Ischemic necrosis: a hypothesis to explain the pathogenesis of spontaneously ruptured enterocystoplasty

Spontaneous enterocystoplasty rupture represents a devastating and potentially fatal late complication. Previously proposed mechanisms of rupture include catheter trauma, chronic infection, avulsion of adhesions between the bowel patch and peritoneum, and chronic overdistension with elevated intravesical pressures. We have witnessed this complication 4 times in 3 patients 5 weeks to 46 months postoperatively. Tissue specimens from 3 episodes in 2 patients with detubularized sigmoid enterocystoplasties were available for histological examination. All patients had a neurogenic bladder from myelomeningocele, all had an AMS800 artificial urinary sphincter and all had a documented history of chronic distension from inadequate emptying of the augmented bladder. At exploration, all of the ruptures were found within the bowel segment near the bladder apex in an area remote from the anastomotic line. In each case tissue specimens from the rupture site showed marked vascular congestion, intramural hemorrhage, abundant hemosiderin laden macrophages, myofiber atrophy and intravascular thrombi. These features are interpreted to reflect the sequelae of vascular compromise and ischemia. We propose that enterocystoplasty rupture results from ischemia, possibly due to chronic overdistension and subsequent vascular compromise. This mechanism may account for many of the previously reported cases of enterocystoplasty rupture.