Perforation
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
|
K+
|
Cl+
|
Notes
|
|
Stomach
|
Alkalosis
|
↓
|
↓
|
Respiratory insufficiency, seizure, arrhythmia
|
|
Jejunum
|
Acidosis
|
↑
|
↓
|
Hyponatremia, azotemia, malabsorption
|
|
Ileum/colon
|
Acidosis
|
↓
|
↑
|
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
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.
Malignancy
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
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.
