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Objective:  Cardiac troponin-I is a known biomarker of myocardial injury in adults and children but its diagnostic utility is unclear in newborns.This study aimed to establish normative data for troponin-I in stable newborns and assess any variation due to maternal diabetes status, mode of delivery, and Apgar scores., Study Design:  Prospective, observational study of stable newborn ≥35 weeks gestation admitted to a well-baby nursery at a single institution. Infants with respiratory distress, congenital infections, malformations, or syndromes were excluded. Troponin-I values were obtained by a validated point-of-care capillary blood sample at 24 hours of age., Results:  A total of 132 patients were included for analysis. Thirteen infants were born to mothers with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) during pregnancy and analyzed as a subgroup, with the remaining 119 infants comprising the base cohort to establish baseline normative troponin-I levels in stable newborn infants. The mean (standard deviation) troponin-I level of infants in the base cohort group was 0.019 ± 0.018 ng/mL and in infants born with maternal SARS-CoV-2 infection during pregnancy troponin-I level was 0.081 ± 0.1 ng/mL ( p  < 0.001). In infants of the base cohort, there was no significant difference in troponin-I levels between diabetic versus nondiabetic mothers, vaginal birth versus cesarean section, and 5-minute Apgar score of <7 versus ≥7., Conclusion:  Cardiac troponin-I level in healthy term newborns was 0.019 ± 0.018 ng/mL, which conforms to healthy children and adult lab values. There was no statistically significant difference in troponin-I levels in infants of maternal diabetes or normal glucose status, mode of delivery, cesarean versus vaginal, or 5-minute Apgar score of <7 or ≥7. Troponin-I levels in asymptomatic neonates born to mothers with a history of SARS-CoV-2 during pregnancy demonstrated an elevation when compared to the baseline group of infants., Key Points: · Troponin-I level, biomarker of myocardial injury, in newborns not requiring delivery-room.. · Resuscitation is comparable to normal pediatric & adult population independent of mode of delivery or maternal diabetes status.., Competing Interests: None declared., (Thieme. All rights reserved.)

Background: Human milk-derived fortifier (HMDF) coupled with human milk feeding in extremely premature infants reduces the adverse outcome risks of early exposure to bovine milk ingredients but may not provide enough nutrients for adequate catch-up growth compared with bovine milk-derived fortifier (BMDF)., Objective: This study aims to compare HMDF and BMDF effects on growth parameters and serum 25-hydroxy vitamin D (25OHD) levels in preterm very low birth weight (VLBW) infants during the first 8 weeks of life., Methods: We present a retrospective chart review of inpatient VLBW infants with birth weight <1,500 g and gestational age <32 completed weeks who received either their mother's milk or donor breast human milk fortified with HMDF or BMDF for the first 8 weeks. Weight, head circumference, length gain, and 25OHD level were calculated at 4 and 8 weeks of age., Results: A total of 139 VLBW infants (91 HMDF + 48 BMDF) received fortified human milk without any supplemental premature formula from birth to 4 weeks of age, of whom 44 (37 HMDF + 7 BMDF) continued until 8 weeks of age. There was no statistically significant difference in the growth parameters between the two groups at 4 and 8 weeks of age. Serum 25OHD level in the HMDF group was significantly higher compared with that in the BMDF group at 4 weeks of age despite receiving lower vitamin D supplementation., Conclusion: Similar gain in growth parameters in HMDF and BMDF groups at 4 and 8 weeks of age was observed, suggesting that HMDF provides adequate nutrients for growth in VLBW infants. A higher 25OHD level in HMDF may suggest better absorption., Competing Interests: KT has been in the speaker's bureau for Prolacta and Medela after completion of this study. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (© 2024 Lavassani, Tauber, Cerone, Ludke and Munshi.)

