The association between AB blood group and neonatal disease.

BACKGROUND: Numerous studies have examined the association between ABO blood groups and adult disease states, but very few have studied the neonatal population. The objective of this study was to determine the relationship between AB blood group and the occurrence of common neonatal disorders such as neutropenia at birth, sepsis, respiratory distress syndrome (RDS), intraventricular hemorrhage (IVH), retinopathy of prematurity (ROP), and patent ductus arteriosus (PDA) compared to all other blood groups. METHODS: We performed a retrospective review on 3,981 infants born at 22 0/7 to 42 6/7 weeks' gestational age and compared the relative risk of neonatal diseases in infants with AB blood group to that of infants with all other blood groups (A, B, and O). RESULTS: When compared to all other blood groups, AB infants demonstrated an increased risk for developing negative clinical outcomes. AB blood group was significantly associated with a 14-89% increased risk of neutropenia at birth, sepsis, RDS, and ROP. Risks for IVH and PDA were not significant. CONCLUSION: We hypothesize that the phenotypic expression of A and B antigens, rather than the antigens themselves, in the AB group may reveal an enhanced susceptibility to injury at the endothelial level resulting in an increased risk for disease development.

The role of fetal inflammatory response syndrome and fetal anemia in nonpreventable term neonatal encephalopathy.

OBJECTIVE: To evaluate asphyxial patterns in term encephalopathic newborns caused by chorioamnionitis or intrapartum blood loss that resulted in cerebral palsy and allegations of obstetrical professional liability. STUDY DESIGN: As an expert witness, JKM identified term newborns with profound neurologic impairment: 18 born in the presence of chorioamnionitis and 14 with significant anemia. RESULT: In both study groups, profound depression with low 10-min Apgars was associated with early-onset seizures (88%), multiorgan failure (94%) and a partial prolonged injury to the cortex and subcortical white matter (94%). A cord arterial pH>7.00 was noted in 68% and deep gray matter injury involving the basal ganglia and thalamus occurred in only 19% of the newborns studied. CONCLUSION: The cord arterial pH and pCO2 values, early-onset seizures and paucity of isolated deep gray matter injury support that significant injury occurred postnatally despite appropriate resuscitation. This unique pattern may refute allegations of obstetrical mismanagement in the intrapartum period.

Factors influencing independent oral feeding in preterm infants.

OBJECTIVE: Determine the mean post-menstrual age when preterm infants attain independent oral feeding skills and whether gestational age, common neonatal morbidities, gender, race, delivery route, or birth year affects this reflex. METHODS: A retrospective chart review of 2700 preterm infants, born before 37 weeks gestational age admitted to a level III NICU between January 1978 and July 2013, to determine the post-menstrual age when independent oral feedings occur. RESULTS: Mean post-menstrual age at achievement of independent oral feeding was 36 + 4/7 weeks ± 14 days. Gestational age under 29 weeks correlated with delayed post-menstrual age at achievement of independent oral feeding at 37 + 3/7 weeks versus 36 + 1/7 weeks for gestational age 29-33 weeks and 36 + 3/7 weeks for late preterm infants (p < 0.0001). Preterm infants with certain morbidities experienced a delay in independent oral feeding: necrotizing enterocolitis at 38 + 6/7 weeks (p < 0.0001), bronchopulmonary dysplasia at 38 + 1/7 weeks (p < 0.0001), severe intraventricular hemorrhage at 37 + 6/7 weeks (p < 0.001). Preterm infants born before the year 2000 achieved independent oral feeding two days later than preterm infants born since the year 2000 (p < 0.0001). Preterm infants delivered vaginally achieved independent oral feeding three days sooner than infants delivered via c-section (p < 0.0001). Female infants orally fed one day sooner than male preterm infants (p = 0.0008). CONCLUSIONS: Preterm infants achieve independent oral feeding at 36 + 4/7 weeks. Factors negatively influencing when the preterm infant will achieve independent oral feeding include gestational age under 29 weeks and major morbidities, whereas vaginal delivery and ongoing advances in neonatal care may accelerate the transition to independent oral feeding.

