Use of the silastic sheath in bladder neck reconstruction.

OBJECTIVE: The study compared two populations of patients undergoing bladder neck reconstruction using the silastic sheath in two major pediatric centers. The success with this technique was markedly different in the two centers. The purpose of the study was to determine factors that might explain the divergent results. PATIENTS AND METHODS: Fifteen patients treated in Indianapolis were compared with 94 patients treated in London with the silastic sheath technique of bladder neck reconstruction. Eighty-seven percent of the Indianapolis patients had myelomeningocele whereas 86% of the London group had exstrophy/epispadias. Median age of the Indianapolis patients was 11 years whereas it was 8.4 years in London. Seventy-three percent of patients in Indianapolis were female and 79% in London were male. Patients were followed for a minimum of eight years in Indianapolis and a mean of seven years in London. Similar surgical technique was employed in the two centers but, over time, the London approach included use of a non-reinforced silastic wrapped loosely around the bladder neck with the interposition of omentum. RESULTS: Both groups achieved continence rates exceeding 90%. Of the Indianapolis patients, two-thirds experienced erosion of the silastic at a mean of 48 months. With modifications in the London technique, the erosion rate of silastic was lowered from 100% to 7%. CONCLUSION: Direct, snug wrap of silastic without omentum around the Young-Dees tube as well as simultaneous bladder augmentation placed patients at increased risk for erosion. The silastic sheath technique may be less applicable to myelomeningocele patients. It seems most applicable to older male patients with exstrophy or epispadias undergoing Young-Dees bladder neck reconstruction who have the ability to void.

Bladder hemangioma as a cause of massive hematuria in a child. A case report and literature review.

A 12-year-old girl with bladder hemangioma presenting with massive hematuria is described. The patient was previously operated for removal of cystic hygroma from the chest wall. The association of those two pathological entities suggests possible common etiology and pathogenesis and the various therapeutic options are reviewed.

Bladder neck reconstruction: long-term followup of reconstruction with omentum and silicone sheath.

PURPOSE: In 1986 we reported the placement of a silicone sheath sandwiched between layers of omentum around a newly reconstructed bladder neck. We now present long-term followup of 94 cases of silicone sheath bladder neck reconstruction. MATERIALS AND METHODS: A total of 94 silicone sheaths was placed in 84 patients between August 1983 and October 1992. We retrospectively reviewed our results and divided the reconstructions into 3 groups according to modifications in surgical technique. We report the results of each modification and current recommendations for use. RESULTS: Each sequential modification of silicone sheath bladder neck reconstruction significantly reduced the risk of erosion from 100%, 32% and 7%, respectively (p < 0.05). Erosion was independent of patient age, sex, pathological condition or whether bladder neck reconstruction was a repeat procedure. Patients who had silicone sheath erosion did not have different continence or loss of urethral continuity than those with no erosion. In 13 patients (16%) artificial sphincter placement was clearly facilitated by the silicone sheath. CONCLUSIONS: Modifications in the surgical technique of silicone sheath placement around a reconstructed bladder neck have resulted in a decrease in the erosion rate to 7%. The primary benefit of silicone sheath placement is ease of subsequent sphincter placement. Currently we reserve silicone sheath placement for a small subset of patients who are most likely to benefit from subsequent artificial sphincter placement.

Lower pole heminephrectomy: its role in treating nonfunctioning lower pole segments.