Continuous improvement in the clinical performance of neonatal intensive care units (NICU) depends on the use of locally relevant, reliable data. However, neonatal databases with these characteristics are typically unavailable in NICUs using paper-based records, while in those using electronic records, the inaccuracy of data and the inability to customize commercial data systems limit their usability for quality improvement or research purposes. We describe the characteristics and uses of a simple, neonatologist-centered data system that has been successfully maintained for 30 years, with minimal resources and serving multiple purposes, including quality improvement, administrative, research support and educational functions. Structurally, our system comprises customized paper and electronic components, while key functional aspects include the attending-based recording of diagnoses, integration into clinical workflows, multilevel data accuracy and validation checks, and periodic reporting on both data quality and NICU performance results. We provide examples of data validation methods and trends observed over three decades, and discuss essential elements for the successful implementation of this system. This database is reliable and easily maintained; it can be developed from simple paper-based forms or used to supplement the functionality and end-user customizability of existing electronic medical records. This system should be readily adaptable to NICUs in either high- or limited-resource environments.

Unintended endobronchial placement is a common complication of neonatal tracheal intubation and a threat to patient safety, but it has received little attention towards decreasing its incidence and mitigating associated harms. We report on the key aspects of a long-term project in which we applied principles of patient safety to design and implement safeguards and establish a safety culture, aiming to decrease the rate of deep intubation (beyond T3) in neonates to <10%. Results from 5745 consecutive intubations revealed a 47% incidence of deep tube placement at baseline, which decreased to 10-15% after initial interventions and remained in the 9-20% range for the past 15 years; concurrently, rates of deep intubation at referring institutions have remained high. Root cause analyses revealed multiple contributing factors, so countermeasures specifically aimed at improving intubation safety should be applied before, during, and immediately after tube insertion. Extensive literature review, concordant with our experience, suggests that pre-specifying the expected tube depth before intubation is the most effective and simple intervention, although further research is needed to establish accurate and accepted standards for estimating the expected depth. Presently, team training on intubation safety, plus possible technological advances, offer additional options for safer neonatal intubations.

Objective: Elevation of serum troponin I has been reported in newborns with hypoxic ischemic encephalopathy (HIE), but it is diagnostic and prognostic utility for newborn under 6 hours is not clear. Study the predictive value of early serum troponin I levels in newborns with HIE undergoing therapeutic hypothermia (TH) for persistent residual encephalopathy (RE) at discharge., Study Design: Retrospective chart review of newborns admitted with diagnosis of HIE to neonatal intensive care unit (NICU) for TH over a period of 3 years. Troponin levels were drawn with the initial set of admission laboratories while initiating TH. Newborns were followed up during hospital course and stratified into three groups based on predischarge examination and their electrical encephalography and cranial MRI findings: Group 1: no RE, Group 2: mild-to-moderate RE, and Group 3: severe RE or needing assisted medical technology or death. Demographic and clinical characteristics including troponin I levels were compared in each group., Results: Out of 104 newborns who underwent TH, 65 infants were in Group 1, 26 infants in Group 2, and 13 newborns in Group 3. All groups were comparable in demographic characteristics. There was a significant elevation of serum troponin in group 2 (mild-to-moderate RE) and group 3 (severe RE) as compared with group 1 (no RE). Receiver operator curve analysis for any RE (groups 2 and 3) compared with group 1 (no RE as control) had 0.88 (0.81-0.95) area under curve, p  < 0.001. A cut-off level of troponin I ≥0.12 µg/L had a sensitivity of 77% and specificity of 78% for diagnosis of any RE, positive predictive value of 68%, and a negative predictive value of 84%., Conclusion: In newborns undergoing TH for HIE, the elevation of troponin within 6 hours of age predicts high risk of having RE at discharge., Key Points: · Troponin I elevation is a biomarker of myocardial ischemia in adults and children.. · Myocardial ischemia may be part of multi-organ injury in neonatal HIE.. · Early elevation of troponin I level may correlate with the severity of neonatal HIE and predict residual encephalopathy in newborn at discharge from initial hospitalization.., Competing Interests: None declared., (Thieme. All rights reserved.)

