Urinary Incontinence

DR/ADEL DR/ADEL FAROUK FAROUK M.D M.D.. ASSISTANT ASSISTANT PROFFESOR PROFFESOR of of

Obstetrics Obstetrics & & Gynecology Gynecology Cairo Cairo university university

URINARY URINARY INCONTINENCE INCONTINENCE IN IN THE THE FEMALE FEMALE

ANATOMY OF THE BLADDER THE BLADDER is a hollow muscular organ normally situated behind the pubis symphysis. It is composed of a syncytium of smooth muscle fibers known as the Detrusor muscle. It is covered superiorly & anteriorly by peritoneum, and is connected to the proximal urethra at the bladder neck which rests on the urogenital diaphragm. The Detrusor muscle has a rich cholinergic parasympathetic supply (S: 2,3,4). Contraction of this meshwork of fibers results in simultaneous reduction of the bladder in all its diameters.

ANATOMY OF THE URETHERA THE URETHRA is 3-5 cm in length. It is a thin-walled muscular tube that drains urine from the bladder to outside the body. The epithelium of the urethra is transitional near the bladder, stratified squamous near the external opening and pseudostratified columnar epithelium in between. Beneath this thick epithelium is a rich vascular plexus which contributes up to 1/3 the uretheral pressure. The urethra has a minimal parasympathetic innervation and its smooth muscles are innervated by sympathetic fibres (T10,11,12). Stimulation of these sympathetic fibres produce urethral contraction via a-adrenergic receptors. b-adrenergic receptors produce urethral and Detrusor muscle relaxation.

URETHERAL SPHINCTERS The internal urethral sphincter (involuntary): at the bladder-urethral junction, a thickening of the detrusor muscle forms. The external urethral sphincter (voluntary): is skeletal muscle and surrounds the urethra as it passes through the urogenital diaphragm. N.B.: The urogenital diaphragm is part of the pelvic diaphragm which is the muscular portion of the pelvic floor that provides a stable base on which the bladder neck and proximal urethra rest.

ANATOMY OF THE BLADDER AND THE URETHERA

Mechanism of continence

The intera-urethral pressure at rest or with the stress of increase intra-abdominal pressure (I.A.P.) remains higher than intravesical pressure by the following factors: A- At rest: - Urethral mucosal resistance. - Periurethral vascular plexus pressure. - Resting intra-abdominal pressure. B- At stress of increased I.A.P.: Kinking of the urethra. Contraction of urogenital diaphragm ↑ pressure in lower urethra

Mechanism of continence Urinary continence is the ability to hold urine at all times except during micturition. Continence control is established via: Intraurethral pressure is higher than the intravesical pressure (neuromuscular). Fascial support around the urethra (anatomical position) or support of urethra at rest. Submucosal vascularity. Abrupt increases in intra-abdominal pressure (IAP) are transmitted equally to the bladder and proximal urethra as it lies above the pelvic diaphragm. Increase IAP leads to kinking effect of the proximal urethra because of strong support of pubocervical fascia posterior to the urethra which stimulates contraction of the pelvic diaphragm.

Micturition As urine accumulates, the bladder stretches and stretch receptors are activated. This causes a reflex that result in relaxation of the detrusor muscle and contraction of the external urethral sphincter. When about 200 ml. of urine has accumulated, impulses are sent to the brain and one begins to feel the urge to urinate. Activation of the micturition centre in the pons signals parasympathetic neurons that stimulate contraction of the detrusor and relaxation of the sphincters.

During micturition 1- Relaxation of pelvic striated muscle (pudendal nerve inhibition). 2- Relaxation of the fascial support (parasympathetic effect) leads to: - Descent of bladder neck. - Funnelling of the urethra. - Increase of urethro-vesical angle → 180° - Increase of urethral pubic angle → 45° 3- Contraction of detrusor muscle (parasympathetic effect).

Urinary incontinence Urinary incontinence is the involuntary loss of urine that is objectively demonstrable and results in social and hygienic problem.

CLASSIFICATION OF URINARY INCONTINENCE A) Extraurethral incontinence: Fistula (vesicovaginal, uretrovaginal, urethrovaginal) B) Urethral incontinence: Urodynamic stress incontinence (USI), also called genuine stress incontinence (GSI). Detrusor overactivity (DO), also called detrusor instability (DI), or (urgency incontinence). Mixed type (commonest). Overflow incontinence (retention with overflow). N.B.: Acute temporary incontinence may occur with child birth, limited mobility, medication side effect or urinary tract infection.

