Placental Abnormalities and Their Relationship to Periventricular White Matter Lesions in Very Low Birth Weight Infants in the First 72 Hours of Life
Nancy G. Mazzitelli, Nora C. Balanian, Claudio L. Solana.
Pathology; Neonatology Departments, Hospital Materno Infantil Ramon Sarda, Buenos Aires, Argentina.
BACKGROUND
Periventricular white matter lesions (WML) are the main cause of cerebral palsy in preterm infants and many of them are of prenatal origin. Placental abnormalities may indicate a risk of WML and adverse neurological outcomes.
OBJECTIVE
To evaluate the relationship between placental lesions (PL) and the appearance of periventricular WML in the first 3 days of life.
DESIGN/METHODS
Patients: all inborn infants with a birth weight 500 -1500 g and less than 32 weeks of gestational age (GA), admitted to the NICU from 4/02 to 10/04, were included in the study. Exclusion criteria were major congenital malformations or proven intrauterine infections. Methods: cranial ultrasound scans were routinely obtained in the first 72 hours after birth and the placentas were submitted for pathological and histological examination. Samples of the umbilical cord, ovular membranes and placental tissue were processed and studied in every case. PL were classified into three groups: 1) inflammation (chorioamnionitis / umbilical-chorionic vasculitis), 2) maternal-fetal vasculopathy or 3) the presence of both lesions. Patients were diagnosed with WML when ultrasonagraphy revealed any of the following abnormalities: periventricular leukomalacia, intraparenchymal hemorrhage, ventricular dilatation, periventricular echodensities or parenchymal hyperechogenity. Confounding factors for the multivariate analyses model included gender, IUGR, prenatal steroids, PROM and twin gestation.
RESULTS
139 infants were included, 38 patients (27%) had WML. PL patients had lower GA and a higher rate of PROM than those with no PL. When both PL (inflammation and maternal-fetal vasculopathy) were present the relationship between PL and WML was statistically significant by univariate (OR: 5.7, 95 % CI: 1.65-19.4) and multivariate analyses (OR: 4.4, 95% CI: 1.1-17.8). Vasculopathy was also associated with WML in multivariate analysis (OR: 5.8, 95% CI: 1.6-20.3). The specificity of PL for WML was 95%, with NPV of 80%.
CONCLUSIONS
In this population, PL (inflammation-vasculopathy/vasculopathy) were associated with WML in the first 72 hours of life with high specificity and NPV. We did not find any statistical association between placental inflammation and WML. Placental examination may suggest a prenatal etiology for WML.
PAS 2005: 57: 2650