INTRODUCTION: Although laparoscopic Nissen fundoplication has been recognized as the standard of care for hiatal hernia (HH) repair, HH recurrence due to breakdown of the hiatoplasty have been reported as a common mechanism of failure after primary repair. Different surgical techniques for diaphragmatic pillars closure have been proposed, but the problem remains unsolved. The authors hypothesized that ultrastructural illness may be implicated in this recurrence. The aim of this study was to investigate the presence of changes at esophageal hiatal area in patients with and without HH. MATERIALS AND METHODS: One hundred and thirty-two laparoscopic samples from phrenoesophageal membrane and diaphragmatic crura were collected from 33 patients with gastroesophageal reflux disease and HH (HH group) and 60 samples from 15 patients without HH enrolled as the control group (NHH group). All specimens were processed and analyzed by transmission electron microscopy. RESULTS: Muscular and connective samples from the NHH group showed no ultrastructural alterations; similar results were found in phrenoesophageal ligament samples from the HH group. In contrast, 94% of the muscular samples obtained from the crura of the HH group have documented four main types of alterations. In 75% of HH patients, the pillar lesions were severe. CONCLUSION: Patients with hiatal hernia have ultrastructural abnormalities at the muscular tissue of the crura that are not present in patients with a normal gastroesophageal junction. There is no difference in the microscopic damage at the connective tissue of the phrenoesophageal membrane surrounding the esophagus of the two groups of patients. The outcome of antireflux surgery could depend not only on the adopted surgical technique but also on the underlying status of the diaphragmatic crura.
INTRODUCTION: Although laparoscopic Nissen fundoplication has been recognized as the standard of care for hiatal hernia (HH) repair, HH recurrence due to breakdown of the hiatoplasty have been reported as a common mechanism of failure after primary repair. Different surgical techniques for diaphragmatic pillars closure have been proposed, but the problem remains unsolved. The authors hypothesized that ultrastructural illness may be implicated in this recurrence. The aim of this study was to investigate the presence of changes at esophageal hiatal area in patients with and without HH. MATERIALS AND METHODS: One hundred and thirty-two laparoscopic samples from phrenoesophageal membrane and diaphragmatic crura were collected from 33 patients with gastroesophageal reflux disease and HH (HH group) and 60 samples from 15 patients without HH enrolled as the control group (NHH group). All specimens were processed and analyzed by transmission electron microscopy. RESULTS: Muscular and connective samples from the NHH group showed no ultrastructural alterations; similar results were found in phrenoesophageal ligament samples from the HH group. In contrast, 94% of the muscular samples obtained from the crura of the HH group have documented four main types of alterations. In 75% of HH patients, the pillar lesions were severe. CONCLUSION:Patients with hiatal hernia have ultrastructural abnormalities at the muscular tissue of the crura that are not present in patients with a normal gastroesophageal junction. There is no difference in the microscopic damage at the connective tissue of the phrenoesophageal membrane surrounding the esophagus of the two groups of patients. The outcome of antireflux surgery could depend not only on the adopted surgical technique but also on the underlying status of the diaphragmatic crura.
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