URINARY INCONTINENCE

URINARY INCONTINENCEGuided ByDr. Pratiksha GuptaPresented By Dr. Jograjiya Department of Obstetrics and Gynecology ESIC-PGIMSR, Basaidarapur, New Delhi-110015.

Bladder innervation

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The inferior hypogastric plexus, also known as the pelvic plexus, is formed by visceral efferents from S2 to S4, which providethe parasympathetic component by way of the pelvic nerves. The superior hypogastric plexus primarily contains sympathetic fibersfrom the T10 to L2 cord segments and terminates by dividing into right and left hypogastric nerves. The hypogastric nerves and ramifrom the sacral portion of the sympathetic chain contribute the sympathetic component to the pelvic plexus. The pelvic plexus dividesinto three portions according to the course and distribution of its fibers: the middle rectal plexus, uterovaginal plexus, and vesical plexus.4Physiology of Micturition

Physiology of urine storage. Bladder distension from filling leads to: (1) -adrenergic contraction of the urethral smoothmuscle and increased tone at the vesical neck (via the T11-L2 spinal sympathetic reflex); (2) activation of urethral motor neurons in Onufnucleus with contraction of striated urogenital sphincter muscles (via the pudendal nerve); and (3) inhibited parasympathetic transmissionwith decreased detrusor pressure. alpha adrenergic receptors; beta adrenergic; M muscarinic (cholinergic).6

Onuf nucleus is found in the ventral horn gray matter of S2 through S4. This nucleus contains the neurons whose fiberssupply the striated urogenital sphincter. The urethrovaginal sphincter and compressor urethrae are innervated by the perineal branch ofthe pudendal nerve. The sphincter urethrae is variably innervated by somatic efferents that travel in the pelvic nerves.7

Physiology of urine evacuation. Efferent impulses from the pontine micturition center results in inhibition of somaticfibers in Onuf nucleus and voluntary relaxation of the striated urogenital sphincter muscles. These efferent impulses also result inpreganglionic sympathetic inhibition with opening of the vesical neck and parasympathetic stimulation, which results in detrusormuscarinic contraction. The net result is relaxation of the striated urogenital sphincter complex causing decreased urethral pressure,followed almost immediately by detrusor contraction and voiding. alpha adrenergic receptors; beta adrenergic; M muscarinic (cholinergic).8DEFINITION The complaint of any involuntary leakage of urine It is a symptom, a sign, and a condition.ICS 2013TYPES:1. True incontinence. 2. False incontinence (ischuria paradoxica). 3. Stress or sphincter incontinence. 4. Urgency incontinence (precipitancy-detrusor overactivity or detrusor dyssynergia).5. Functional / Transient / Reversible incontinence.

Incidence of Subtypes of Urinary Incontinence in WomenStress Incontinence 49% Urge Incontinence 21% Mixed 30%-Berek and Novak's Gynecology, 15th Edition 1. True (continuous) incontinenceIn this case, urine escapes continuously by day and by night. It is caused by: (a) Urinary fistulae as vesicovaginal fistula; (b) Ectopia vesica.2. False incontinence (Overflow incontinence) It is involuntary loss of urine following overdistension of the bladder. Overflow incontinence, usually short-term, can occur after vaginal deliveryespecially if epidural anesthesia was used. Other causes include diabetes, neurological diseases, severe genital prolapse, and post surgical obstruction.4. Urgency incontinence (precipitancy-detrusor instability or detrusor dyssynergia). The woman feels the desire to micturate but before she reaches the bathroom, urine passes involuntarily. It is due to irritability of the bladder muscle and so the patient cannot inhibit it. It is due to :emotional disturbance, neurologic diseases, and bladder diseases as cystitis, stone or tumour.Overactive bladder, is a condition in which the bladder contracts involuntarily in response to filling. It was called detrusor dys-synergia in the past. It commonly presents as urge incontinenceleakage of urine associated with a strong desire to void. No cause is identified in more than 90% of these patients. Advancing age is an important risk factor. Detrusor overactivity (DO)Detrusor overactivity (DO) caused by neurologic diseases such as cerebrovascular disease, multiple sclerosis, or spinal cord injury is called detrusor hyperreflexia. Irritation of the bladder by inflammation (such as urinary tract infection) or prior pelvic surgery can also cause detrusor overactivity.

