Sphincter-like motion following mechanical dilation of the internal inguinal ring during indirect inguinal hernia procedure.

INTRODUCTION: Even today, there is still great speculation as to the underlying pathogenesis of inguinal hernia. As a result, it could be extrapolated that the vast majority of repairs are based upon conjecture. Most current repairs are founded upon the principle of "closing the defect" in the anatomy, either by suturing closed under tension, covering with a mesh or obliterating the defect with a plug. Many variants of each method are refined to achieve better clinical outcomes. Yet few, if any, strive to understand a fundamental question: "What has gone wrong with the normal physiological and anatomical mechanisms that prevent abdominal structures protruding through the abdominal wall?" We consider, in the normal subject, the muscular structures that converge and wrap around the inguinal canal as a highly dynamic structure, which forms a reactive barrier to the augmentation of intra-abdominal pressures. In effect, the structures work together like a "striated sphincter complex." Through years of surgical experience, we have seen the formation of adhesions and fibrosis in these delicate and key structures, and hypothesised that they may impair its shuttering action, thus, creating a patency of this jammed inguinal ring leading to hernia. Based upon these observations, we have created a hernia repair variant that tries to "unblock" the muscles prior to repair, thus, hopefully restoring a degree of physiologic function.
METHODS: A retrospective study describes the results of 47 patients operated for indirect inguinal hernia with a standardised procedure consisting of meticulous adhesiolysis of the hernia area and mechanical dilation (divulsion) of the inguinal orifice in order to break stiff fibres within the muscle, allowing viable muscle fibres to contract freely once more. After dilation, a proprietary lamellar-shaped implant was delivered into the canal. Its form and function are designed to eliminate impingement of the cord structures and give a gentle outwards force to induce a reactive contraction of the sphincter-like muscle complex during healing. This gentle contraction offers the possibility to eliminate fixation of the implant.
RESULTS: The removal of scar tissue, dilation and the introduction of the implant into the internal inguinal ring induced a forceful "gripping" contraction by the sphincter complex in all patients. Even without fixation, it became almost impossible to pull the implant out of the canal. After obliterating the orifice with the lamellar implant, it was clear that there was no dilative compression upon the cord structures.
CONCLUSION: The results of this combined procedure, scar removal, dilation and implant delivery, led to thoughtful suggestions regarding the anatomy and the physiology of the inguinal canal. The procedural adhesiolysis during indirect inguinal hernia repair has always shown the well described concentric muscular arrangement formed by the internal oblique and transversus muscles. This circular-shaped muscular structure is often recognised as a static barrier that, due to weakness and/or together with other causes, fails in its role and allows indirect inguinal hernia protrusion. According to the results of our observations, we consider this concentric muscular complex as a dynamic formation: we will use the term "striated sphincter complex." Its steady tightening motion after divulsion and the insertion of a lamellar implant is always accompanied by a strong gripping action, which is not seen prior to divulsion. This indicates that it could correspond to a sphincter: the "inguinal sphincter." The impairment of this sphincter could be the cause of the inguinal canal's patency and the development of hernia.