The biomechanics of uterine prolapse impact rectal intussusception, ODS and surgical restoration

Excerpt

Prior to commencement of labor, the collagen of connective tissue in the birth canal depolymerizes and loses 95% of its strength [1]. Depolymerization plasticizes all connective tissues, so it can stretch, but does not rupture. The biomechanics of uterine prolapse commence at the entry to the birth canal. At 10 cm dilatation of the cervix, the cardinal (CL) ligaments may stretch to cause a cystocele and further down, a recto-peri-neocele; the uterosacral ligaments (USLs), may lengthen to cause uterine prolapse (Fig. 1). The USLs are attached to the lateral wall of the rectum by filamentous ligament-like structures. Extreme USL damage may cause the USLs to lengthen considerably, resulting in 3rd- or 4th-degree uterine prolapse. When the uterus descends, the USLs lengthen and invariably splay laterally, to create an enterocele. Lateral displacements of USLs carry the lateral rectal wall with them (Fig. 1). Consequently, the anterior rectal wall stretches laterally, widening it, so it prolapses inwards to cause intussusception, (Fig. 1). Such anatomical distortion would naturally alter the morphological and biomechanical properties of the anterior rectal wall.

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