Bladder augmentation and urinary diversion in patients with neurogenic bladder: Non-surgical considerations

Abstract

Segments from almost all parts of the bowel have been used for urinary diversion. As a result, the available absorptive surface area of the bowel is reduced, and the incorporation of bowel segments into the urinary tract may have metabolic consequences. This is an area somewhat neglected in the literature. Metabolic complications are rare, but sub-clinical metabolic disturbances are quite common. Several studies have demonstrated that some of the absorbent and secreting properties of the bowel tissue are preserved after incorporation into the urinary tract. Hyperchloraemic metabolic acidosis can occur if ileal and/or colon segments are used, as well as malabsorption of vitamin B (12) and bile acid after the use of ileal segments. These metabolic effects are not as severe as may be suspected and can be prevented by prophylactic substitution. Secondary malignancies can develop as a long-term consequence of bladder augmentation. Using colonic segments, tumours are most likely to occur at the ureteral implantation site. To prevent metabolic complications, careful patient selection and meticulous and lifelong follow-up, as well as prophylactic treatment, are mandatory. Endoscopy for early detection has been recommended, starting 10 years postoperatively for patients who underwent surgery for a benign condition. Editorial CommentThis a nice review on the topic of non surgical complications implicated in bladder augmentation and urinary diversion in pediatric neurogenic bladder patients. Although the article does not bring any outrageously new fact out it does remind us of the severe implications that may take place following this type of surgery, notably in children. There should be a concern regarding this specific population as less invasive treatments lack efficacy and must be repeated continuously and regularly for a lifelong period.Although the use of intestinal segments have been widely used for many years it seems clear that it is far from being the ideal solution. Research in tissue engineering may bring a more suitable alternative in the future.

Orthotopic neobladder reconstruction

“…These ions are absorbed in exchange with sodium and bicarbonate from the blood stream, thus resulting in hyperchloremic, hyperkalemic metabolic acidosis and salt-loss syndrome. [ 6 7 ] These conditions can manifest clinically with lethargy, fatigue and dehydration. It is important to detect and treat metabolic acidosis early as it can induce calcium resorption from bone and hypophosphatemia thus leading to osteoporosis and osteomalacia.…”

Emerging Concepts in Transitional Care of Congenital Genitourinary Reconstructions

“…While gastric augmentation is currently rarely employed, alkalosis and hematuria are demonstrated complications [75]. Patients with chronic acidemia are at risk for osteomalacia and osteoporosis as adults [76]. Thus, acidosis should be promptly corrected, and dietary supplementation with calcium and vitamin D may be necessary.…”

Growth morbidity in patients with cloacal exstrophy: a 42-year experience

“…Abnormalities of the upper urinary tract are seen in up to two thirds of patients, and lower urinary tract reconstruction may be complicated by metabolic and infectious sequelae (5). Mild to moderate metabolic acidosis is reported in 15% of patients with incontinent urinary conduits and in approximately half of patients with continent urinary diversions, likely due to the longer segment of bowel used and the longer dwell time of urine within the pouch (5). Gastrocystoplasty does not result in metabolic acidosis, and also has the advantage of enteral sparing for patients who have relatively short bowel (6).…”

“…It results in increased in urine calcium loss (as calcium is committed to H + as a buffer), increased intestinal sulfate absorption, which inhibits renal tubule calcium reabsorption, and the direct activation of osteoclasts causing growth disturbance and reduced bone mineral density (5, 7). Acidosis also blunts the release of growth hormone, and animal models have shown suppressed serum IGF-1, hepatic IGF-1 mRNA and hepatic growth hormone receptor mRNA, and decreased gene expression of IGF-1 at the growth plate of the long bones (8).…”

“…Renal insufficiency is an important risk factor for uncompensated acidosis, and the majority of patients have upper urinary tract anomalies, including renal agenesis, pelvic kidneys, horseshoe kidneys, fusion anomalies, hydronephrosis, or ureteral anomalies (5). A predilection for renal impairment may be compounded by recurrent urinary tract infections (4).…”