Acute drop in blood monocyte count differentiates NEC from other causes of feeding intolerance.

OBJECTIVE: Necrotizing enterocolitis (NEC) is characterized by macrophage infiltration into affected tissues. Because intestinal macrophages are derived from recruitment and in situ differentiation of blood monocytes in the gut mucosa, we hypothesized that increased recruitment of monocytes to the intestine during NEC reduces the blood monocyte concentration and that this fall in blood monocytes can be a useful biomarker for NEC. STUDY DESIGN: We reviewed medical records of very-low-birth-weight (VLBW) infants treated for NEC and compared them with a matched control group comprised of infants with feeding intolerance but no signs of NEC. Clinical characteristics and absolute monocyte counts (AMCs) were recorded. Diagnostic accuracy of AMC values was tested using receiver-operator characteristics (ROC). RESULT: We compared 69 cases and 257 controls (median 27 weeks, range 26 to 29 in both the groups). In stage II NEC, AMCs decreased from median 1.7 × 10(9) l(-1) (interquartile range (IQR) 0.98 to 2.4) to 0.8 (IQR 0.62 to 2.1); P < 0.05. In stage III NEC, monocyte counts decreased from median 2.1 × 10(9) l(-1) (IQR 0.1.5 to 3.2) to 0.8 (IQR 0.6 to 1.9); P < 0.05. There was no change in AMCs in control infants. ROC of AMC values showed a diagnostic accuracy (area under the curve) of 0.76. In a given infant with feeding intolerance, a drop in AMCs of > 20% indicated NEC with sensitivity of 0.70 (95% confidence interval (CI) 0.57 to 0.81) and specificity of 0.71 (95% CI 0.64 to 0.77). CONCLUSION: We have identified a fall in blood monocyte concentration as a novel biomarker for NEC in VLBW infants.

Sepsis-induced alteration in T-cell Ca(2+) signaling in neonatal rats.

Sepsis-induced suppression in T-cell proliferation follows deranged Ca(2+) signaling in adult rats. In preliminary studies, we observed suppression in T-cell proliferation in septic neonatal rats as well. In this study, we assessed splenic T-cell cytosolic Ca(2+) concentration, [Ca(2+)](i), as its elevation plays an important role in T-cell proliferation. Also, we investigated the role of PGE(2) in sepsis-related changes in T-cell [Ca(2+)](i) in animals pretreated with cyclooxygenase-1 (COX-1) inhibitor (resveratrol) and cyclooxygenase-2 (COX-2) inhibitor (NS-398). Sepsis was induced in 15-day-old rat pups by intraperitoneal implantation of fecal pellets containing Escherichia coli and Bacteroides fragilis. The sham group consisted of pups implanted with sterile fecal pellets. Septic and sham pups were sacrificed 24 h after implantation and their spleens were removed. The spleens from sham and septic pups, along with spleens from unoperated control pups, were processed for single cell suspensions, and T cells were isolated using nylon wool columns. Fura-2 fluorophotometry was employed for the measurement of [Ca(2+)](i) (in nM units) in T cells stimulated with concanavalin A (ConA). Our results show that ConA-mediated T-cell [Ca(2+)](i) response is significantly suppressed in septic neonatal rats. Pretreatment of pups with COX-2, but not COX-1 inhibitor, prevented the decrease in the [Ca(2+)](i) response. These findings suggest that PGE(2) might induce the attenuation in T-cell Ca(2+) signaling during sepsis in neonatal rats.

Neonatal-perinatal risk factors for the development of persistent pulmonary hypertension of the newborn in preterm newborns.

