The influence of urinary diversion on experimental gastrocystoplasty

Gastrocystoplasty is used to augment the bladder of patients with decreased renal function to prevent development or worsening of metabolic acidosis. We recently observed a perforated peptic ulcer in the gastric portion of a defunctionalized gastrocystoplasty. We postulated that the lack of buffering action of urine precipitated peptic ulcer disease in the gastrocystoplasty. To explore this possibility further, we conducted an experiment. In 12 adult female mongrel dogs (weight 15 to 26 kg.) the bladder was divided into right and left segments. One kidney was removed and both hemibladders were capped with a vascularized segment of gastric body. Thus, 1 side (wet) remained exposed to urine, while the other side (dry) was drained to the abdominal wall with a cystostomy tube. The animals were divided into 2 groups: 9 in group 1 received no drugs to modify gastric secretion and 3 in group 2 received a hydrogen (H2) blocker. Three animals in group 1 had perforation of the vesical part of the dry gastrocystoplasty 2 to 3 weeks postoperatively and were sacrificed. The others were sacrificed 3 to 6 weeks postoperatively. Serum gastrin levels remained normal in all animals. Gross and histological examinations of the augmented bladders in group 1 revealed ulcerations of the bladder segment of the wet and dry gastrocystoplasties but the lesions were more numerous and prominent on the dry side in all animals, particularly those in which the perforations occurred. A peptic ulcer was noted in the gastric portion of the dry gastrocystoplasty in 1 animal. The bladder epithelium of the dry gastrocystoplasty showed glandular metaplasia in several animals in this group. In group 2 the wet gastrocystoplasty showed normal histology except in 1 dog that had mild inflammation and focal superficial ulceration in the vesical portion. On the other hand, the dry gastrocystoplasty showed severe inflammation and ulcerations in 2 animals, and mild inflammation of the vesical portion in 1. There were no perforations in this group. This experiment demonstrates that gastrocystoplasty produces cystitis but that these changes are more prominent in the absence of urine, as indicated by the severity of the lesions, perforations and metaplasia. Peptic ulcer disease occurred in the gastric portion of the dry gastrocystoplasty in 1 animal. The use of H2 blockers decreases the incidence of ulceration in wet gastrocystoplasty but it seems to have less influence on the ulceration of dry gastrocystoplasty. Clinicians must be alerted to the risk of perforation of dry gastrocystoplasty.