With any major abdominal surgery there are associated cardiovascular, respiratory, and gastrointestinal complications. Postoperative mortality rates have been reported between 0 and 3.2% [49, 78, 80–87] and were generally the result of postoperative myocardial infarction (0–2.7%) and pulmonary embolus/deep vein thrombosis (0–7%) [39]. There have been a small number of reports of other severe complications, such as major bleeding requiring reoperation [39] and necrosis of the bowel segment [8, 87].

Small bowel obstruction requiring operative intervention may occur in 3–6% of patients, and approximately 5–6% of patients may develop a wound infection or dehiscence [49]. Anastomotic leak from the bladder occurs in 2–4% of patients. Postoperative ileus is common, and prolonged ileus occurs in approximately 5% of patients [49]. Severe postoperative complications are less frequent in contemporary case series [49].

Several groups have reported long-term functional outcomes in adult and pediatric populations. Blavias and colleagues [70] reported on 65 adult patients who underwent augmentation cystoplasty (primarily with an ileocecal segment) with or without creation of an abdominal stoma (and included an additional 11 patients who had a continent diversion). At a mean follow-up of 5 years, 70% considered themselves cured, and 18% considered themselves improved. Failures consisted almost exclusively of interstitial cystitis patients. Mean bladder capacity increased from 166 to 572 mL, and mean maximal detrusor pressure fell from 53 to 14 cmH₂O. Flood and coworkers [42] reported on 122 augmentation cystoplasties (67% ileocystoplasty, 30% ileocecocystoplasty) with a mean follow-up of 3 years. They had a primarily adult population. They reported similar urodynamic improvements, a 75% cure rate, and a 20% improvement rate in incontinence.

Quek and Ginsberg [88] reported durability of the urodynamic improvements and 96% patient satisfaction among 24 patients with a mean follow-up of 8 years (range 4–13).

Herschorn and Hewitt [78] preformed a cross-sectional survey of 59 adults who underwent augmentation cystoplasty (usually with additional simultaneous reconstructive procedures) at a median follow-up of 6 years. Sixty -seven percent of patients reported complete continence, and 30% reported only mild incontinence (requiring on average 1–2 pads per day). Almost all patients were very satisfied with their urologic management.

Results in the pediatric populations are similar although the majority of patients require additional reconstructive procedures such as ureteral reimplantation, bladder neck procedures, and creation of catheterizable channels. Lopez Pereira and coworkers reported on 29 children with a mean follow-up of 11 years [89]. Mean postoperative bladder capacity increased from 90 to 521 mL, and mean maximal detrusor pressure fell from 45 to 10 cmH₂O. Shekarriz and coworkers reported a 95% continence rate among 133 pediatric patients at a mean follow-up of 5 years [58].

A number of authors have compared the outcomes of ileum, ileocecal, and sigmoid segments and have not shown any consistent advantages of any segment in terms of urinary continence or renal function [87, 90–92]. Urodynamically demonstrated contractions might persist postoperatively with colonic segments [56, 93].

Small case series by Mundy and Nurse [94] and Wagstaff and coworkers [95] were the first to suggest there is a decrease in linear growth in children after augmentation cystoplasty. Since then, several additional studies have been published, of which 2 suggested there is approximately a 15% decrease in linear growth after augmentation and 6 which did not demonstrate a significant change to linear growth [96, 97]. There is also contradictory evidence as to whether decreased bone mineral density or osteopenia is a result of the augmentation [97]. In a case series of 24 children followed for an average of 9 years after augmentation, Hafez and coworkers reported a 20% incidence of significant osteopenia [98]. The osteopenia is likely a result of buffering of the acidosis by the skeletal system, which leads to changes in bone mineralization [99]. Correction of this acidosis may improve bone density [100]. Other mechanisms of osteopenia include reduced renal tubular reabsorption of calcium and intestinal malabsorption of calcium [101]. In a recent study, Haas and colleagues demonstrated that bone mineral density was significantly related to ambulatory status and secondarily to neurological level rather than to the presence or absence of augmentation cystoplasty [102]. The long-term impact of the osteopenia and how it affects children as adults is still unknown [97].

Management includes appropriate screening and treatment of postoperative metabolic acidosis. Patients with renal failure are more likely to have uncompensated acidosis and should be followed closely and treated for this complication. Some authors have advocated bone mineral density measurements after augmentation [98].

The expected pattern of metabolic abnormality is dependent on the segment of bowel used in the augmentation cystoplasty. Other factors that influence the severity of the electrolyte imbalance include the surface area of the augmentation, urine pH, and the urine contact time [101].

Deterioration of renal function may occur in 0–15% of patients after augmentation [49]. It is unknown whether this is a direct result of the augmentation or due to associated complications [113]. Renal insufficiency occurs independent of the bowel segment selected [114, 115]. The etiology of renal dysfunction may be urinary stone disease, bacteriuria, high detrusor pressures, vesicoureteral reflux, unrecognized obstruction, and lack of compliance with catheterization [114]. One study suggests approximately 5% of patients will have renal dysfunction after augmentation without a clear etiology [114]. Some authors have demonstrated that baseline renal function is a significant predictor of renal deterioration after augmentation cystoplasty, with an increased risk when creatinine clearance is <40 mL/min [8, 49, 116, 117]. Other studies in children and adults with baseline renal dysfunction did not appear to demonstrate that they have accelerated renal failure after augmentation cystoplasty [51, 78].