Background and Objective: Vitamin D supplementation in preterm infants has been recommended by American Academy of Pediatrics (AAP); however, its efficacy and safety has not been well studied. To study 25-hydroxy vitamin D (25OHD) levels as a marker of vitamin D status of very low birth weight infants while on vitamin D supplementation during neonatal intensive care unit hospitalization., Methods: Retrospective study of preterm infants with birth weight <1500 g admitted to our unit from January 2013 to December 2015 who were on oral vitamin D3 400 IU supplementation. Serum 25OHD level were checked at 4, 8, and 12 weeks of age or before discharge and the levels were stratified as deficient <20 ng/mL, insufficient 20 to 29 ng/mL, normal 30 to 60 ng/mL, high 61 to 100 ng/mL and very high >100 ng/mL., Results: A total of 301 infants were enrolled, 186 very low birth weight (VLBW; 1000-1499 g) infants and 115 extremely low birth weight (ELBW; <1000 g) infants. Approximately 80% of both VLBWs and ELBWs had deficient or insufficient 25OHD levels at 4 weeks of age. On oral vitamin D supplementation, VLBW infants increased their 25OHD levels significantly by 8 and 12 weeks of age, whereas ELBW infants lagged behind at 8 weeks and increased their 25OHD levels by 12 weeks of age., Conclusions: Eighty percent of ELBW and VLBW infants have either deficient or insufficient vitamin D status at 4 weeks of age. Vitamin D supplementation helps in improving the vitamin D levels, VLBW infants significantly more than ELBW infants. AAP recommendation appears to be safe; however, if using higher supplement dosing, 25OHD level should be monitored to avoid high and very high vitamin D levels.

It is unknown how often preterm infants in neonatal intensive care units achieve the American Academy of Pediatrics-recommended daily intake of 400 international units of Vitamin D. We studied 378 preterm infants with birth weight 1500 g or less admitted to our neonatal intensive care unit, 151 infants before and 227 infants after daily vitamin D-intake monitoring was introduced. Infants were stratified into 2 groups: extremely low birth weight (<1000 g) and Very low birth weight (1000-1500 g). Monitoring of daily intake coincided with significant improvement in vitamin D intake in both extremely low birth weight and very low birth weight groups.

Objectives: To assess neonatologists' practices, knowledge, and opinions regarding the prevention of endobronchial intubation., Design: Anonymous survey., Subjects and Setting: Program Directors of Neonatology Fellowship Programs in the United States, surveyed by mail, and neonatologists who volunteered to respond while attending the Vermont-Oxford Network Annual Meeting., Interventions: None., Measurements and Main Results: Program directors (response rate 66%) and other practitioners contributed equally to the 132 survey responses, which were statistically indistinguishable between groups. Deep intubation frequency was estimated at greater than 5% by 39% of respondents, and 38% believed that it contributes to neonatal morbidity equally or more than medication errors. Quality assurance surveillance of intubations was uncommon. Neonatologists had remarkably varied responses when identifying the recommended vocal cord-level marking from a triple set of distal safety markings on a commonly used endotracheal tube; most had never seen recommendations or package insert directions for the use of such markings, and 86% desired improvements in endotracheal tube features to promote safer intubations., Conclusions: Neonatologists perceive endobronchial intubation as a consequential but underreported complication. Most are uncertain about the use of common vocal cord markings on endotracheal tubes, and few have seen specific instructions on this feature. We suggest that standardizing endotracheal tube safety features and making clear directions available to users may decrease the risk of endobronchial intubation in neonates.

