Neutrophils contribute to ischemic brain injury in adult animals. The role of neutrophils in perinatal hypoxic-ischemic (HI) brain injury is unknown. Allopurinol reduces neutrophil accumulation after tissue ischemia and is protective against HI brain injury. This study was designed to investigate how neutrophils contribute to perinatal hypoxic ischemic brain injury and how neutropenia compared with allopurinol in its neuroprotective effects. A HI insult was produced in the right cerebral hemisphere of 7-d-old rats by right common carotid artery ligation and systemic hypoxia. Half the rats were rendered neutropenic with an anti-neutrophil serum (ANS). At 15 min of recovery from hypoxia, half the neutropenic and nonneutropenic rats received allopurinol (135 mg/kg, s.c.). The protective effect of the four treatment combinations was determined on brain swelling at 42 h of recovery. Neutropenia reduced brain swelling by about 70%, p < 0.01. Allopurinol alone produced similar protection so that the relatively small number of animals studied did not permit assessment of an additive effect. Neutrophil accumulation in cerebral hemispheres was measured by myeloperoxidase (MPO) activity assay and by neutrophil counts in 6-microm sections stained by MPO and ANS immunostaining. MPO activity peaked between 4 and 8 h of recovery in both hemispheres. Hemispheric neutrophil counts peaked at the end of the HI insult and again at 18 h of recovery. Neutrophils were stained within blood vessels and did not infiltrate the injured brain before infarction had occurred. We conclude that neutrophils contribute to HI brain injury in the neonate and that neutrophil depletion before the insult is neuroprotective.

We examined the contribution of chromosomal abnormalities, mendelian disorders, and birth defects to mortality in a regional neonatal intensive care unit by medical record review of neonatal deaths in that unit. Of a total of 296 infant deaths during the 5-year period June 1986 to May 1991, 69 (23.3%) had a genetic disorder. By diagnostic category, 18.8% had a chromosomal abnormality, 10.1% had a mendelian condition, 42% had a single primary defect in development, and 29% had an unrecognized pattern of malformation. The rate of autopsy and genetic evaluation differed markedly between these diagnostic categories. A comparison was made of underlying cause of death determined from medical records with underlying cause as classified by vital statistics nosologic procedures. No death certificate was on file for two of the deaths; for the remaining 67, 27 (40.3%) had an erroneous or misleading underlying cause of death as determined from vital statistics. The important contribution of genetic disorders to neonatal mortality in this high-risk population and the relative underrecognition of these disorders by vital statistics sources indicate that efforts aimed at reducing neonatal mortality will require a full range of preventive health activities, including preconception, prenatal and perinatal assessment, and counseling. Improved data collection techniques need to be developed to understand the contribution of this group of conditions to total neonatal mortality.

Nosocomial infections are significant causes of morbidity and mortality in patients who require newborn intensive care. The most common bacterial pathogens are Gram-positive bacteria, including Staphylococcus epidermidis, Staphylococcus aureus, and Enterococcus species. Gram-negative enteric bacilli and Gram-negative environmental bacteria are involved in outbreaks and occasional cases of nosocomial infection. The incidence of fungal infection has increased over the past 10 years; fungemia is the most commonly recognized infection. Surveillance for nosocomial infection is essential to identify outbreaks and detect unsuspected reservoirs of pathogens. A variety of molecular techniques can be used to determine the genetic relatedness of pathogens. Prevention of infection requires the identification of contaminated equipment, education regarding infection control methods including hand washing, and the judicious use of antimicrobial agents.

Objective:To evaluate the implementation of early screening for critical congenital heart defects (CCHDs) in the neonatal intensive care unit (NICU) and potential exclusion of sub-populations from universal screening.Study Design:Prospective evaluation of CCHD screening at multiple time intervals was conducted in 21 NICUs across five states (n=4556 infants).Results:Of the 4120 infants with complete screens, 92% did not have prenatal CHD diagnosis or echocardiography before screening, 72% were not receiving oxygen at 24 to 48 h and 56% were born ⩾2500 g. Thirty-seven infants failed screening (0.9%); none with an unsuspected CCHD. False positive rates were low for infants not receiving oxygen (0.5%) and those screened after weaning (0.6%), yet higher among infants born at <28 weeks (3.8%). Unnecessary echocardiograms were minimal (0.2%).Conclusion:Given the majority of NICU infants were ⩾2500 g, not on oxygen and not preidentified for CCHD, systematic screening at 24 to 48 h may be of benefit for early detection of CCHD with minimal burden.