In a recent review of 80 patients treated at the Mayo Clinic with ileocystoplasty and simultaneous bladder neck outlet procedure after a median follow-up of 14 years (range, 8–45 years), Husmann reported upper tract deterioration in 40% (32/80) of the patients. Development of ≥ stage 3 chronic renal failure occurred in 38% (12/32) of the patients with scarring, i.e., 15% (12/80) of the total patients. Prior to the development of the renal scarring, 69% (22/32) of the patients had been noncompliant with intermittent catheterization. He attributed the new onset renal deterioration largely to patient noncompliance with medical directive [118].

Although there is no published consensus on the order of performing augmentation cystoplasty and renal transplant, there are no significant differences between pretransplant and posttransplant AC. It therefore seems reasonable to perform the AC before a kidney is transplanted to avoid damage to the graft from the hostile bladder [17]. Graft survival and function after AC also appear to be similar to those in children with normal bladders [17].

Postoperatively, patients should have renal imaging and serum creatinine measurements to screen for renal insufficiency [106]. Serum creatinine can be difficult to interpret in this population, due to a low muscle mass in neurogenic patients, and increased reabsorption of urine creatinine by the ileum. Nuclear renograms may be better for definitive measurement.

Vitamin B12 is bound to intrinsic factor in the duodenum which allows is to be absorbed in the terminal ileum. With ileocystoplasty, the most distal 15 cm of the ileum should be preserved to prevent this complication [106]. Vitamin B12 deficiency may cause megaloblastic anemia and neurologic changes [106]. In nutritionally normal individuals, it takes up to 3 years for the liver’s store of B12 to be depleted and the resulting deficiency to manifest. The incidence of B12 deficiency related to ileal resection is 3–20% [106, 119].

This complication may be treated prophylactically with B12 supplementation if more than 50 cm of ileum is used for the bladder augmentation [120]. Otherwise, patients should have complete blood counts in follow-up to screen for pernicious anemia.

Bladder cancer has been reported in young patients after augmentation [79, 121, 122]. It has also been reported that spinal cord injury patients and spina bifida patients develop bladder cancer at a young age (40–50 years), have an increased risk of locally advanced disease, an increased number of adenocarcinomas and squamous cell carcinomas, and a short median survival after diagnosis [77, 123]. In a matched cohort study from a registry of patients with bladder dysfunction due to neurologic abnormalities, exstrophy, and posterior urethral valves, Higuchi and colleagues did not find a significant difference in the incidence of bladder cancer among patients with augmentation cystoplasty (using ileum or colon) compared to patients managed with intermittent catheterization [76]. The authors did demonstrate that the incidence of bladder cancer was higher in both groups with congenital bladder anomalies independent of augmentation status when compared to the SEER database. Possible reasons for a higher rate of bladder cancer in patients with neurogenic bladder may be reduced intracellular antioxidant activity (leading to increased rates of DNA mutation) [124], impaired DNA repair in the bowel due to the hyperosmolar urine [125], and immunosuppressant use in patients after renal transplantation [76]. However, patients who have undergone a gastric augmentation may have a higher cancer risk compared to other bowel segments [76]. In a subsequent report, Rove and Higuchi presented more case series to illustrate that congenital bladder anomalies alone are a risk factor for malignancy [126]. Current screening tests such as cystoscopy and cytology are not cost effective and have not diagnosed the cancers.

In a recent systematic review of 57 articles involving malignancy and AC, Biardeau and colleagues [127] concluded that AC is associated with a risk of malignancy. In spite of its limitations, annual cystoscopy surveillance is the only validated tool available for diagnosis. It should be started 10 years after surgery and accompanied by clinical examination and surveillance imaging [127].

Urologists should have a particular awareness of the potential for aggressive bladder cancer in this population whether or not they have had an AC. Symptoms such as hematuria, frequent urinary infections or penile/scrotal discharge need to be aggressively investigated; visual changes in the bladder due to the augmentation, recent infections, or catheterization can make cystoscopy challenging, and biopsy or CT should be considered if there is any uncertainty [123].

Bladder perforation is a potentially life-threatening complication that occurs in approximately 6–13% of patients [23, 128–132]. Patients with neurogenic bladders, those with competent bladder necks, those without a catheterizable channel and those who abuse alcohol appear to be at an increased risk [23, 49, 133, 134]. Perforation can occur at any time postoperatively, even years after surgery. It can present with fever, abdominal pain, and distension with intraperitoneal extravasation of urine, nausea and vomiting, referred shoulder pain, peritonitis, and septic shock [58, 130]. Because of neurologic abnormalities of these patients, the presenting symptoms are often nonspecific. Diagnosis can be made with a CT cystogram; standard fluoroscopic cystography has a 10–20% false negative rate [58, 129, 135]. CT or US can demonstrate intraperitoneal fluid which is an important sign that bladder perforation has occurred [136]. Due to the augmentation, extraperitoneal ruptures are rare [137]. The area of perforation is usually at the bowel-bladder anastomosis or within the weaker bowel wall [129]. The etiology of bladder perforation is thought to be from traumatic catheterization, acute over distension, increased intravesical pressure, chronic overdistension (from CIC noncompliance), or infection leading to localized areas of ischemia and necrosis [135, 138].