Neonatal necrotizing enterocolitis which develops after feeding preterm infants is characterized by severe intestinal inflammation and profound systemic metabolic acidosis. The fermentation of undigested dietary carbohydrate by colonic flora yields gases (CO2 and H2) and short chain organic acids. These organic acids can disrupt the intestinal mucosa and initiate inflammation driven predominantly by resident mast cells and by granulocytes which are recruited from blood. A systemic acidosis ensues derived from intestinal acids, not classic lactic acidosis produced from anaerobic metabolism. The systemic acidosis further compromises inflamed bowel leading to bowel necrosis., (Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.)

Pericardial tamponade associated with central catheters is often lethal, unless promptly identified. We report our experience with two infants who suffered this complication but were successfully resuscitated. In each case, associated radiographs showed the tip of the central catheter beyond the superior vena cava-right atrium (SVC-RA) junction. Identifying the clinical triad of (1) sudden cardiovascular collapse unresponsive to usual resuscitative measures, (2) thoracic transillumination not suggestive of air leak, and (3) unexpected resistance to external cardiac compression led to the working diagnosis of pericardial tamponade and therapeutic pericardiocentesis. Prompt recovery followed. Central catheters within the RA seem prone to cause pericardial tamponade.

Objectives: To determine whether endothelin-1 (ET-1) in tracheal aspirates (TA) is a specific marker for acute lung injury in preterm infants with respiratory distress syndrome (RDS) who progress to bronchopulmonary dysplasia (BPD); and to investigate the relationship between TA ET-1 and the proinflammatory cytokines, interleukin-6 (IL-6) and IL-8, as early mediators of BPD., Study Design: We measured TA ET-1, IL-6, and IL-8 levels in preterm infants whose lungs were mechanically ventilated for RDS, categorized into two groups, BPD or non-BPD, on the basis of oxygen requirement at 36 weeks' postconceptional age., Results: A total of 106 TA samples were obtained from 34 infants with gestational ages ranging from 24 to 28 weeks on days 1, 3, 5, and 7 of life. There was a wide range of ET-1 concentration. TA ET-1 levels were significantly elevated on days 1, 3, and 7 in infants in whom BPD developed, in comparison with the non-BPD group (Mann-Whitney U test: p < 0.01). TA IL-8 levels were elevated on days 1, 3, 5, and 7 in the BPD group (p < 0.01); TA IL-6 levels were elevated (p < 0.05) only on day 5. There was a similarity in pattern of increase of TA ET-1 and TA IL-8 levels in the BPD group, with both being elevated in the first 24 hours of life and through the first week. There was no correlation between ET-1 and IL-8 values., Conclusion: Early significant increase in the TA ET-1 and IL-8 concentrations in preterm infants with acute lung injury correlates with subsequent progression to BPD.

The influx of inflammatory mediators and cells into the tracheobronchial effluent of preterm infants with respiratory distress syndrome (RDS) appears to be important in signaling the development of bronchopulmonary dysplasia (BPD). The mechanism that initiates this early inflammatory response is not well understood. The purpose of this study was to test the hypothesis whether increased interleukin-8 (IL-8), a potent chemoattractant for human neutrophils, appears in the airways of preterm infants with RDS in whom BPD develops before the influx of neutrophils. In addition, airway secretions were analyzed for the cytokine interleukin-6 (IL-6) to test the hypothesis whether this pro-inflammatory cytokine is an early marker of inflammation in preterm infants with RDS who progress to BPD. Sixty-five infants less than 32 weeks gestation with RDS were enrolled on the first day of life and 56 infants completed the study, with 31 recovering from RDS (Non-BPD) and 25 infants progressing to BPD. Infants were excluded from enrollment in the presence of maternal chorioamnionitis, infection at birth, or infection within the first week of life. There were no significant differences in birthweight, gestational age, or prolonged rupture of membranes between the two groups. Serial tracheal aspirates (TA) were collected on days 1, 3, 5, and 7 while the infants remained intubated. Significant elevations of TA neutrophil counts were detected in the BPD group on days 5 and 7. Cell-free TA revealed marked elevations of IL-8 in the BPD group compared to the Non-BPD group [median (25th percentile, 75th percentile), ng/ml epithelial lining fluid (ELF)] on day 1 [BPD 485 (195, 840); Non-BPD 63.1 (28.3, 197), P < 0.05] and day 3 [BPD 740 (319, 1310); Non-BPD 111 (54.3, 337); P < 0.05], while on days 5 and 7, the differences were not statistically significant. Interleukin-6 (IL-6) was measured as a marker of acute inflammation and was not different in the two groups on day 1, but was significantly elevated on day 3 [median (25th percentile, 75th percentile), ng/ml ELF; BPD 297 (62.1, 702); Non-BPD 72 (32.8, 266), P < 0.05] and on day 5 [BPD 270 (136, 672); Non-BPD 86.4 (57.8, 138), P < 0.05]. These studies demonstrate that elevation of IL-8 and IL-6 levels precedes the marked neutrophil influx seen in the TA of preterm infants in whom BPD develop. The presence of IL-8 and IL-6 in TA from these infants suggests that these cytokines either initiate the acute inflammatory cascade in the lungs, or they are early markers of the inflammatory process that places preterm infants at high risk for BPD.