Detrusor overactivity (DO)5. Functional/Transient incontinence It occurs in situations in which a woman cannot reach a toilet in time because of physical, psychological, or mentation limitations. It is medically reversible conditions.Cause of Reversible IncontinenceD DeliriumI InfectionA Atrophic urethritis and vaginitisP Pharmacologic causesP Psychological causesE Excessive urine productionR Restricted mobilityS Stool impactionResnick NM, Yalla SV. Management of urinary incontinence in the elderly. N Engl J Med 1985;313:800805.

STRESS INCONTINENCE )SPHINCTER INCONTINENCE-GENUINE STRESS INCONTINENCE) DEFINITIONIt is involuntary escape of few drops of urine with increased intra-abdominal pressure as during straining, sneezing, coughing, laughing, exercise, Valsalva ... etc.DEGREES OF STRESS INCONTINENCEGrade I Incontinence occurs only with severe stress, such as coughing, sneezing, etc Grade II Incontinence with moderate stress, such as rapid movement or walking up and down stairsGrade III Incontinence with mild stress, such as standing. The patient is continent in the supine positionPHYSIOLOGICAL ANATOMYThe bladder neck and upper third or half of the urethra are above the level of the pelvic floor. With increased intra-abdominal pressure, the pressure is equally transmitted to the bladder and upper urethra and urine will not escape. PHYSIOLOGICAL ANATOMY

Is an involuntary muscle which surrounds the bladder neck and urethra.The internal urethral sphincter (bladder sphincter)The external urethral sphincter is a voluntary muscle found between the superficial and deep perineal membranes and surrounds the middle part of the urethra.(1) the sphincter urethrae(2) the urethrovaginal sphincter (3) the compressor urethrae

Striated urogenital sphincter anatomy. The perineal membrane is removed to show the three component muscles of thestriated urogenital sphincter. This sphincter receives most of its somatic innervation through the pudendal nerve.29

It empties the urethra after the act of micturition, Interrupts the flow of urine on desireIt acts as a secondary defensive mechanism against escape of urine.The external urethral sphincter At rest the urethra makes an angle of 90-100 degrees with the base of the urinary bladder called the : posterior urethrovesical angle. The urethra also makes an angle of less than 30 degrees with the vertical line.

During micturition the following changes occur:1. Descent of the bladder neck with complete loss of the posterior urethrovesical angle (angle becomes 180 degrees).2. Opening (funneling) of the bladder neck and upper urethra.3. Descent of the urethra leading to increase in the angle between it and vertical line, so the angle becomes more than 30 degrees.In stress incontinence, one or all of the above changes occur with increased intra-abdominal pressure.The uroepithelium is supported by A connective tissue layer, which is thrown into deep folds, also known as plications. A rich capillary network runs within its subepithelial layer.This vascular network aids in urethral mucosal approximation, also termed coaptation, by acting like an inflatable cushionUrethral Mucosal Coaptation(Fig. 23-9). In women who are hypoestrogenic, this submucosalvasculature plexus is less prominent. In part, hormone replacementtargets this diminished vascularity and enhances coaptationto improve continence.

