Neonatal serial creatinine levels as an adjunct biomarker in timing of fetal neurologic injury.

Objective: To investigate the rise and clearance of newborn creatinine in perinatal asphyxia as an adjunct biomarker to support or refute allegations of acute intrapartum asphyxia. Study design: In this retrospective chart review, newborns > 35 weeks gestational age were evaluated from closed medicolegal cases of confirmed perinatal asphyxia and reviewed for causation. Data collected included newborn demographic data, patterns of hypoxic ischemic encephalopathy, brain magnetic resonance imaging, Apgar scores, cord and initial newborn blood gases, and serial newborn creatinine levels during the first 96 h of life. Newborn serum creatinine values were collected at 0-12, 13-24, 25-48, and 49-96 h. Newborn brain magnetic resonance imaging was used to define 3 patterns of asphyxial injury: acute profound, partial prolonged, or Both. Results: Two hundred and eleven cases of neonatal encephalopathy from multiple institutions were reviewed from 1987 to 2019 with only 76 cases having serial creatinine values during the first 96 h of life. A total of 187 creatinine values were collected. Partial prolonged and Both had significantly greater degree of metabolic acidosis in the first newborn arterial blood gas in comparison to acute profound. Acute profound and Both had significantly lower 5- and 10- minute Apgar scores in comparison to partial prolonged. Newborn creatinine values were stratified by asphyxial injury. Acute profound injury showed minimally elevated creatinine trends with rapid normalization. Partial prolonged and Both demonstrated higher creatinine trends with delayed normalization. Mean creatinine values were significantly different between the three types of asphyxial injuries within 13-24 h of life at the time when creatinine values peaked (p = 0.01). Conclusion: Serial newborn serum creatinine levels taken within the first 96 h of life can provide objective data of timing and duration of perinatal asphyxia.

ABO blood group and procoagulant factors: the hypercoagulation hypothesis ABO and Procoagulant Factors.

BACKGROUND: The correlation between procoagulant levels-factor VIII (FVIII), von Willebrand factor (vWF), and fibrinogen-and risk of thrombosis has been well documented in adult populations. We hypothesize that interaction of passively transferred isoagglutinins in premature neonates with a compromised immune system may trigger an immune response that can target the immature gastrointestinal tract. The objective of this study is to evaluate if there are procoagulant level differences in preterm newborns stratified by ABO blood group. METHODS: VWF, FVIII, and fibrinogen levels were analyzed in neonates ≤32 weeks and/or birthweight ≤1500 g over the first 6 weeks of life. Demographic, blood type, and transfusion data were collected. RESULTS: Elevations in vWF and FVIII were found to be statistically significant in the third week of life in non-O neonates vs. type O neonates. FVIII was also found to be significantly elevated in week 1. Transfused neonates also showed elevations between weeks 0 and 3. CONCLUSION: There appears to be a time-dependent variation in procoagulant factor levels in preterm newborns. Although the clinical significance remains unclear, prothrombotic factors vWF and FVIII are significantly higher in non-O blood-type preterm neonates in the third week of life.

Influence of perinatal factors in short- and long-term outcomes of infants born at 23 weeks of gestation.

OBJECTIVE: Investigate the influence of perinatal factors on short- and long-term outcomes for infants born at 23 weeks of gestation. STUDY DESIGN: This is a retrospective study over a 25-year period (1987-2011) of 87 successfully resuscitated infants at 23 weeks of gestation. We investigated the effects of poor prenatal care, race, gender, chorioamnionitis, antenatal corticosteroids, delivery route/location, low 5-minute Apgar score, birth weight, and multiple births on short- and long-term outcomes. RESULTS: The mortality rate was 43% (37/87). A total of 88% (44/50) of the survivors were followed at 2 years corrected age with 66% (29/44) diagnosed with a moderate-to-severe neurological impairment. Outborn and multiple birth infants had significantly higher mortality (p-value 0.042 and 0.006, respectively). Lack of exposure to antenatal steroids and lower birth weight significantly increased the disability score (p-value 0.042 and 0.003, respectively). CONCLUSION: Multiple perinatal factors significantly influence outcomes at the threshold of viability.

Long-term follow-up of 2 newborns with a combined birth weight of 540 grams.