PURPOSE: We assessed the role and long-term outcome of lower pole heminephrectomy in the treatment of nonfunctioning lower renal moieties in children with duplex kidneys. MATERIALS AND METHODS: Between 1979 and 1994, 54 lower pole heminephrectomies were performed in 53 patients 1 to 192 months old (mean age 54) with duplex systems. A total of 15 patients was prenatally diagnosed, while the others presented with a urinary tract infection (36), orchiepididymitis (1) and failure to thrive (1). The surgical technique was essentially similar to that of upper pole heminephrectomy. RESULTS: Operative course was uneventful except for intraoperative bleeding in 5 cases, which necessitated blood transfusion, and a postoperative urinary tract infection in 1. Followup ranged from 3 to 168 months (mean 56.9). Postoperative renograms available in 34 cases showed unchanged differential function in 12 and an ipsilateral 2 to 14% decrease (mean 5.65%) in 22. No late complications were detected except in 1 patient, who had postoperative urinary tract infections and subsequently underwent removal of the ureteral stump. Our series includes 4 patients with solitary ipsilateral upper poles (after the contralateral kidney was removed or nonfunctioning) who had good renal function at long-term followup despite the reduced parenchymal mass. CONCLUSIONS: Based on our experience it seems that lower pole heminephrectomy is the treatment of choice in cases of nonfunctioning dilated lower segments of duplicated kidneys.

Nicotine has no effect on rat gastric mucosal prostaglandin generation in vitro.

Previous studies have shown that cigarette smoking depresses prostaglandin generation by human gastric mucosa, but the component of smoke that is responsible for that action is not known. To investigate whether nicotine has a direct effect on gastric mucosal prostaglandin generation, we performed the following study. Eight rats were sacrificed and the stomachs removed. Using a biopsy forceps, small pieces of gastric mucosa were resected and placed in incubation vials containing either buffered Krebs solution alone (control), Krebs solution plus indomethacin (5 micrograms/ml), or Krebs solution plus one of several concentrations of nicotine ditartrate (10, 100, 500, 1000 ng/ml). The nicotine concentrations we used ranged below and above the plasma nicotine concentrations of smokers shortly after smoking cigarettes. Three separate incubations of gastric mucosa were performed per experimental group from each animal. After 30 min of incubation, prostaglandin E2 and 6-keto-prostaglandin F1 alpha concentrations in the incubation medium were measured by radioimmunoassay. We found that nicotine at any concentration tested had no effect on the generation of prostaglandin E2 and 6-keto-prostaglandin F1 alpha by rat gastric mucosa. Thus, this study indicates that, if nicotine is involved in the depression of prostaglandin generation in the gastric mucosa of smokers, its role is an indirect one and not by direct action on the gastric mucosa.

Effects of stress on gastric mucosal prostaglandin generation in intact, adrenalectomized, and sham-operated rats.

UNLABELLED: To study the effects of (a) cold restraint stress and (b) adrenalectomy in association with cold restraint stress on gastric mucosal ulceration and prostaglandin generation, we performed two experiments. In the first, 40 rats were divided into four groups of 10 rats each: (a) unstressed and (b) stressed for 0.5 h, (c) stressed for 2 h, and (d) stressed for 4 h. In the second experiment, another 80 rats were divided into four groups of 20 rats each: (a) adrenalectomy plus cold restraint stress for 2 h, (b) adrenalectomy plus no stress, (c) sham operated plus 2 h of stress, and (d) sham operated plus no stress. In both experiments we recorded an ulcer index and measured mucosal generation of prostaglandin E2 (PGE2) and prostaglandin I2 (6-keto-PGF1a). IN CONCLUSION: (a) Cold restraint stress is associated with a time-dependent decrease in gastric mucosal PGE2 generation, but no change in 6-keto-PGF1a generation, and an increase in mucosal injury that is maximal by 2 h. (b) Adrenalectomy augments the effects of stress on mucosal injury but has no effect on prostaglandin generation; thus, the ulcerogenic effect of adrenalectomy appears to be independent of an effect on prostaglandin generation.

Active smoking depresses prostaglandin synthesis in human gastric mucosa.