Urinary incontinence Common symptoms associated with incontinence: Urgency: a sudden desire to void. Frequency: urination 7 or more times a day or waking more than once at night to void. Stress incontinence: loss of urine on physical effort. It is not a diagnosis.

I. URODYNAMIC STRESS INCONTINENCE ((USI) (Genuine Stress incontinence) involuntary leakage of urine through the urethra when the intravesical pressure exceeds the maximal urethral pressure in absence of detursor activity (Genuine type ). It occurs during periods of increased intraabdominal pressure e.g. coughing, sneezing, exercise. It results from incompetent closure mechanisms at the urethra and the bladder neck.

Incidence –Genuine stress incontinence occurs in about 20% of females at certain time of their life. Prevalence and severity increase with age, parity and obesity (5% before 45 years, 10% between 45-60 years and 30% above 65 years).

Etiology of stress incontinence Stress incontinence occurs due to weakness of the urethro-vesical junction resulting from Weakness of the musculo-fascial support of this region. Descent of the urethro-vesical junction so that the upper urethra is not situated above the urogenital diaphragm and consequently it is not compressed by the raised intra-abdominal pressure at stress.

The bladder neck and proximal urethra are normally situated in an intraabdominal position above the pelvic floor and are supported by the pubourethral ligaments. This position allows increases in IAP to be transmitted equally to the bladder and proximal urethra maintaining urethral closure and continence. Damage to either the pelvic floor musculature (levator ani) or pubourethral ligaments may result in descent of the proximal urethra, and bladder neck, such that they will become no longer intraabdominal organs. This descent prevents transmission of IAP to the proximal urethra leading to an increase in the intravesical pressure over the intraurethral pressure during straining with a consequent leakage of urine per urethra during stress. This typically occurs in women that experience loss of support in the anterior vaginal wall leading to prolapse and descent of the bladder neck and urethra. Reduction in the resting urethral closure pressure occurs due to fibrosis, scarring or oestrogen deficiency, with resultant weakness of the internal urethral sphincter.

Etiology of stress incontinence A) Predisposing Factors: Congenital weakness “Racial and familial”. Traumatic weakness: Child birth trauma (overstretching of pelvic floor muscles and ligaments). Direct trauma (fracture pelvis). Fibrosis of the urethra and periurethral support: Secondary to bladder neck surgery or surgery for prolapse. Secondary to radiotherapy Postmenopausal atrophy that leads to further weakness of the pelvic fascia as well as decrease the mucosal resistance (due to oestrogen deficiency). B) Precipitating Factors: Obesity, ascites, constipation, chronic cough, pelvic mass.

Causes of stress incontinence Congenital or developmental weakness of the internal sphincter. Traumatic: resulting from childbirth causing overstretech and damage of the fascia around the bladder neck. Operative trauma: operations causing excessive fibrosis around the bladder neck Hormonal: postmenopausal atrophy of the pelvic floor muscles, ligaments and fascia around the sphincter. Genital prolapse: due to descent of the urethra and the bladder neck below the level of the pelvic diaphragm and stretching of the internal uretheral sphincter.

Descent of bladder neck

Descent of the urethro-vesical junction so that the upper urethra is not situated above the urogenital diaphragm and consequently it is not compressed by the raised intra-abdominal pressure at stress.

Types of stress incontinence –Genuine stress incontinence (anatomical weakness of the bladder neck).it may be classified into –Grade I ( incontinence with severe stress), –Grade II (with moderate stress rapid movement, walking up or down stairs). – Grade III (with mild stress as standing). –Detreusor instability: involuntary contractions of the detrusor muscles during filling. It may be due to neurological lesions as DS (detrusor hyperreflexia) or urinary tract infection, it may lead to incontinence.

Diagnosis of stress incontinence Symptoms:

Dribbling of urine with increases I.A.P.

(coughing-sneezing, laughing, walking or other activities). Loss of urine is brief, usually in spurts and corresponds precisely to the period of increase in I.A.P., limited to the upright or sitting position and not associated with desire to urinate

• Urgency, frequency may be present • Awareness of prolapse especially in multiparous women.

