Poor growth is an under-recognised yet significant long-term sequelae of oesophageal atresia (OA) repair. Few studies have specifically explored the reasons for growth impairment in this complex cohort. The association between poor growth with younger age and fundoplication appears to have the strongest supportive evidence, highlighting the need for early involvement of a dietitian and speech pathologist, and consideration of optimal medical reflux management prior to referring for anti-reflux surgery. However, it remains difficult to reach conclusions regarding other factors which may negatively influence growth, due to conflicting findings, inconsistent definitions and lack of validated tool utilisation. While swallowing and feeding difficulties are particularly frequent in younger children, their relationship with growth remains unclear. It is possible that these morbidities impact on the diet of children with OA, but detailed analysis of dietary composition and quality, and its relationship with these complications and growth, has not yet been conducted. Another potential area of research in OA is the role of the microbiota in growth and nutrition. While the microbiota has been linked to growth impairment in other paediatric conditions, it is yet to be investigated in OA. Further research is needed to identify the most important contributory factors to poor growth, the role of the intestinal microbiota, and effective interventions to maximise growth and nutritional outcomes in this cohort.

A brief resume of the highlights in the history of oesophageal atresia is presented. This is followed by research into the etiology, ontogeny and embryology, and microbiological studies. A revised classification of risk factors with consequent survival statistics is presented. Lessons learned in the management of the condition over a 40-year period are reported with particular emphasis on the management of the preterm infant with associated severe respiratory distress, right-side aortic arch, upper pouch fistula, 'long-gap' atresia, and the use of gastrostomy and intercostals drains. The incidence and treatment of early and late complications is discussed.

Thirty-nine Staphylococcus isolates with different mechanisms of resistance were recovered from the feces of 50 healthy children and tested for their susceptibilities to 17 antibiotics. The percentages of resistance of the staphylococci to some antibiotics were as follows: penicillin, 87%; erythromycin, 64%; tobramycin, 36%; tetracycline, 20.5%; kanamycin, 15%; and gentamicin, 13%. The mecA gene was detected in nine coagulase-negative staphylococci.