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AETIOLOGYIt is due to either :Weakness of the internal urethral sphincter or Descent of bladder neck below the level of the pelvic floor.AETIOLOGY1. Congenital weakness of the internal urethral sphincter, seen in the young nullipara.2. Congenital defects as:Epispadias, Short urethra (less than 1 cm), Wide bladder neck, and Separation of symphysis pubis.3. Trauma to the region of the bladder neck due to vaginal delivery or operation. The incidence of stress incontinence increases with parity due to repeated birth trauma. AETIOLOGYIn fact vaginal delivery is the commonest cause of stress incontinence.4. Menopause: Lack of oestrogen leads to atrophy of bladder neck supports.5.Pregnancy and continuous administration of oestrogen-progestogen preparation to induce psuedopregnancy state to treat endometriosis. The hormonal imbalance with increased progesterone weakens the internal urethral sphincter.AETIOLOGY6. Genital prolapse: If the bladder neck descends below the level of the pelvic floor, the increased intra-abdominal pressure will be transmitted to the bladder and not to the upper urethra leading to escape of urine.7. Organic nervous diseases as disseminated sclerosis.

AETIOLOGYPathophysiology of Stress IncontinenceThe basic pathology is urethral incompetence. This can be either due to:A) Urethral hypermobility (80 - 90% )B) Intrinsic Sphincter Dysfunction (10 - 20% )A) Urethral hypermobility (80 - 90%)This results from loss of the normal pelvic anatomical support mechanism of the bladder and urethra due to: Trauma and stretching during vaginal delivery Hysterectomy Hormonal changes ( Menopause) Pelvic denervation Congenital weakness As the bladder neck support is weakened, the increase in intra-abdominal pressure is transmitted to only the bladder not to bladder neck and upper urethra, therefore instantaneous leakage occurs.A) Urethral hypermobility (80 - 90%)

B) Intrinsic Sphincter Dysfunction (10 - 20%)The urethra maintains continence through the combination of Urethral mucosal coaptation- The underlying urethral vascular plexus, The combined viscous and elastic properties of the urethral epithelium,Contraction of intrinsic sphincterAll of above damage due to:Prior pelvic reconstructive surgeriesTrauma Radiation Diabetic neuropathyNeuronal degenerative diseasesAtrophic changes: lack of estrogen. Denervation and/or Devascularizationscarring of the urethra and its supporting tissueLead pipe UrethraWhich lead to

DiagnosisA. HistoryA detailed history differentiates between the different types of incontinence. Stress incontinence and detrusor instability frequently occur together.Gradual onset after menopause suggests oestrogen deficiency.History of vaginal repair or operation in the region of the bladder neck and history of any neurologic disease.B. Diagnostic Tests1. Stress TestThe bladder must be moderately full. The patient in the lithotomy position, the two labia are separated, and the patient is asked to cough. If urine escapes, the patient is incontinent. If no urine escapes, the test is repeated while the index and middle fingers in the vagina press on the perineum to abolish reflex contraction of the levator ani muscles during straining. If still no urine escapes, the test is repeated while the patient is standing with the legs separated.2. Bonney testIt is indicated in case of a positive stress test associated with a cystocele. To know if incontinence is due to descent of bladder neck or weakness of the sphincter. The index and middle fingers are placed on both sides of the urethra to elevate the bladder neck upwards. If no urine escapes on stress it means that the incontinence is due to descent of the bladder neck, but if urine still escapes it means weakness of the sphincter.Indicated in case of a negative stress test associated with a large cystocele to diagnose hidden stress incontinence. The cystocele is reduced, the cervix is grasped with a volsellum and pushed upward, then the patient is asked to cough. If urine escapes, it indicates that the patient was continent because of kinking of the urethra.3. Yousef Test4. Examination of UrineUrinalysis, culture and sensitivity to exclude cystitis.

To exclude lesions in the urethra and bladder. The bladder neck is examined. It should close in response to straining. However, it opens in case of stress incontinence.5. CystourethroscopyA radio-opaque dye is injected by a catheter into the bladder. On straining, the lateral view will show absence of the posterior urethrovesical angle in more than 90% of cases. Funneling of the bladder neck in the antero-posterior view may be seen in some cases. The procedure is recorded on video tape (video Cystourethrography) to facilitate diagnosis and for education purposes.6. Cystourethrography7. UrodynamicsMedical science concerned with the study of urine transport from kidney to bladder as well as its storage and evacuationClassification:1.Cystometrogram( most important test), Filling Cystometry and Voiding Cystometry2.Urethral pressure profile3.Uroflow4.ElectromyographyCystometrogramTo measure the intravesical pressure while the bladder is filled with sterile water or carbon dioxide gas. It diagnoses stress incontinence and detrusor overactivity. The most important test.

