Monday, March 11, 2013

Augmentation Cystoplasty (part 11)


Approximately 6% of patients who undergo augmentation cystoplasty experience perforation.[26] These patients may present with various signs and symptoms, including acute abdomen or a vague illness with nausea, vomiting, fever, or abdominal distention. Patients are generally quite ill, and sepsis and death are possible.
Neurologically impaired patients with decreased abdominal sensation may present with different symptoms or may present later in the course than patients without neurologic impairment.
Traditional or computed tomographic (CT) cystography (imaging after retrograde administration of intravesical contrast) is the best method of evaluation if the patient is clinically stable. Patients diagnosed with perforation of the augmented bladder and those who are hemodynamically unstable with suspected perforation require urgent operative exploration and repair.
Early perforation usually occurs along the anastomosis and is usually due to poor healing or technical issues. The etiology of late perforation is unclear; however, ischemia, infection, inflammation, or overdistention may be involved. Injury with self-catheterization may be responsible for some cases of perforation. Rivas et al showed in an animal model that augmented bladders stressed with infused volume tend to rupture within the dome (7 of 11 cases) and at a suture line (4 of 11 cases).[27]
Consultation with a neurosurgeon should be considered in patients with a ventriculoperitoneal shunt who experience bladder perforation.

Urolithiasis and mucus

Stone formation, both of the kidney and of the bladder, occurs in 18-50% of patients after augmentation. Struvite is the most common stone composition; thus, treatment should be initiated immediately for bacteriuria with urea-splitting organisms.
Other risk factors for stone formation include incomplete emptying (by poor voiding or by catheterization through a stoma) and increased mucus (which can serve as a nidus for stone formation). Large intestine creates more mucus than small intestine, and gastric patches produce little mucus. Gastrocystoplasty is also slightly protective against stones because of the increased acidity, which minimizes bacteria.
At present, there are no uniform recommendations to guide the metabolic workup in patients with augmented bladders who form stones. A 24-hour urine profile for pH, volume, citrate, calcium, phosphorous, oxalate, and sodium, along with serum electrolytes and urine culture, is appropriate. A surveillance abdominal plain film obtained annually may be used to identify a few small stones before they grow into multiple large stones that require more involved treatment.
Treatment options for stones in the augmented bladder include the following:
·         Extracorporeal shockwave lithotripsy
·         Endoscopic fragmentation or removal through the urethra or a catheterizable stoma
·         Percutaneous fragmentation or removal
·         Open surgery
In addition to serving as a nidus for urolithiasis, mucus can obstruct the outlet and increase the possibility of infection or perforation. Daily irrigation may decrease the risk of these complications. Irrigants can include tap water, saline, urea, N -acetylcysteine, or 3% sodium chloride.

Metabolic derangements

Except for stomach segments, which cause hypokalemic hypochloremic metabolic alkalosis, most intestinal segments used for augmentation cystoplasty can cause metabolic acidosis (see Table 2 below).[28]
Table 2. Metabolic Changes Caused By the Use of Various Tissues in Augmentation Cystoplasty
Intestinal Segment
Acid-Base Effect
Respiratory insufficiency, seizure, arrhythmia
Hyponatremia, azotemia, malabsorption
Diarrhea with loss of colon, ileocecal valve

Jejunal segments, which are rarely used, can cause volume contraction and hyperkalemia, whereas ileal and colon segments can cause hyperchloremia. The acidosis caused by these segments is of concern in younger patients who are susceptible to growth retardation and bone density loss due to occult or recognized acidosis. The exact mechanism has yet to be elucidated, but oral bicarbonate replacement may obviate some of these effects.
In addition, patients with baseline renal insufficiency are at significantly greater risk for the development of marked serum acidosis. This can manifest as weakness, fatigue, thirst, and failure to thrive. Screening for patients who need bicarbonate replacement is also helpful in this setting.
Because of the effects on volume and electrolytes, the use of jejunal segments is typically avoided in bladder augmentation, urinary reservoirs, and urinary conduits. The use of gastric segments may decrease the potential need for bicarbonate replacement in patients with renal insufficiency who have acidosis; however, severe metabolic derangements may still develop. Rink et al reported on episodes of severe hypokalemic hypochloremic metabolic alkalosis developing after GI illness.[29]

Hypercontractility and hypocontractility

Hypercontractility and poor compliance are more common with the use of sigmoid bowel segments but can occur with any segment despite adequate detubularization. In some cases, this complication can necessitate reaugmentation.
Hypocontractility of the augmented bladder with incomplete voiding is also a possibility that patients should understand before surgery. Patients must be physically and emotionally prepared to perform intermittent catheterization for life.


Incontinence may occur if the enteric segment used for augmentation provides insufficient volume or has forceful contractions. Preoperative assessment of urine output is helpful in determining the desired volume for the augmented bladder. In addition, proper detubularization is crucial to prevent forceful contractions of the enteric segment, especially when sigmoid colon is used.
Retained mucus or stones may reduce the effective volume of the augmented bladder, and urine may leak through a poorly constructed catheterizable stoma. Urinary tract infection (UTI) may also lead to detrusor instability and incontinence. Poor outlet resistance at the bladder neck or external sphincter will cause urinary leakage if it is not diagnosed before augmentation cystoplasty and addressed at the time of surgery.

Hematuria/dysuria syndrome

A symptom complex characterized by hematuria, dysuria, or both occurs with voiding or catheterization in as many as 33% of patients after augmentation gastrocystoplasty. Continence is particularly important in patients with gastrocystoplasty because of the perineal and peristomal skin irritation that can occur as a consequence of low urine pH. Patients with renal insufficiency, low urine volume (acting as acid buffer), incontinence, and a sensate abdomen and pelvis may be at an increased risk for this syndrome.
Treatment options include type II histamine blockers or proton pump blockers, and failed medical treatment may necessitate takedown and reaugmentation with ileum.


Augmented bladders appear to be at greater risk for malignancy.[30]Adenocarcinoma is the most commonly observed tumor, and all segments seem to be associated with the same level of risk. The average time to malignancy after augmentation is around 2 decades, but cancer has been found as early as 4 years after surgery.
For this reason, some begin surveillance cystoscopy as soon as 2 years after surgery. Filmer and Spencer recommend that patients with augmentation cystoplasty undergo yearly cytology and endoscopy and that they undergo biopsy beginning 10 years after surgery.[31] Some advocate general anesthesia during surveillance cystoscopy, on the grounds that thorough examination is crucial and should not be limited by patient discomfort.

Small bowel obstruction

Approximately 3% of patients may develop a small bowel obstruction at any time after augmentation cystoplasty. Parastomal hernia, internal hernia, and volvulus can also occur.


Diarrhea can result from the removal of the ileocecal valve from the intestinal tract in the course of the augmentation procedure. This is more likely in pediatric patients with neurogenic bladder and intestinal dysfunction. Removal of the ileocecal valve may yield a decreased stool transit time or may allow retrograde colonization of the distal small intestine, with fat malabsorption in this segment. Increased delivery of bile salt to the colon may cause secretory diarrhea.

Other complications

The removal of the terminal ileum from the alimentary tract leads to compromised vitamin B-12 and bile salt reabsorption. In addition, retrograde colonization of colonic bacteria into the small bowel can interfere with absorption. These can lead to megaloblastic anemia and diarrhea.
Early satiety after gastrocystoplasty is uncommon and is usually self-resolving.



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