Stress incontinence can be demonstrated when asking the patient to cough while the bladder is full (better in erect position but can be demonstrated more commonly in lithotomy position). Presence and degree of associated genital prolapse

Examination of a case of stress incontinence Demonstrate the presence of stress incontinence by asking the patient to cough. There should be some urine in the bladder before asking the patient to cough to diagnose the presence of stress incontinence.

Examination of a case of stress incontinence In some cases of stress incontinence loss of urine may not appear (hidden stress incontinence) this may be due to The presence of large cystocele causing knick •The of the urethra (reexamination after elevation of the cystocele) (Yossef test). Empty bladder (the bladder should be half •Empty filled before demonstrating the presence of stress incontinence. Examination in recumbent position (so •Examination reexamination in the standing position might be needed). 

Examination of a case of stress incontinence Try to find the cause: Some degree of pelvic relaxation usually exists (urethrocele or cystocele). With straining excessive mobility of urethrovesical junction (detected by Q Tip test).

Examination of a case of stress incontinence The Q Tip test is done by application of lubricated applicator in the urethra and asking the lady to strain; normally the applicator moves not more than 15º above the horizontal plane excessive mobility with the angle is up to 50-70º indicates detachment of the urethra from the symphysis pubis.

Q Tip test

Bonney’s test: The bladder neck is elevated by 2 fingers placed in the vagina on each side of the urethra without compressing it. The patient is asked to cough or strain to produce an elevation in IAP. If no urine escapes during coughing, then bladder neck descent is the cause, and surgical repair will be successful. If urine escapes on coughing then weakness of bladder neck will be the cause.

Examination of a case of stress incontinence • Bonney’s test: to detect the etiology & to suggest prognosis

Bonney’s test • Bonney’s test: If urine escapes from the urethra

on coughing, the test is repeated after elevation of the bladder neck upwards (by 2 fingers in the vagina on either side of the region of the bladder neck). If no urine escapes on coughing, this means that the cause is descent of the bladder neck treated by elevation of the bladder neck region (uretheropexy), but if urine escapes, this means that the cause is due to weakness of the region of the bladder neck (not due to descent of the bladder neck) (treated by uretheroplasty).

Detrusor overactivity (DO) • (previously called Detrusor instability) is a urodynamic observation characterized by involuntary Detrusor contractions during the filling phase which may be spontaneous or provoked. • Incidence: It is the second most common cause of female incontinence, after USI, and accounts for 30-40% of cases.

Detrusor overactivity (DO) • Aetiology: • Local bladder irritation (e.g. infection, stone, ulcer, polyps, ....). • In association with other evidence of neuropathy e.g. DM, DS, spinal cord or brain lesions. • Idiopathic (most common). • Associated symptoms include; urgency, frequency, urgency incontinence, nocturia, stress incontinence, voiding difficulty and dysuria. • Diagnosis: • The diagnosis can only be made by urodynamic investigation tests when there is failure to inhibit Detrusor contractions during cystometry.

III. OVERFLOW INCONTINENCE

Definition: Insidious failure of bladder emptying that may lead to chronic urinary retention and overflow incontinence. Aetiology: Hypotonic bladder; as in lower motor neurone diseases, spinal cord injury or autonomic neuropathy e.g. (D.M.) Outflow obstruction: External or urethral (large cervical myoma). Acute retention with overflow e.g. postoperative, postpartum or infection. Iatrogenic e.g. anticholinergic and anticonvulsant drugs

OVERFLOW INCONTINENCE Clinical presentation: A) Symptoms: Patients usually present with various symptoms including dribbling of urine, straining to void with poor stream, and unawareness of urine loss. B) Physical examination: General examination: weight, gait, chronic chest disease. Abdominal examination: abdominal mass, hernia. Pelvic examination: Atrophy, displacement, weak perineal muscle. Examination for neurologic disorder: Muscle weakness, paralysis, deep tendon reflex.

Investigations 

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Urine analysis, A midstream urine for culture and sensitivity of urine to exclude urinary tract infection Cystoscopy to exclude cystitis or any bladder lesion. Rodiological studies: Cystourethrography: In cases of stress incontinence there is funneling of the bladder neck in the antero-posterior view and obliteration of the posterior urethro-vesical angle in the lateral view.

