Inguinal Hernia: The Destiny of the Inferior Epigastric Vessels and the Pathogenesis of the Disease

INTRODUCTION: While many scientific reports deal with inguinal hernia, including treatment methods and prosthetic devices proposed to provide a cure, few studies have sought to deepen our understanding of the etiology of this disease. The genesis of inguinal protrusion seems to be a neglected subject, even though addressing hernia genesis may be helpful for improving techniques and materials for surgical treatment. To clarify the source of inguinal protrusions, macroscopic and histological alterations of the inferior epigastric vessels in the herniated groin have been studied. These vascular structures exhibit significant features that could help to illuminate hernia genesis. MATERIAL AND METHODS: In patients with double ipsilateral inguinal hernia, composed of distinct direct and indirect protrusions, a tissue septum separates the two defects. Macroscopic observation and histological examination of this septal arrangement were carried out in 23 patients to highlight characteristics of the inferior epigastric vessels in the posterior aspect of this anatomical area. RESULTS: The examined inferior epigastric vessels presented notable alterations of the gross anatomy and histologically significant damage, with a typical trait of chronic compressive damage. All degrees of degeneration were observed, including complete disbanding of the vascular structure. CONCLUSIONS: In pantaloon hernias, excised inferior epigastric vessels suffered from chronic compressive degeneration but had no contact with the protrusions. Therefore, protrusion expansion does not produce the degenerative injuries seen in the epigastric vessels. In the inguinal area, there is no source of chronic compression except visceral impact. Consequently, orthostatic visceral impact could be hypothesized to cause structural weakening of the groin, leading to tissue disbanding and visceral protrusion through the weakened inguinal floor.