Background & Aims: Inflammatory bowel disease is characterized by increased synthesis of nitric oxide. The aim of this study was to determine if inducible NO synthase (iNOS) was responsible for tissue injury, potentially via peroxynitrite formation, in the guinea pig model of gut inflammation., Methods: Inflammation was induced in guinea pig ileum by intraluminal administration of the hapten trinitrobenzene sulfonic acid in 50% ethanol. iNOS gene expression was assessed by reverse-transcriptase polymerase chain reaction and Western blotting, immunohistochemistry was determined by its localization, and activity was inhibited with the specific inhibitor aminoguanidine administered via the drinking water for 7 days. Nitration of tyrosines was assessed by immunohistochemistry., Results: In control animals, iNOS gene expression was minimal to absent, whereas, in hapten, inflammation-marked iNOS gene expression was evident from day 1 to 7. Nitrotyrosine and iNOS immunohistochemistry were colocalized, and positive staining was most intense in epithelia and neurons. Inhibition of NO formation prevented nitrotyrosine formation. Aminoguanidine inhibited the inflammatory response and restored morphology., Conclusions: The colocalization of tyrosine nitration with iNOS immunoreactivity suggests that iNOS may be responsible for tissue injury and the formation of NO-dependent nitrating species, potentially peroxynitrite. Inhibition of iNOS may afford a new therapeutic approach to the treatment of inflammatory bowel disease.

Objective: Our purpose was to determine the effects of nitric oxide synthase inhibition on maternal and fetal health in the last third of pregnancy., Study Design: Pregnant rats were treated from gestational day 13 to day 19 or 20 with the nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester, which was administered in the drinking water ad libitum. Control animals received the inactive enantiomer NG-nitro-D-arginine methyl ester or no treatment. Maternal blood pressure, blood chemistry studies, and placenta and pup size were determined. A separate group of rats received nitroprusside sodium in conjunction with NG-nitro-L-arginine methyl ester., Results: NG-nitro-L-arginine methyl ester caused a dose-dependent reduction in placenta and pup size. Amniotic fluid levels of cyclic guanosine monophosphate were significantly reduced at 0.1 mg/ml but not at higher doses. Hemorrhagic necrosis of fetal hind limbs occurred only with treatment with NG-nitro-L-arginine methyl ester and was prevented by coadministration of nitroprusside sodium. Maternal blood pressure and blood and urine chemistry studies were unaffected by NG-nitro-L-arginine methyl ester., Conclusion: Chronic reductions of nitric oxide production in the last third of pregnancy result in significant intrauterine growth retardation and hemorrhagic disruptions of hind limbs. Maternal complications were minimal and did not mimic preeclampsia.

