Rehabilitation of Patients with Benign Prostate Hyperplasia with Urinary Bladder Decompensation

The article is devoted to the problem of bladder decompensation and related complications in patients with BPH.

The objective: to study the effectiveness of certain methods of restoring the functional capacity of the detrusor in patients with BPH with bladder decompensation.

Materials and methods. The results of treatment of 149 patients with BPH with bladder decompensation aged 47 to 83 years (68,3±7,9) were analyzed, the proportion of which was 39,11 % of the total number of operated on BPH. Two groups of patients were formed by random sampling – every 2–3 patients. Group I included 30 people who underwent cystostomy. Group II included 30 people who, in addition to cystostomy, underwent metabolic-corrective and anticholinesterase therapy. The complex of drugs included B vitamins: octothiamine – 25 mg, riboflavin – 2,5 mg, pyridoxine hydrochloride – 40 mg, cyanocobalamin – 0,25 mg 3 times a day for 4 weeks; Anticholinesterase drug – ipidacrine 20 mg 3 times a day for 4 weeks.

Results. According to the results of pathomorphological examination in both groups of observation there was desquamation of the urothelium, growth of connective tissue, bundles of nerve fibers with the phenomena of dystrophy. Degenerative changes in smooth muscle cells were accompanied by a decrease in the proportion of muscle tissue and a decrease in the diameter of leiomyocytes. However, in patients who underwent preoperative metabolism-corrective therapy, the diameter of the lumen of the arterioles was 20.21 % larger (p<0,05), the wall thickness of the arterioles – 31,73 % smaller (p<0,05), the Kernogan index is 28,22 % lower (p<0,05), the diameter of the capillaries is 3,52 % higher (p>0,05). The diameter of leiomyocytes was 45,26 % larger (p<0,05), the proportion of connective tissue in the bladder wall – 29,14 % lower (p<0,05). Compared with patients who underwent only cystostomy, after metabolic-corrective and anticholinesterase therapy in the short and long postoperative period were better indicators of functional capacity of the detrusor. 6 months after the second stage of the operation according to uroflowmetry Qmax was higher by 32,92 % (p<0,05), Qave – higher by 62,27 % (p<0,05), IPSS – lower by 33,18 % (p<0,05) and the QoL index is better by 29,54 % (p<0,05).

Conclusions. Bladder decompensation due to untimely removal of the obstructive component is the main cause of unsatisfactory treatment results in patients with BPH. Anticholinergic exercise may be an additional factor in bladder decompensation in patients with BPH. Metabolism-correcting and anticholinesterase therapy permit to restore detrusor function by eliminating microcirculatory disorders and energy deficiency, stimulating neurotransmitter, neuromuscular conduction and smooth muscle contraction. In patients with megacystis, additional surgical correction by duplication allows the bladder to be emptied.