Long-term growth and developmental data are presented for the smallest and third smallest surviving newborns in the world literature to 5 and 20 years of age, respectively. Both patients exhibited normal motor and language development. Although head circumference for both newborns demonstrated catchup growth, significant differences in height and weight growth velocities persisted.

Does the International Classification of Disease (ICD-9) code accurately identify neonates who clinically have hypoxic-ischemic encephalopathy?

BACKGROUND/AIMS: Hypoxic-ischemic encephalopathy (HIE) refers to neonatal neurological signs and symptoms of hypoxia and/or ischemia. Our aim was to determine the accuracy of ICD-9 codes to identify newborns with HIE confirmed by umbilical cord blood analysis. METHODS: ICD-9 codes in the newborn chart for birth trauma, birth asphyxia, intrauterine hypoxia, and fetal distress were used to identify newborns with suspected HIE by neonatal personnel. Maternal charts were reviewed for umbilical cord gases meeting the HIE clinical criteria. RESULTS: There were 21,008 deliveries at center I and 17,540 at center II. ICD-9 codes identified 172 neonates, 49 infants (2.3‰ births) at center I and 123 neonates (7‰) at center II. Only 3 neonates (6%) were ≥34 weeks and none met ACOG criteria [umbilical artery pH <7.00 or base excess (BE) ≥12 mmol/l at center I]. At center II, 80 infants were ≥34 weeks but only 5/123 (4%) met the ACOG clinical criteria for HIE (pH <7.00, BE ≥12 mmol/l, and Apgar ≤3 at 5 min). CONCLUSIONS: ICD-9 codes are unreliable in identifying birth asphyxia and cannot identify newborns meeting the clinical criteria for intrapartum HIE.

A proposed evidence-based neonatal work-up to confirm or refute allegations of intrapartum asphyxia.

OBJECTIVE: To propose a clinical work-up in term and near-term newborns to address the nine American College of Obstetricians and Gynecologists (the College) and American Academy of Pediatrics criteria to define an acute intrapartum event sufficient to cause cerebral palsy. METHODS: We examined our experience as neonatal expert witnesses in 103 closed claims of alleged intrapartum asphyxia with poor newborn outcome over a 21-year period from 1987 to 2008. We estimated how often the clinical components of this proposed work-up were not obtained or recorded in the medical record. RESULTS: Cord arterial blood gases and placental pathology were not obtained or sent in 38% and 32% of the 103 cases, respectively. Routine neonatal laboratory tests, including a complete blood count with differential, nucleated red blood cells, electrolytes, calcium, coagulation profile, and renal and liver function tests, were frequently absent. Cranial imaging in ultrasonograms, computed tomography, and magnetic resonance imaging were absent in more than 50% of the cases reviewed and were often not scheduled at optimal times. CONCLUSION: The medical record of newborns with poor outcomes frequently has a paucity of objective, evidence-based data. This leads to speculation and unethical expert testimony. The protocol will assist in confirming or refuting allegations of intrapartum asphyxia. LEVEL OF EVIDENCE: III.

Pericardial effusion in a preterm infant resulting from umbilical venous catheter placement.

Pericardial effusion in neonates is a rare occurrence associated with malpositioning of central venous catheters. This report describes a case of pericardial effusion in which echocardiographic determination of line position, typically considered one of the most reliable means of placement verification, was misleading. The infant ultimately did well after pericardiocentesis, with complete resolution of symptoms and no further complications.

Annular pancreas in identical twin newborns.

Annular pancreas is a rare congenital anomaly occurring in 1 of every 12,000 to 15,000 live births [Nerwich N, Shi E. Neonatal duodenal obstruction: a review of 30 consecutive cases. Pediatr Surg Int 1994;9:47-50]. It may remain asymptomatic throughout life, present in adulthood, or present in infancy as a high intestinal obstruction. Review of the literature demonstrates only 8 cases of familial annular pancreas and no case of twins exhibiting the disease. We will describe a case of identical (monochorionic diamniotic) female twins with neonatal presentation of duodenal obstruction and annular pancreas, and discuss data supportive of a genetic etiology.

Orthopaedic implications of multiple gestation pregnancy with triplets.

