Gastrocystoplasty in Patients with an Areflexic Low Compliant Bladder

Aim: This study was performed with the aim of evaluating gastrocystoplasty as a method of management of patients with an areflexic low compliant bladder. Patients and Methods: We performed gastrocystoplasty in 30 patients (19 males and 11 females) with an areflexic low compliant bladder. The mean age of the patients was 23.4±11 years (range 4–32). The etiology of lower urinary tract dysfunction was myelodysplasia in 26 patients and spinal cord injury in 4. Twenty-three patients had normal renal function and 7 had impaired renal function (creatinine 2.0–5.0 mg%). Additionally, 4 patients had an artificial urinary sphincter implanted and seven had an antireflux procedure performed. Results: Renal function remained stable or improved in 29 patients. Postoperatively, there was a 225% increase from mean preoperative capacity and a 52% decrease from the preoperative end filling pressure. Nineteen patients voided spontaneously and 11 used clean intermittent catheterization to empty the bladder. Twenty-five patients were continent with augmentation alone, four with augmentation and artificial sphincter implantation while one remained incontinent, as sphincter implantation could not be performed due to the young age of the patient. Five patients (17%) had transient hematuria and dysuria after augmentation. There were no mortalities and complications included prolonged urinary leakage in one patient and mild gastric bleeding in another two. Conclusion: The use of the stomach for augmenting the areflexic low compliant bladder is clearly advantageous over other tissues as it increases bladder capacity and compliance with consequent achievement of continence and preservation of upper tracts. An artificial urinary sphincter can be safely implanted in the same session. Because of its inherent fibromuscular properties, the gastric patch contributes to the force of urination resulting in better bladder emptying. Patients with impaired renal function are protected from hyperchloremic metabolic acidosis.