Co-morbidity and interstitial herniation in the adult: an hypothesis

Whereas interstitial hernias of infancy are a result of congenital abnormalities, those in adults have been blamed on anatomical banding. Many of the latter are associated with systemic, genetic, or acquired connective tissue disease, however. This results in attenuated aponeuroses, ruptured tendons, and atrophied fascia from collagen malformation and destruction. Muscle contractility is compromised by loss of connective tissue septae, reducing capillary density. The result is wasting and disaggregation, which explains interstitial defects filled with herniated extraperitoneal fat, which account for 1% of primary inguinal herniae. These were originally described in the transversus and internal oblique musculature by Hessert (Surg Gyn Obstet 16:566–568, 1913). Similar slits are seen with Spigelian herniae, all of which are interstitial. This hypothesis, if proven, would imply treatment of the pervasive co-morbidity with the protrusions.