As nitric oxide reduces gut epithelial permeability, we designed a study to determine if chronic nitric oxide synthase inhibition predisposes the gut to inflammation. Nitric oxide synthase (NOS) inhibitors were administered in the drinking water ad libitum, for seven days: aminoguanidine (10 micrograms/ml), a selective inhibitor of the inducible form of nitric oxide synthase; and NG-nitro-L-arginine methyl ester (L-NAME, 1, 10, and 100 micrograms/ml), which inhibits both the constitutive and inducible forms. Control animals drank tap water only or water with D-NAME, the inactive enantiomer. After one week, circulating leukocyte count and tissue myeloperoxidase activity were measured. L-NAME (100 micrograms/ml), but not D-NAME or aminoguanidine, caused a twofold increase in a circulating leukocyte numbers. This increase in leukocyte numbers was time- and dose-dependent, but the differential count was unaltered. Tissue myeloperoxidase (MPO) activity as an index of granulocyte infiltration was comparable in all groups in the stomach, jejunum, colon, liver, lung, kidney, heart, and skeletal muscle. However, ileal MPO activity was elevated threefold in the L-NAME-(100 micrograms/ml) treated group (P < 0.05). Results in the D-NAME and aminoguanidine groups were similar to controls. L-NAME administration resulted in a reduction in NOS activity ([14C]citrulline formation) in the ileum but not jejunum, whereas cGMP levels were elevated in both ileum and jejunum. We conclude that chronic inhibition of the constitutive form of nitric oxide synthase predisposes the ileum to inflammation and leads to a progressive leukocytosis.

We studied the effects of seven day treatment with the nitric oxide synthase (NOS) inhibitor NG-nitro-L-arginine (L-NAME), administered in the drinking water (100 micrograms/ml ad lib) of female guinea pigs. The effects of NOS inhibition were evaluated in naive animals and in guinea pigs with ileitis induced by intraluminal trinitrobenzenesulfonic acid (TNBS). After 7 days, animals were anesthetized, a sterile saline lavage injected into an ileal loop and removed after 30 min for analysis. In naive guinea pigs, L-NAME caused a marked increase in ileal myeloperoxidase activity and conversion of the mucosa from an absorptive to a secretory state. TNBS-treated guinea pigs has a similar, marked increase in granulocyte infiltration and a mucosal secretory response. However, in contrast to naive animals, L-NAME treatment was anti-inflammatory, reverting all responses to the basal state. We conclude that intestinal nitric oxide serves an anti-inflammatory role under basal conditions, whereas in the TNBS model of chronic ileitis, nitric oxide is a critical mediator of gut injury.

Forty eight neonates, born to mothers suffering from pregnancy induced hypertension and receiving labetalol for control of blood pressure, were studied for the possible adverse effects of the drug. These were compared with eighty one neonates matched for gestation and weight and born to mothers with pregnancy induced hypertension treated with drugs other than labetalol. Incidence of birth asphyxia and intrauterine growth retardation (IUGR) in the study population was 10.4 and 22.9%, respectively and in the control group 5 and 19.7%, the difference between two groups was not statistically significant (p > 0.05). However, the incidence of hypoglycemia was significantly higher (p < 0.01) in the study group (47.9%) as compared to the control group (17.2%). Two-thirds of the hypoglycemic babies in the study population were asymptomatic and they were managed with sugar-fortified milk feeds. In the study population, the symptomatic hypoglycemic babies had hypoglycemia for prolonged duration of 43.3 +/- 23.3 hours as compared to 11.5 +/- 6.3 hours in symptomatic hypoglycemic babies of the control group (p < 0.01). The mothers of the symptomatic babies in the study group received higher doses of labetalol in the range of 287.6 +/- 142.3 mg/day while rest of the mothers in the same group whose babies had either asymptomatic hypoglycemia or normal blood glucose levels, received 239.5 +/- 118.5 mg/day, though the difference was not statistically significant. It is concluded that maternal labetalol therapy is associated with increased risk of neonatal hypoglycemia.