Endothelin-1 levels and renal function in newborns of various gestational ages.

BACKGROUND: Renal failure is common in the NICU; Acute Kidney Injury (AKI) occurs in 8-24% of admissions. Although AKI is preventable with early diagnosis, no reliable AKI biomarkers exist. Endothelin-1 (ET-1) has been implicated in renal pathogenesis, and elevated urinary ET-1 (uET-1) levels may correlate with progression of renal dysfunction. The study objectives were to determine whether uET-1 levels correlate with renal function parameters and/or fetal growth restriction, and if uET-1 is a potential neonatal AKI biomarker. METHODS: Sixty-three neonates were enrolled and divided into gestational age (GA) groups by weeks: 1) (24-30 6/7; n = 24); 2) (31-36 6/7; n = 26); and 3) (37-42; n = 13). Additional preterm subgroups for fetal growth restriction analysis included: 1) Appropriate for GA (AGA; n = 40), and 2) Small for GA (SGA; n = 10). ET-1 levels, measured using enzyme linked immunosorbent assay, were collected at birth (cord blood) and 24 h ( ± 4) of life (blood/urine). RESULTS: No correlation was found between uET-1 and blood plasma levels at birth (r = 0.15; p > 0.05) or 24 h (r = 0.17; p > 0.05). uET-1 negatively correlated with GA (r = -0.44; p < 0.001) and GFR (r = -0.34; p < 0.01). uET-1 levels did not correlate with creatinine (r = 0.13; p > 0.05), BUN (r = 0.19; p > 0.05), BUN/Cr ratio (r = 0.15; p > 0.05), or urinary output (r = 0.12; p > 0.05). In fetal growth restriction subgroup analyses: uET-1 levels negatively correlated with GFR in the PT-AGA subgroup (r = -0.38; p = 0.017), but not with PT-SGA (r = 0.01; p > 0.05). CONCLUSION: Plasma and uET-1 levels did not correlate; therefore, renal ET-1 excretion may reflect renal ET-1 production. uET-1 levels correlated negatively with GA and GFR. uET-1 may be a marker of impaired neonatal circulatory regulation and consequent renal injury.

Prenatal Oxycodone Exposure Alters CNS Endothelin Receptor Expression in Neonatal Rats.

Prenatal opioid exposure such as oxycodone is linked to significant adverse effects on the developing brain. Endothelin (ET) and its receptors are involved in normal development of the central nervous system. Opioid tolerance and withdrawal are mediated through ET receptors. It is possible that adverse effect of oxycodone on the developing brain is mediated through ET receptors. We evaluated brain ETA and ETB receptor expression during postnatal development in rats with prenatal oxycodone exposure. Timed pregnant Sprague-Dawley rats received either oxycodone or placebo throughout gestation. After birth, male rat pups were sacrificed on postnatal day (PND) 1, 7, 14 or 28. Brain ETA and ETB receptor expression was determined by Western blot analysis. Oxycodone pups compared to placebo demonstrated congenital malformations of the face, mouth, and vertebrae at the time of birth [4/69 (5.7%) vs. 0/60 (0%); respectively] and intrauterine growth retardation [10/69 (15%) vs. 2/60 (3.3%); respectively]. On PND 28, oxycodone pups compared to placebo had lower body and kidney weight. ETA receptor expression in the oxycodone group was significantly higher compared to placebo on PND 1 (p=0.035), but was similar on PND 7, 14, or 28. ETB receptor expression decreased in oxycodone compared to placebo on PND 1 and 7 (p=0.001); and increased on PND 28 (p=0.002), but was similar on PND 14. Oxycodone-exposed rat pups had lower birth weight and postnatal weight gain and greater congenital malformations. ETB receptor expression is altered in the brain of oxycodone-treated rat pups indicating a possible delay in CNS development.

Emission of volatile organic compounds from medical equipment inside neonatal incubators.

OBJECTIVE: To determine emission of volatile organic compounds (VOCs) from plastic medical equipment within an incubator. STUDY DESIGN: Air samples from incubators before and after adding medical equipment were analyzed using EPA TO-15 methodology. Headspace analysis was used to identify VOC emissions from each medical equipment item. Air changes per hour (ACH) of each incubator were determined and used to calculate the emission rate of identified VOCs. RESULTS: Cyclohexanone was identified in all incubator air samples. At 28 °C, the mean concentration before and after adding medical equipment items was 2.1 ± 0.6 and 57.2 ± 14.9 µg m(-3),respectively (P<0.01). Concentrations increased to a mean of 83.8 ± 23.8 µg m(-)(3) (P<0.01) at 37(o)C and 93.0 ± 45.1 µg m(-)(3) (P=0.39) after adding 50% humidity. Intravenous tubing contributed 89% of cyclohexanone emissions. ACH were determined with access doors closed and open with means of 11.5 ± 1.7 and 44.1 ± 6.7 h(-1), respectively. Cyclohexanone emission rate increased from a mean of 102.2 µg h(-1) at 28(°C to 148.8 µg h(-1) (P<0.01) at 37 °C. CONCLUSION: Cyclohexanone was quantified in all incubator air samples containing plastic medical equipment. The concentration of cyclohexanone within the incubator was inversely related to ACH in the closed mode. The cyclohexanone concentration as well as the emission rate increased with higher temperature.

