Developmental changes in brainstem neurons regulating lower airway caliber.

Premature infants are at risk for lower airway obstruction; however, maturation of reflex pathways regulating lower airway patency is inadequately studied. We hypothesized that postnatal maturation causes developmental change in brainstem efferent airway-related vagal preganglionic neurons (AVPNs) within the rostral nucleus ambiguus (rNA) that project to the airways and in pulmonary afferent fibers that terminate in the nucleus tractus solitarius (NTS). Ferrets aged 7, 14, 21, and 42 d received intrapulmonary injection of cholera toxin (CT)-beta subunit, a transganglionic retrograde tracer. Five days later, their brainstem was processed for dual immunolabeling of CT-beta and the cholinergic marker, choline acetyl transferase. CT-beta-labeled AVPNs and CT-beta-labeled afferent fiber optical density (OD) were analyzed. There was a significantly higher CT-beta-labeled cell number within the rNA at the youngest compared with older ages. All efferent CT-beta-labeled cells expressed choline acetyl transferase. OD of CT-beta-labeled afferent fibers was also higher at 7 d compared with 14 d. We conclude that the number of efferent AVPNs and afferent fiber OD both diminish over the second postnatal week. We speculate that exposure to injurious agents in early postnatal life may inhibit natural remodeling and thereby enhance later vulnerability to airway hyperreactivity.

Obstetrical correlates and perinatal consequences of neonatal hypoglycemia in term infants.

OBJECTIVE: To determine independent perinatal and intrapartum factors associated with neonatal hypoglycemia. METHOD: Of singleton pregnancies delivered at term in 2013; 318 (3.8%) neonates diagnosed with hypoglycemia were compared to 7955 (96.2%) neonate controls with regression analysis. RESULTS: Regression analysis showed that independent prenatal factors were multiparity (odds-ratio [OR] = 1.61), gestational age (OR = 0.68), gestational diabetes (OR = 0.22), macrosomia (OR = 4.87), small for gestational age neonate [SGA] (OR = 6.83) and admission cervical dilation (OR = 0.79). For intrapartum factors, only cesarean section (OR = 1.57) and last cervical dilation (OR = 0.92) were independently significantly associated with neonatal hypoglycemia. For biologically plausible risk factors, independent factors were cesarean section (OR = 4.18), gentamycin/clindamycin in labor (OR = 5.35), gestational age (OR = 0.59) and macrosomia (OR = 5.62). Mothers of babies with neonatal hypoglycemia had more blood loss and longer hospital stays, while neonates with hypoglycemia had worse umbilical cord gases, more neonatal hypoxic conditions, neonatal morbidities and NICU admissions. CONCLUSION: Diabetes was protective of neonatal hypoglycemia, which may be explained by optimum maternal glucose management; nevertheless macrosomia was independently predictive of neonatal hypoglycemia. Cesarean section and decreasing gestational age were the most consistent independent risk factors followed by treatment for chorioamnionitis and SGA. Further studies to evaluate these observations and develop preventive strategies are warranted.

A 5-hour-old male neonate with cyanosis.

Methemoglobin (MetHb) is a form of hemoglobin in which heme iron is oxidized and unable to bind oxygen; its normal basal production is counteracted by an efficient MetHb-reduction pathway. The causes of methemoglobinemia are classified as congenital or acquired. Shortly after his birth, the 5-hour-old male Caucasian neonate, whose case we present herein, developed central cyanosis that was unresponsive to supplemental oxygen. Oxygen saturation as determined via pulse oximetry was normal. In contrast, blood gas testing by multiwave CO-oximetry indicated decreased fractional oxyhemoglobin and an elevated MetHb fraction. The patient was subsequently diagnosed with a congenital cytochrome b5 reductase deficiency. This case emphasizes causes of methemoglobinemia and differences among analytical methods used to measure oxygen status when MetHb is present.