There is a long-held belief that preterm newborns lack sufficient arteriolar musculature to maintain a prolonged elevated pulmonary vascular resistance (PVR) after birth. Net ductal flow is thought to be minimal, with the developing pulmonary circulation incapable of significant vasoconstriction. We identified retrospectively 15 premature newborns over a 10-year period weighing < or = 1500 g and with a gestational age of < or = 30 weeks with documented persistent pulmonary hypertension of the newborn (PPHN) in the first 24 hours after birth. We matched 36 newborns of similar weight and gestation with no clinical evidence of shunting. The control group weaned to an FiO2 < or = 0.50 by 12 hours after birth. Despite similar gestational ages, the PPHN group (n = 15) had significantly higher birth weights than the control group (n = 36). The duration of ruptured membranes, maternal tobacco use, and use of antenatal steroids were significantly higher in the PPHN group. We speculate that these three factors might act in a synergistic relationship with which to accelerate pulmonary vascular smooth muscle development in premature newborns.

Severe rhinorrhea and respiratory distress in a neonate exposed to fluphenazine hydrochloride prenatally.

OBJECTIVE: To report a case of respiratory distress with severe rhinorrhea in a newborn exposed prenatally to fluphenazine hydrochloride. CASE SUMMARY: The safety of phenothiazines during pregnancy and the effect on the fetus and newborn are not well known. We describe a newborn who had severe rhinorrhea, vomiting, and respiratory distress after being exposed in utero to fluphenazine hydrochloride. Sepsis, choanal atresia, and congenital syphilis were excluded as causative factors for rhinorrhea. The rhinorrhea and upper airway obstruction responded to treatment with pseudoephedrine. CONCLUSIONS: Severe rhinorrhea, vomiting, and respiratory distress that occurred in this infant have not been reported previously following prenatal fluphenazine hydrochloride exposure. Awareness of this problem would be helpful to clinicians and should be considered in the differential diagnosis of rhinorrhea in newborns.

Myelopathy secondary to neonatal bacterial meningitis.

Myelopathy is an infrequently reported complication of bacterial meningitis. Four patients with neonatal meningitis and cervical myelopathy are reported. This complication may be more frequent than presumed and should be closely assessed during evaluation. The conditions of most previously reported survivors improved or resolved and the majority involved the cervical spinal cord.

Mediastinal cystic hygroma: prenatal decompression with neonatal resection and recurrence at 19 months of age.

A case of an anterior mediastinal cystic hygroma detected prenatally at 22 weeks' gestation is reported. Because of progressive nonimmune hydrops, cardiac compromise, and mediastinal shift compressing the lungs, in utero decompression was successfully performed at 24 weeks. This newborn infant was delivered at 37 weeks' gestation with no respiratory distress. Operative excision of a large thoracic cystic hygroma was performed shortly after birth. At 19 months of age, this patient appeared with unilateral wheezing and fever. Operative findings confirmed recurrence of a cystic hygroma.

An association of pulmonary hypoplasia with unilateral agenesis of the diaphragm.

During a period of 5 years, 33 newborns with congenital diaphragmatic hernia were treated. Three groups presenting with respiratory distress in the delivery room were identified. These included 8 newborns with agenesis (group 1) and 4 newborns with nonagenesis (group 2), all of whom died. There were 19 nonagenesis survivors (group 3), giving an overall survival rate of 61%. Two newborns who presented beyond 6 hours of life were excluded. No one specific arterial blood gas value or ventilation parameter obtained preoperatively could predict survival. Postmortem right and left lung weights, lung/body weight ratio, and radial alveolar counts demonstrate that agenesis is a unique subgroup with profound pulmonary hypoplasia and a dismal prognosis.

Intact survival of a 280-g infant: an extreme case of growth retardation with normal cognitive development at two years of age.

The care of infants born weighing less then 500 g is not only controversial but is also associated with medical uncertainties. We report the management of a growth retarded infant who weighed 280 g at birth after 26.9 weeks' gestation. The child not only survived but appears developmentally normal at two years of age. Although the infant is the smallest survivor reported, the case demonstrates the importance of gestational assessment in deciding delivery room management.