Intrauterine crowding has been implicated as a risk factor in several orthopaedic conditions, such as developmental dysplasia of the hip (DDH), metatarsus adductus, and torticollis. The goal of this study was to see whether orthopaedic conditions associated with intrauterine crowding were more frequent in multiple gestation pregnancies, specifically in triplets. The authors reviewed their experience over a 10-year period with 261 children who were products of triplet pregnancies. They surveyed 13 orthopaedic conditions and found only one condition, torticollis, that had a greater incidence than that reported in single gestation pregnancies. A 0% incidence of DDH was found in these patients. Routine ultrasound screening cannot be recommended in these patients based on these results.

A randomized trial comparing beractant and poractant treatment in neonatal respiratory distress syndrome.

AIM: To compare the effects of beractant and poractant in neonatal respiratory distress syndrome (RDS). METHODS: Infants with RDS were randomized to receive beractant or poractant. The primary outcome measure was fraction of inspired oxygen (FiO2) requirement in the first 48 h after surfactant therapy. RESULTS: 58 infants completed the study. The mean gestational ages for the poractant and beractant groups were 29.6+/-3.6 and 29.3+/-2.9 wk, with average birthweights of 1394+/-699 and 1408+/-534 g, respectively. In the first 48 h, infants who received poractant had a lower FiO2 requirement compared to those who received beractant (p=0.018). The prevalence of patent ductus arteriosus (PDA) was lower in the group of infants that received poractant (17%) compared to the group that received beractant (45%) (p=0.02). CONCLUSIONS: Infants with RDS treated with poractant had a lower FiO2 requirement during the first 48 h compared to infants who received beractant. Infants who received poractant also had fewer PDAs than infants who received beractant. The difference in FiO2 was not associated with a difference in age of first extubation, total intubation time, or incidence of bronchopulmonary dysplasia between groups.

Amniotic band syndrome with significant orofacial clefts and disruptions and distortions of craniofacial structures.

Amniotic band syndrome (ABS) is a rare disorder in which bands of mesoderm that emanate from the chorionic side of the amnion and insert on the fetal body can generate a wide variety of disfiguring and disabling malformations. It usually is sporadic, and the incidence is approximately 1 in 15,000 live births, and affected children typically require involvement of several pediatric surgical subspecialties. The authors describe a case of ABS with extensive craniofacial anomalies.

T-cell proliferative responses following sepsis in neonatal rats.

Both experimental and clinical evidence suggest a suppression of T-cell function in burn and sepsis. The objective of the present study was to evaluate splenocyte and purified T-cell proliferative response and IL-2 production in septic neonatal rats. We also examined if alterations in T-cell proliferation and IL-2 production in neonatal sepsis is due to elevation in PGE2. PGE2 is known to play a significant role in T-cell suppression during sepsis in adults. Sepsis was induced in 15-day-old neonatal Sprague-Dawley rats by implanting 0.1 cm3 of fecal pellet impregnated with Escherichia coli (50 CFU) and Bacteroides fragilis (10(3) CFU). Animals receiving fecal pellets without the bacteria were designated as sterile. A group of septic and sterile rats were treated with PGE2 synthesis inhibitors, NS398 and resveratrol. These treatments of animals allowed us to evaluate the role of PGE2 in T-cell suppression during neonatal sepsis. Splenocytes as well as purified T cells were prepared and then proliferative response and IL-2 productive capacities were measured. A significant suppression of splenocyte proliferation and IL-2 production was noticed in both sterile and septic animals compared to the T cells from unoperated control rats. In contrast, the proliferation and IL-2 production by nylon wool purified T cells in sterile rats was not significantly different from control rats, whereas, a significant suppression in Con A-mediated T-cell proliferation and IL-2 production noticed in septic rat T cells compared to the sterile and control rat T cells. Such decrease in T-cell proliferation and IL-2 production was accompanied with 20-25% deaths in neonates implanted with septic pellets. No mortality was noted in sterile-implanted neonates. Treatment of animals with COX-1 inhibitor had no effect on T-cell proliferation response in both septic and sterile groups, whereas COX-2 inhibitor abrogated the decrease in T-cell proliferative response in the septic group. The treatment of animals with COX-2 inhibitor also significantly prevented the sepsis-associated mortality in neonates. In conclusion, the present study demonstrated T-cell suppression during neonatal sepsis is accompanied by a decrease in IL-2 production. Such suppressions were ameliorated with COX-2 inhibitor suggesting a role for PGE2 in the suppressed T-cell-mediated immune function in neonatal sepsis.