Micro-premature infants in New Jersey show improved mortality and morbidity from 2000-2018.

BACKGROUND: Micro-premature newborns, gestational age (GA) ≤ 25 weeks, have high rates of mortality and morbidity. Literature has shown improving outcomes for extremely low gestational age newborns (ELGANs) GA ≤ 29 weeks, but few studies have addressed outcomes of ELGANs ≤ 25 weeks. OBJECTIVE: To evaluate the trends in outcomes for ELGANs born in New Jersey, from 2000 to 2018 and to compare two subgroups: GA 23 to 25 weeks (E1) and GA 26 to 29 weeks (E2). METHODS: Thirteen NICUs in NJ submitted de-identified data. Outcomes for mortality and morbidity were calculated. RESULTS: Data from 12,707 infants represents the majority of ELGANs born in NJ from 2000 to 2018. There were 3,957 in the E1 group and 8,750 in the E2 group. Mortality decreased significantly in both groups; E1, 43.2% to 30.2% and E2, 7.6% to 4.5% over the 19 years. The decline in E1 was significantly greater than in E2. Most morbidities also showed significant improvement over time in both groups. Survival without morbidity increased from 14.5% to 30.7% in E1s and 47.2% to 69.9% in E2s. Similar findings held for 501-750 and 751-1000g birth weight strata. CONCLUSIONS: Significant declines in both mortality and morbidity have occurred in ELGANs over the last two decades. These rates of improvements for the more immature ELGANs of GA 230 to 256 weeks were greater than for the more mature group in several outcomes. While the rates of morbidity and mortality remain high, these results validate current efforts to support the micro-premature newborn.

Evaluation of critical congenital heart defects screening using pulse oximetry in the neonatal intensive care unit.

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.

Nosocomial infections in the neonatal intensive care unit.

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.

The role of neutrophils in the production of hypoxic-ischemic brain injury in the neonatal rat.

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.

Precise control of nitric oxide concentration in the inspired gas of continuous flow respiratory devices.

Inhaled NO has become widely used for diagnosis and therapy of pulmonary hypertension. The potential hazards of NO inhalation include the formation of methemoglobin, formation of NO2, and generation of free radicals in the presence of humidity and oxygen. Careful monitoring of NO and NO2 concentration, and titration of the dose according to a patient's clinical response is essential to minimize toxicity. This paper describes a formula and method that permits calculation and precise control of NO concentration in the inspired gas. The accuracy of the delivery system was assessed by a comparison of calculated and measured NO and NO2 concentrations in a continuous flow ventilator circuit. A comparison of electrochemical detector (ECD) versus chemiluminescence detector (CLD) monitoring techniques showed agreement between the instruments within approximately 2 ppm, with the ECD averaging a higher reading than the calculated or CLD measured values. We deemed a 2 ppm discrepancy between instruments clinically acceptable, and concluded that the instruments could be used interchangeably for clinical purposes to measure NO1 and that the ECD was preferable to CLD for measuring NO2. Details about the equipment are given and techniques are discussed to avoid the risk of inhalation of toxic concentrations of NO and NO2. This method provides the possibility of using inhaled NO with appropriate safety precautions in the range 0-60 ppm in a variety of continuous flow respiratory devices.

Nitric oxide reversal of recurrent pulmonary hypertension and respiratory failure in an infant with CDH after successful ECMO therapy.

Nitric oxide (NO) represents a new therapeutic modality for treating neonatal pulmonary hypertension and may obviate the need for extracorporeal membrane oxygenation (ECMO) in a number of cases of neonatal respiratory failure. Recently, the authors treated an infant with a congenital diaphragmatic hernia and pulmonary hypertension with NO on two separate occassions. During the initial period of stabilization, NO failed to reverse the pulmonary hypertension and prevent the development of progressive respiratory failure. After a successful course of ECMO, recurrent pulmonary hypertension developed that was successfully treated with continuous low-dose NO therapy for over 1 month. Prolonged administration of NO in varying doses titrated to clinical and echocardiographic parameters was well tolerated by the infant and prevented the need for a second run of ECMO.

Contribution of genetic disorders to neonatal mortality in a regional intensive care setting.

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.