Bladder Decompensation in Patients with Benign Prostatic Hyperplasia: Causes, Complications, Rehabilitation

Background Despite the high efficiency of surgical methods in correction of bladder outlet obstruction (BOO) caused by benign prostatic hyperplasia (BPH), a significant proportion of patients (up to 35%) remains after surgery with impaired contractile function of the bladder and lower urinary tract symptoms (LUTS). Both are consequences of structural and functional changes of the detrusor due to long-term exposure to obstructive factor. Today there is a lack of systematic reviews that provide a specialist with an integrative conception of pathological changes in the bladder wall caused by BPH associated prolonged BOO and evidence based methods of detrusor rehabilitation. The objective: systematization of modern conceptions about structural and functional changes in the bladder of patients with BPH caused by prolonged BOO, and methods of their correction. Materials and methods. An analytical review of the literature covering pathogenesis of bladder remodeling due to BPH associated long-term BOO and methods of bladder rehabilitation was performed. Literature sources were searched in PubMed, Google Scholar, Scopus and Web of Science databases by keywords. The search depth was 40 years. 74 relevant publications were selected for analysis. Results. Bladder remodeling due to obstructive factor is a complex staged process that involves all layers of the wall at the tissue, cellular and subcellular levels, affecting not only the executive structures (urothelium, smooth-muscle syncytium, fibrous connective tissue matrix), but also the system metabolism. Depending on the nature of the changes, there are 3 stages of this process: compensation, subcompensation and decompensation. In the compensatory stage, an increase of the load on the bladder leads to hypertrophy of smooth muscle fibers. At the same time, there is a reorganization of the vascular bed – neoangiogenesis, which should provide increased energy needs of muscles. In the stage of subcompensation, vicarious hypertrophy and neoangiogenesis cease. The most prominent disorders of the structure and function of the bladder are observed in the stage of decompensation. It includes a number of pathological processes: hypoxia, anaerobic metabolism, oxidative stress, inflammation, changes in the paracrine environment (increased levels of HIF-1α, vascular endothelial growth factor (VEGF) and angiopoietin-1). It is characterized by progressive loss of contractile function of the detrusor due to the death of smooth muscle cells and neurons, deterioration of viscoelastic characteristics of the bladder wall due to excessive collagen synthesis by fibroblasts, loss of barrier properties of the mucous membrane due to dystrophy. It was found that the severity of these pathological changes correlates with the severity of LUTS in patients who underwent surgery for BPH. The current arsenal of measures for bladder rehabilitation is quite diverse and includes periodic sterile catheterization, pharmacotherapy (cholinesterase inhibitors, antioxidants), physiotherapy (electrical stimulation, muscles training) and plastic surgery. However, there is still a lack of high-level studies to prove their effectiveness in patients who have undergone prostate surgery for BOO caused by BPH. Conclusions. Persistence of LUTS in patients who have undergone prostate surgery due to BOO may be caused by bladder decompensation. Long-term bladder decompensation due to prolonged exposure to obstructive factor is a complex process that includes decreased contractile activity, deterioration of the viscoelastic characteristics of the bladder, and impaired mucosal barrier function. Further research is needed to develop an effective bladder rehabilitation protocol