Airborne concentrations of volatile organic compounds in neonatal incubators.

OBJECTIVE: To identify and quantify airborne volatile organic compounds (VOCs) inside neonatal incubators during various modes of operation within the neonatal intensive care unit (NICU) environment. STUDY DESIGN: Air samples were taken from 10 unoccupied incubators in four operational settings along with ambient air samples using air sampling canisters. The samples were analyzed following EPA TO-15 using a Tekmar AutoCan interfaced to Agilent 6890 Gas Chromatograph with a 5973 Mass Spectrometer calibrated for 60 EPA TO-15 method target compounds. Non-target compounds were tentatively identified using mass spectral interpretation and with a mass spectral library created by National Institute for Standards and Technology. RESULT: Two non-target compounds, 2-heptanone and n-butyl acetate, were found at elevated concentrations inside the incubators compared with ambient room air samples. Increase in temperature and addition of humidity produced further increased concentrations of these compounds. Their identities were verified by mass spectra and relative retention times using authentic standards. They were quantified using vinyl acetate and 2-hexanone as surrogate standards. CONCLUSION: The emission pattern of these two compounds and background measurements indicate that they originate inside the incubator. There is evidence that exposure to some VOCs may adversely impact the fetal and developing infants' health. Currently, as there is no definitive information available on the effects of acute or chronic low-level exposure to these compounds in neonates, future studies evaluating the health effects of neonatal exposure to these VOCs are needed.

Incidence and duration of hepatitis B surface antigenemia after neonatal hepatitis B immunization.

After immunization with recombinant hepatitis B vaccine, 19 infants were tested serially for hepatitis B surface antigen (HBsAg); 65% of infants had test results positive for HBsAg at least once, the incidence peaking 2 to 3 days from the time of immunization. The longest documented duration of antigenemia was 8 days; in all patients, HBsAg test results were negative by 18 days.

Intrathrombic urokinase reverses neonatal renal artery thrombosis.

A term infant with aortic and renal artery thrombosis is described, in whom the right kidney experienced complete ischemia for 5 days. A continuous intrathrombic urokinase infusion induced complete clot lysis and reperfusion of the right kidney. Follow-up studies of renal function and renal growth have been normal. This is the first report to describe complete pharmacological salvage of a neonatal kidney after prolonged warm ischemia. This case underscores both the ability of the neonatal kidney to recover from prolonged ischemia and the need to effect thrombolysis before irreversible renal injury occurs. The intrathrombic use of fibrinolytic agents in similarly affected infants warrants consideration and further study.

Grief reaction to sudden unexpected cardiorespiratory arrest in a normal newborn nursery.

The authors report two cases of sudden unexpected cardiorespiratory arrest occurring in a normal newborn nursery. They discuss the impact on the families and hospital personnel. The nursing and medical staff demonstrated many of the reactions experienced by families of sudden infant death syndrome (SIDS) victims, including shock, anger, guilt, disbelief, fear, and doubt. The manner in which hospital personnel were supported and counseled is discussed. Specific clinical implications of these cases, including the need to provide for appropriate monitoring and resuscitation in normal newborn nurseries, are presented.

Distal ileostomy drip feedings in neonates with short bowel syndrome.

When a newborn infant presents with high intestinal atresia, the proximal segment of the bowel is usually grossly distended and atonic. The anastomosis of this segment to the smaller and unused distal segment will usually result in little or no propulsion of contents distally. Many techniques have been employed to correct this problem. A common surgical approach is immediate end-to-end anastomosis, followed by parenteral alimentation until return of normal function. This can take many weeks, and requires special attention to fluid loss and complications associated with parenteral alimentation. In this paper we report two infants in whom we utilized a new technique to circumvent these problems. The technique involves continuous drip ileostomy feedings through the distal ileostomy, while basic nutritional needs are being met parenterally. In addition, the secretions from the proximal stoma are collected and infused with the elemental feeding. The distal bowel, now being fully utilized, is stimulated to accommodate, and when the two ends are joined at a second operation, nearly normal anatomical bowel is present.

The role of RBC transfusion in the premature infant.

Fifty-six premature infants with a mean gestational age at birth of 30 weeks were randomly assigned to a transfusion group, for whom the hemoglobin level was kept above 10.0 g/dL, and a nontransfusion group, who were transfused only for specific clinical indications. The groups were followed up longitudinally with weekly determinations of reticulocyte count, the partial pressure of oxygen at which 50% of hemoglobin is saturated, and hemoglobin F percentage, as well as weight gain, length of stay, hospital cost, and frequency and severity of apnea. At birth, there was no significant difference in birth weight, gestational age, and hemoglobin level between the two groups. At discharge, laboratory differences were noted between the two groups, but there was no clinical difference. We found no clinical advantage to the use of "booster" RBC transfusions in growing premature infants.