84%) preterm infants (GA <34 wks) with a typical PVHI and 14/19 (74%) with an atypical presentation of PVHI.
RESULTS: Using univariate analysis clinical factors significantly associated with a typical PVHI were mechanical ventilation (p = 0.00), while fetal heart rate abnormalities (p = 0.00), a planned caesarean section (p = 0.00) and hypertensive disorders (p = 0.01) were associated with an atypical PVHI. Placental pathology was different between the typical vs atypical group with respect to chorioamnionitis (p = 0.04), funisitis (p = 0.05), fetal thrombosis (p = 0.01) and placental infarction (p = 0.00).
CONCLUSION: Chorioamnionitis and funisitis were significantly more common in infants with a typical PVHI. Fetal thrombosis and placental infarction were significantly more often associated with an atypical PVHI. Placental pathology in infants with PVHI reflects underlying disease processes and clinical conditions which may interact with the pathogenic mechanism of PVHI.