Overactive bladder: treatment

Treatment of a hyperactive bladder, first of all, is aimed at restoring the lost control of the memory function of the bladder. With all forms of the hyper-reactive bladder, the main method of treatment is medication. The standard drugs of choice are anticholinergics (m-holinoblokatory). As a rule, medication is combined with behavioral treatment, biological feedback or neuromodulation. The mechanism of action of anticholinergic drugs is the blockade of postsynaptic (m2, m1) detrusor muscarinic cholinergic receptors. This reduces or prevents the action of acetylcholine on detrusor, reducing its hyperactivity and increasing the capacity of the bladder.

Until recently, the treatment of a hyperactive bladder was the administration of oxybutynin (driptane). The maximum dose of the drug is usually 5-10 mg 2-3 times a day. In recent years, new medicines have been proposed for the treatment of the hyperreactive bladder, such as trospium chloride (spasmox) 10-15 mg 2-3 times a day, tolterodine (detrusitol) 2 mg 2 times a day and solifenacin (vesicar) 5 -10 mg once a day. All anticholinergics have side effects associated with blocking m-cholinergic receptors of other organs and tissues. Dry mouth, the main side effect of anticholinergics, causes a block of muscarinic salivary gland receptors. Other systemic side effects of anticholinergic drugs blocking muscarinic cholinergic receptors of various organs include visual impairment, decreased tonus of smooth muscle organs (bowel peristalsis, constipation), tachycardia, in some cases central effects (drowsiness, dizziness), etc. It should be noted that trospium chloride is the only quaternary compound in this group and, unlike tertiary amines, it does not penetrate the blood-brain barrier and does not cause side effects from the side of the central nervous system.

By all accounts, trospium chloride, tolterodine and solifenacin have a better safety profile than oxybutynin. With prolonged use of colinollectics in patients with a hyperreactive bladder (especially with non-irogenic detrusor hyperactivity), detrusor contractile activity may develop with the development of chronic urinary retention, ureterohydronephrosis, and chronic renal failure. It is especially dangerous to prescribe anticholinergic drugs for patients with a hyper-reactive bladder in combination with impaired detrusor activity. For the timely monitoring of possible side effects, it is necessary to monitor residual urine.

Treatment of a hyperactive bladder is also performed by other drugs, myotropic antispasmodic relaxants, slow calcium channel blockers (nifedipine, verapamil), tricyclic antidepressants (imipramine). However, the results of treatment with drugs of these groups are much inferior to blockers of muscarinic receptors, and therefore they are usually used in combination with the latter.

In severe cases of non-irogenic detrusor hyperactivity, when anticholinergic drugs are ineffective, intracerebral administration of botulinum neurotoxin type A and intravesical administration of drugs possessing neurotoxic activity, such as capsaicin, are used.

The mechanism of action of botulinum neurotoxin type A is the presynaptic blockade of acetylcholine release, which leads to a detrusor relaxation and an increase in the volume of the bladder. 200-300 units of botulinum neurotoxin type A diluted in 10-20 ml of isotonic sodium chloride solution is injected at 20-30 points into the detrusor. In the vast majority of patients to maintain the clinical effect, repeated administration of the drug is necessary with a periodicity of 3-12 months.

Capsaicin causes the exorbitant stimulation of non-myelinated C-fibers located in the subepithelial layer of the bladder wall. The neurotoxic effect of capsaicin * is accompanied by a decrease in the detrusor's increased contractile activity and an increase in the capacity of the bladder. The homovanilic acid derivative capsaicin * is obtained from red hot pepper. The effect of a single intravesical installation of capsaicin lasts an average of 3-4 months. After which the repeated administration of the drug is required. Side effects are manifested in the appearance of burning sensation and acute reflex contractions of the bladder in the first minutes after administration.

Treatment of a hyperactive bladder also requires the use of neuromodulation, that is, the process of forming a lost urination mechanism by direct or indirect stimulation of the afferent fibers of the somatic division of the peripheral nervous system by a weak electric current. Fibers are a part of various nerve trunks, but are formed mainly from the third sacral nerve. The effect on them reduces the parasympathetic activity of the pelvic nerve and increases the sympathetic activity of the hypogastric nerve. This leads to inhibition of the detrusor's increased contractile activity. The most effective are the tibial and sacral electrostimulation.

The technique of electrostimulation of the tibial nerve consists in its stimulation by a weak electric current. To do this, use a needle electrode, which is injected at a depth of 3-4 cm through the skin to a point 5 cm from the medial malleolus cranial. A passive electrode is placed in the region of the ankle joint. One treatment lasts 30 minutes. Conduct 12 procedures. One per week. Patients with disappearance or improvement of symptoms of a hyperactive urinary bladder are included in the so-called final protocol. This means that in the future it. Depending on the results of treatment, one procedure is performed for 2-3 weeks. This treatment of a hyperactive bladder does not cause side effects.

The technique of sacred nervous electrostimulation assumes a consistent performance of the test of acute stimulation, temporary stimulation and the installation of a permanent electrostimulator. At the first stage, before the implantation of the electrode for temporary stimulation, an acute stimulation test is performed. After infiltration anesthesia, a 0.5% solution of procaine (novocain) on the posterior surface of the sacrum is performed by the search puncture of the third sacral orifice. The search needle is connected to an external electrostimulation device and an acute stimulation test is performed to determine the position of the needle tip. Irritation by electric current of nerve fibers at the level of S3 leads to a reduction in perineal muscles and plantar flexion of the big toe on the side of stimulation, which is regarded as a positive test. After this, an electrode is introduced into the third sacral hole along the needle. The location of the electrode is monitored radiographically in the anteroposterior and lateral projections. After implantation, the electrode is fixed to the skin and connected to a portable device for nervous stimulation. They are acted upon by monophase, rectangular pulses of a width of 210 Mcs. Frequency of 25 Hz and a voltage of 0.5-5 V. The temporary stimulation is carried out for 3-5 days. The time stimulation test is considered positive when the symptoms decrease during the stimulation period by more than 50% of the baseline values and the resumption of symptoms after cessation of stimulation. Positive results of the temporary stimulation test serve as indications for subcutaneous implantation of a permanent stimulant for sacral neuromodulation. Implantation involves the installation in the area of the third sacral nerve electrode with connection to a constant stimulant. Placed under the skin in the gluteal region. Complications of sacral neuromodulation: electrode migration and infectious-inflammatory processes.

Surgical treatment of the hyper-reactive bladder is used extremely rarely, and it consists in replacing the bladder with a gut (thin or thick) area or in a myectomy with an increase in the volume of the bladder.

[1], [2], [3], [4], [5], [6], [7], [8], [9], [10]