Maturational changes in the gut start in utero and rapidly progress after birth, with some functions becoming fully developed several months or years post birth including the acquisition of a full gut microbiome, which is made up of trillions of bacteria of thousands of species. Many factors influence the normal development of the neonatal and infantile microbiome, resulting in dysbiosis, which is associated with various interventions used for neonatal morbidities and survival. Extremely low gestational age neonates (<28 weeks’ gestation) frequently experience recurring arterial oxygen desaturations, or apneas, during the first few weeks of life. Apnea, or the cessation of breathing lasting 15–20 s or more, occurs due to immature respiratory control and is commonly associated with intermittent hypoxia (IH). Chronic IH induces oxygen radical diseases of the neonate, including necrotizing enterocolitis (NEC), the most common and devastating gastrointestinal disease in preterm infants. NEC is associated with an immature intestinal structure and function and involves dysbiosis of the gut microbiome, inflammation, and necrosis of the intestinal mucosal layer. This review describes the factors that influence the neonatal gut microbiome and dysbiosis, which predispose preterm infants to NEC. Current and future management and therapies, including the avoidance of dysbiosis, the use of a human milk diet, probiotics, prebiotics, synbiotics, restricted antibiotics, and fecal transplantation, for the prevention of NEC and the promotion of a healthy gut microbiome are also reviewed. Interventions directed at boosting endogenous and/or exogenous antioxidant supplementation may not only help with prevention, but may also lessen the severity or shorten the course of the disease.

Respiratory syncytial virus (RSV) is the most common respiratory pathogen in infancy and childhood. To compare the compliance and biologic efficacy of a home health care agency dosing-compliance program to treatment provided in a physician’s office setting during a single RSV season (November to May). AAP guidelines were used to identify neonates who were eligible for RSV prophylaxis before discharge from a neonatal intensive care unit setting. Parents were asked to choose to receive the recommended treatment for their child either in their pediatrician’s office setting or through a sequence of periodic nursing visits to their home. All home health care records were reviewed for demographics, number of doses received and hospitalization rate. Pediatricians office records were surveyed by telephone interview of their office staff and parents. Compliance data were calculated based on actual monthly injections given during the RSV season. We followed prospectively 1446 infants who received palivizumab during a single RSV season (November 1, 2000 through April 30, 2001). Of these infants 67% (969 of 1446) received their monthly injections in the home setting where 98% of the doses were given on schedule. In contrast 477 infants (33%) received their injections in a pediatrician’s office (parent’s choice) with a compliance of only 89% for completion of all recommended doses (P < 0.001 vs. home setting). There were 9 RSV hospitalizations (0.93%) in the home setting group and 8 RSV hospitalizations (3.57%) in the office setting (P < 0.001). More parents indicated that the in-home prophylaxis program was more convenient than was true for those receiving treatment in the physician’s office setting (P < 0.01). Better compliance with home injections was associated with a decrease in the hospitalization rate for RSV with a higher degree of parental satisfaction.

The term "euthyroid sick syndrome" (ESS) has been used to describe a pattern of thyroid hormone changes during the course of critical illness in adult patients without thyroid disease, often associated with reduced thyroid hormone secretion. To describe the thyroid hormone profile in full-term newborns critically ill compared with thyroid hormone profile of healthy infants, and determine if alterations could be related to the severity of the disease and outcome. A cross-sectional, observational, and prospective study of full-term infants admitted to the neonatal intensive care unit (NICU) of the Hospital de Pediatría J.P. Garrahan between July 2007 and April 2008. Serum T3, T4, and thyroid stimulating hormone (TSH) levels were measured at admission and severity of the disease was evaluated through SNAP, lactic acid, respiratory assistance and number of organs affected. Sick newborns showed significantly lower T3 and T4 levels compared with healthy infants [T3: -0.97 μg/dL (95% CI -0.89, -1.13) and T4: -4.37 μg/dL (95% CI -2.95, -5.78)]. Only 29 out of 94 (31%) infants presented a normal profile; 37 (39%) infants showed isolated low T3 levels, 20 (21%) infants had low T3 and T4 levels and eight (9%) infants had low TSH, T3, and T4. Of this latter group, five of eight (62%) children died suggesting a significantly higher risk of death for patients with low T3 associated with low T4 and TSH [Risk ratio (RR) 10.75 95% CI 3.93, 29]. Full-term sick newborns frequently have lower thyroid hormone levels than healthy ones. These observed thyroid hormones changes might be related to the underlying disease and could be used as a prognostic marker of the severity and fatal outcome of the patient.