Introduction and Aim. Disorders of esophageal motility causing dysphagia and gastroesophageal reflux are frequent in survivors to esophageal atresia (EA) and distal tracheoesophageal fistula (TEF). The aim of the present study was to investigate the histologic and immunohistochemical features in both esophageal atretic segments to further understand the nature of the motor disorders observed in these patients. Material and Methods. Esophageal specimens from 12 newborns with EA/TEF and 5 newborns dead of unrelated causes were examined. The specimens were fixed in 5% buffered formalin, included in paraffin and cut in 5 micron sections that were stained with hematoxilin and eosin (H and E), and immunohistochemical stainings for Actin, S-100 protein, Neurofilament, Neuron-Specific-Enolase, Chromogranin A and Peripherin were evaluated under the microscope. Results. In controls, the distribution of the neural elements was rather homogenous at both levels of the esophagus. In contrast, the atretic segments showed quantitative and qualitative differences between them with sparser nervous tissue in the distal one in comparison with the proximal one and with controls. Conclusions. These results further support the assumption that histomorphological alterations of the muscular and nervous elements within the esophageal wall might contribute to esophageal dysmotility in patients surviving neonatal operations for EA/TEF.

Esophageal atresia and tracheo-esophageal fistula (EA + TEF) are often associated with malformations of neural crest origin. Esophageal innervation is also derived from the neural crest and it is abnormal in EA + TEF in which there is motor dysfunction. Our aim was to examine the intrinsic esophageal innervation in children with isolated EA in which different embryogenic mechanisms might be involved. Specimens from the proximal and distal esophageal segments of 6/35 patients who had esophageal replacement for isolated EA between 1965 and 2006 were suitable for the study. They were sectioned and immunostained with anti-neurofilament (NF) and anti-S-100 antibodies. The muscle and neural surfaces on each section were measured with the assistance of image processing software. The surface of the ganglia and the number of neurons per ganglion were determined at high power microscopy. The findings were compared with those of six autopsy specimens from newborns dead of other diseases by means of standard statistical tests and a significance threshold of P < 0.05. Unmatched age/size of babies in isolated EA and control groups precluded comparison of the relative surfaces occupied by neural elements. Patients with pure EA had denser fibrilar network and larger ganglia than controls. The number of neurons/ganglion were similar in both groups although the cells from EA patients were larger. The findings were similar at both esophageal levels studied. In spite of methodologic biases, it seems that intrinsic esophageal fibrilar network is denser and the intramural ganglia larger with larger cells in patients with pure EA than in controls on both esophageal ends of the organ. These neural anomalies are only in part reminiscent of those described in regular EA/TEF but may as well explain esophageal dysfunction in patients with repaired isolated EA.