To determine the effect of smoking on gastroduodenal mucosal prostaglandin synthesis, endoscopies were done after an overnight fast on 10 nonsmokers, 12 active smokers who smoked four cigarettes in the hour before endoscopy, and then 11 of the smokers who refrained from smoking for 12 hours. Biopsy samples of fundic, antral, and duodenal mucosae were incubated, and the accumulation of prostaglandin E2 and 6-keto-prostaglandin F1 alpha in the incubation medium was measured by radioimmunoassay. We assumed that accumulation of prostaglandins in the medium reflected mucosal synthesis. Comparison of active and inactive smoking showed that active smoking significantly depressed 6-keto-prostaglandin F1 alpha synthesis in antral and fundic mucosa and prostaglandin E2 synthesis in antral mucosa. Comparison of nonsmokers and inactive smokers showed no difference in prostaglandin synthesis. Active smoking causes a transient decrease in prostaglandin synthesis in fundic and antral mucosae. This depression of prostaglandin synthesis may help explain slower ulcer healing and predisposition to ulcer recurrence in smokers.

Effect of chronic cimetidine ingestion on fundic and antral epithelial proliferation in the rat.

Recent reports of the association of cimetidine treatment with the development of gastric carcinoma stimulated us to study the effect of chronic cimetidine ingestion on epithelial proliferation in the stomach of male Wistar/Lewis rats. One group of rats received cimetidine in the drinking water to deliver 150-200 mg/kg/day. Control rats received plain water. To label proliferating cells, the rats were injected by tail vein with tritiated thymidine 1 hr before sacrifice at 1, 6, and 12 months. Sections of fundus and antrum were processed for light autoradiography. We found no histological evidence for malignant change and no effect on the measurements of epithelial proliferation by cimetidine in either fundus or antrum at any of the times studied, with the possible exception of an upward shift in the distribution of labeled cells within the proliferative zone of the fundus after 6 months. Thus, under the conditions of our experiments we have been unable to identify an effect of cimetidine on epithelial proliferation which would implicate it as a chemical carcinogen.

Effect of chronic aspirin ingestion on epithelial proliferation in rat fundus, antrum, and duodenum.

We studied the effect of chronic aspirin ingestion on gastroduodenal epithelial proliferation by feeding rats aspirin in the drinking water. A control group of rats received plain water. At the end of 4 wk, [3H]-thymidine was given intravenously to label proliferating cells, and the rats were killed 1 h later. Sections of fundus, antrum, and proximal duodenum were processed for light autoradiography. We found that chronic aspirin ingestion stimulated epithelial proliferation in fundic mucosa but had no effect in the antrum. In the duodenum, aspirin increased proliferation in the lowest four crypt-cell positions, which most likely indicates an increase in stem-cell production. None of the tissues contained evidence of inflammation or ulceration. The proliferative effects of aspirin may help explain the previously observed phenomenon of mucosal adaptation in the rat after repeated exposure to aspirin. Further, if human gastroduodenal epithelium responds in a similar manner to chronic aspirin exposure, the effects on proliferation may explain in part the distribution of aspirin-associated ulcers.

Effect of N-methyl-N'-nitro-N-nitrosoguanidine on gastroduodenal epithelial proliferation in Wistar/Lewis rats.

The effect of N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) on gastroduodenal epithelial proliferation p]rior to the development of frank neoplasia was studied in inbred LEW rats with or without gastric ulcers. The rats received either MNNG (100 gm/liter) in the drinking water or plain water. After 4 weeks, some rats in the MNNG-treated and control groups were given injections of tritiated thymidine and killed 1 hour later. In other rats, either an ulcer of the fundic mucosa was formed by a suction biopsy tube at laparotomy or a sham operation was performed. At 2 and 4 weeks after the operation, these rats were given injections of tritiated thymidine and killed 1 hour later. Sections of fundus, antrum, and duodenum were prepared for light autoradiography. MNNG treatment stimulated gastroduodenal epithelial proliferation, expanded the proliferative zone (PZ), and in the duodenum caused marked villus blunting and elongation of the crypts. No additional effect of the fundic ulcer or sham operation on gastroduodenal proliferation could be determined. The MNNG-induced expansion of the PZ occurred in a downward direction. Thus theories of carcinogenesis should include not only the expansion of the PZ toward the mucosal surface but also the possibility of expansion of the PZ toward the base of the mucosa.