CystometrogramInvolves filling the bladder to measure volume-pressure relationships. As the bladder is filled to its normal capacity of 300-500 ml, the pressure inside the bladder should remain low. The patient usually experiences the first urge to void at 150-200 ml. Patients with DO often have reduced bladder capacity (< 300 ml) and demonstrate urinary incontinence that is associated with involuntary bladder contractions (pressure increase above baseline) CystometrogramIn patients with GSI, incontinence is demonstrated when the patients coughs or strains (e.g., Valsalva maneuver). The intravesical pressure at which leakage is noted (leak point pressure) is generally < 60 cm of water pressure if intrinsic sphincter deficiency is present.Cystometrogram

Interpretation of multichannel urodynamic evaluation: cystometrogram. A catheter is placed in the bladder to determinethe pressure generated within it (Pves). The pressure in the bladder is produced from a combination of the pressure from theabdominal cavity and the pressure generated by the detrusor muscle of the bladder. Bladder pressure (Pves) pressure in abdominalcavity (Pabd) detrusor pressure (Pdet). A second catheter is placed in the vagina (or rectum if advanced-stage prolapse is present) todetermine the pressure in the abdominal cavity (Pabd). As room-temperature saline is instilled into the bladder, the patient is asked tocough every 50 mL and the external urethral meatus is observed for leakage of urine around the catheter. The volume at first desireto void and the bladder capacity is recorded. Additionally, the detrusor pressure (Pdet) channel is observed for positive deflections todetermine if there is detrusor activity during testing. The detrusor pressure (Pdet) cannot be measured directly by any of the catheters.However, from the first equation, we can calculate the detrusor pressure (Pdet) by subtracting the abdominal pressure (Pabd) from thebladder pressure (Pves):Detrusor pressure (Pdet) bladder pressure (Pves) pressure in abdominal cavity (Pabd)I. Urodynamic Stress Incontinence (USI)Urodynamic stress incontinence is diagnosed when urethral leakage is seen with increased abdominal pressure, in the absence of detrusorpressure.a. USI (Column 1): Abdominal pressure is generated with Valsalva maneuver or cough. This pressure is transmitted to the bladder, anda bladder pressure (Pves) is noted. The calculated detrusor pressure is zero. Leakage is observed, and diagnosis of USI is assigned.b. No USI (Column 2): Abdominal pressure is generated with Valsalva maneuver or cough. This pressure is transmitted to the bladder,and a bladder pressure (Pves) is noted. The calculated detrusor pressure is zero. Leakage is not observed. The patient is not diagnosed ashaving USI.II. Detrusor Overactivity (DO)Detrusor overactivity is diagnosed when the patient has involuntary detrusor contractions during testing with or without leakage.a. DO (Column 3): Although no abdominal pressure is observed, a vesicular pressure is noted. A calculated detrusor pressure isrecorded and noted to be present. A diagnosis of DO is made regardless of whether leakage is seen.b. DO (Column 4): In this example, an abdominal pressure is observed as well as a vesicular pressure. Using only the Pabd and the Pveschannels, it is difficult to tell whether or not the detrusor muscle contributed to the pressure generated in the bladder. On subtraction, acalculated detrusor pressure is recorded. Thus, a diagnosis of DO is made, again regardless of whether leakage is seen.In addition to these channels, occasionally a channel to detect electromyographic activity is used.Pabd pressure in abdominal cavity; Pdet detrusor pressure (calculated); Pves bladder pressure.65

Approximate Normal Values of Female Bladder Function

Residual urine 15 mL/sec with a detrusor pressure of