ABSTRACT
OBJECTIVE: To identify risk factors implicated in the development of periventricular leukomalacia (PVL) and to evaluate the possible association between PVL with neonatal morbidity. DESIGN: Retrospective case control study. SETTING: Medical records of neonates admitted to a University Hospital between January 2000 and December 2005. POPULATION: Sixty-nine neonates with PVL born at gestational ages from 24 to 34 weeks. Forty-three of these had a cystic form of PVL (cPVL), whereas 26 had transient periventricular echodensities (PVE). METHODS: Each case was matched for gestational age and year of birth with one control. The maternal and neonatal medical records were searched. All data was compared between cases with PVL and controls, as well as between cases with cPVL and those with PVE. Stepwise logistic regression analysis was conducted to identify the independent predictors of PVL. RESULTS: Neonates with PVL suffered more frequently from intraventricular hemorrhage (IVH), respiratory distress syndrome type I (RDS I), seizures, sepsis, required more days of both mechanical ventilation and oxygen administration, while the duration of their hospitalization was longer compared to controls. Also, they were born more frequently to mothers who suffered from preterm premature rupture of membranes (PPROM) and clinical chorioamnionitis. We found that male gender, PPROM, preeclampsia, hypocarbia and IVH were independently associated with PVL. CONCLUSIONS: This study revealed that preterm neonates born to mothers with PPROM or preeclampsia, as well as neonates who presented with hypocarbia or suffered from IVH, appeared to be at high risk for the development of PVL.
Subject(s)
Fetal Membranes, Premature Rupture/diagnosis , Infant Mortality/trends , Infant, Premature , Leukomalacia, Periventricular/epidemiology , Leukomalacia, Periventricular/etiology , Pre-Eclampsia/diagnosis , Case-Control Studies , Female , Fetal Membranes, Premature Rupture/epidemiology , Follow-Up Studies , Humans , Incidence , Infant, Newborn , Infant, Premature, Diseases/diagnosis , Infant, Premature, Diseases/epidemiology , Infant, Small for Gestational Age , Intensive Care Units, Neonatal , Leukomalacia, Periventricular/diagnostic imaging , Logistic Models , Male , Pre-Eclampsia/epidemiology , Pregnancy , Probability , Reference Values , Respiratory Distress Syndrome, Newborn/complications , Respiratory Distress Syndrome, Newborn/diagnosis , Retrospective Studies , Risk Assessment , Severity of Illness Index , Statistics, Nonparametric , UltrasonographyABSTRACT
Very few people do not express any Kell antigens on their red blood cells (K0 phenotype). They can be immunized by transfusion or pregnancy and develop antibodies against Kell system antigens. These maternal antibodies can cause severe hemolytic disease of the fetus/newborn, as a result of the suppression of erythropoiesis and hemolysis. Multiple intrauterine transfusions in the management of severe hemolytic disease have been shown to cause erythropoietic suppression as well. Recombinant erythropoietin has been successfully used in the management of late anemia of infants with Rh hemolytic disease and in 1 case of KEL1 (Kell)-associated hemolytic disease. The authors present the case of severe hemolytic disease of a newborn due to KEL5 (Ku) isoimmunization of his K0 phenotype mother. Regular intrauterine transfusions were performed to manage the severe fetal anemia (Hb 3 g/dL). A male infant was born at the 36th week of gestation having normal hemoglobin (15.8 g/dL) and developed only mild hyperbilirubinemia. On the 15th day of life, the infant's hematocrit had fallen to 27.3%, with low reticulocyte count and low erythropoietin level. The infant was managed successfully with recombinant erythropoietin.