Background Determine the tube-related complications and feeding outcomes of infants discharged home from the NICU with nasogastric (NG) tube feeding or gastrostomy (G-tube) feeding. Material & Methods We performed a chart review of 335 infants discharged from our NICU with home NG tube or G-tube feeding between January 2009 – December 2013. The primary outcome was the incidence of feeding tube-related complications requiring emergency department (ED) visits, hospitalizations, or deaths. Secondary outcome was feeding status at 6 months post-discharge. Univariate and multivariate analyses were conducted. Results There were 322 infants discharged with home enteral tube feeding, 84 NG tube and 238 G-tube, with available out-patient data for the 6 month post-discharge period. A total of 115 ED visits, 28 hospitalizations, and 2 deaths were due to a tube-related complication. The incidence of tube-related complications requiring an ED visit was significantly higher in the G-tube group compared to the NG tube group (33.6% vs 9.5%, p < 0.001). Two patients died due to a G-tube related complication. By 6 months post-discharge, full oral feeding was achieved in 71.4% of infants in the NG tube group compared to 19.3% in the G-tube group (p < 0.001). Type of feeding tube and percentage of oral feeding at discharge were significantly associated with continued tube feeding at 6 months post-discharge. Conclusion Home NG tube feeding is associated with fewer ED visits for tube-related complications compared to home G-tube feeding. There may be some infants who could benefit from a trial home NG tube feeding.

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The presentation may be confused with other neonatal endocrinological problems like congenital adrenal hyperplasia, hypoaldosteronism, and Barter syndrome. Type I PHA is further subdivided into 2 distinct entities. 2 The autosomal dominant trait (adPHA1) results from the mutations in the gene encoding mineralocorticoid receptor (NR3C2). 3 The clinical course is mild and is restricted to kidneys. Prognosis for adPHA1 form is good and spontaneous remission is observed over time. The autosomal recessive trait (arPHA1) results from mutations of the genes (SCNN1A, SCNN1B, and SCNN1G) encoding the 3 homologous alpha beta gamma subunits of the amiloride-sensitive epithelial sodium channel (ENaC). 4 This causes loss of function or a decrease in ENaC channel activity. 4 The arPHA1 not only affects kidneys but also affects colon, lung, sweat, and salivary glands. 4 Patients with arPHA1 are reported to have recurrent pulmonary infections with pseudomonas species similar to those seen in cystic fibrosis. 5