Investigations Urodynamics study: these are group of tests determine the pressure changes in the bladder (cystometery) and in the urethra (urethrometery), the functional length of the urethra (the length of the urethra at which the intra-uretheral pressure is higher than the intravesical pressure) and pressure changes during the act of micturition (Uroflwmetry). Urodynamics are indicated to differentiate genuine stress incontinence from detrusor instability

Urodynamics study These are tests which are employed to determine bladder function. They are indicated whenever multiple symptoms are present, mixed types of incontinence suspected, or where difficulties arise in differentiating USI from DO. Cystometry: measures the pressure volume relationship within the bladder. It can detect intravesical pressure and intraurethral pressure during rest and voiding. Cystometry can differentiate between USI and DO in the majority of cases. Uroflowmetry: rate of urine flow through urethra (N= 15 ml/sec.) Urethral pressure profile: traces intraurethral pressure along urethral length DO: is diagnosed if there is rise of the bladder pressure during the filling phase > 15 cm H2O. USI: is diagnosed if leakage occurs as a result of increased intra-abdominal pressure in the absence of rise in detrusor pressure.

Parameters of normal bladder function 1) Residual volume < 50 ml. 2) First desire to void between 150-200 ml. 3) Capacity (strong desire between 400-600 ml. 4) Detrusal pressure during filling < 15 cm H2O 5) Absence of systolic detrusor contraction. 6) No leakage on cough.

MANAGEMENT OF URODYNAMIC STRESS INCONTINENCE A) Prophylactic measures: Avoid prolonged 2nd stage of labour and minimize child birth trauma. Pelvic floor exercises especially in the puerperium, or after pelvic surgery Avoid marked obesity and overweight. Proper treatment of chronic cough and constipation especially in the post menopausal period

MANAGEMENT OF URODYNAMIC STRESS INCONTINENCE B) General measures and exercise: Restrict fluid drinking to 1 litre / day Weighed vaginal cones inserted in the vagina; to stimulate pelvic floor muscle contractions, as a sort of muscle exercise. Maximum electrical stimulation C) Medical treatment: Oestrogen in cases of menopausal atrophy. Alpha sympathomimetics (phenylpropanolamine) Combination of both is the best.

Treatment of stress incontinence  

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1-Postmenopausal cases are treated by combined estrogen and androgen preparations. 2- Pelvic floor exercises by (Kegel’s) perinometer for 3-6 months after labor may cure or improve some post-partum cases these exercises strengthen the levator ani. 3- ∝ adrenergic agonists as Ephedrine, impiramine these drugs increase the tone of the bladder neck. 4- Electrical stimulation therapy of the pelvic floor muscles. These measures are indicated in patients unfit for or refusing surgery or cases with uncontrolled detrusor instability. 5- Surgical treatment in patient fit for surgery.

Kegel’s perinometer

Kegel’s perinometer

Surgical treatment of USI Surgery is the gold standard in treatment of USI, aiming at; Restoration of the proximal urethra and the bladder neck by their elevation to the region of intraabdominal pressure transmission (i.e., elevation to a retropubic position). Increase urethral resistance

Surgical treatment of stress incontinence Basic operations can be grouped into 1. Colposuspension operations (e.g.: Burch colposuspension) 2. The sling procedures. 3. Kelly’s placation with anterior colporrhaphy 4. Periuretheral injection of collagen. 5. Needle suspension

1. Colposuspension operations (e.g.: Burch colposuspension): Attachment of the upper vagina on each side to the Cooper’s or the pectineal ligament at the inferior border of the pubic arch by an abdominal approach. Associated with the highest success rate (95% after 1 year, & 75% after 15 years)

Retropubic bladder neck suspension (urethrocystopexy). Burch operation: Suturing the paraurethral tissues to the pectineal part of inguinal ligament.

Laparoscopic Bursh operation

2. The sling procedures. Autologous materials; using fascia and rectus sheath. Synthetic material (Tension free vaginal tape- TVT). This has an advantage of very high success rate, up to 90%, shorter stay in the hospital as it is performed under local anaesthesia. It is considered now by many the treatment of choice for stress incontinence.

Sling operations Organic materials as Aldridge operation used in severe or recurrent cases were a fasial sling from the anterior rectus sheath is passed below the neck of the bladder to raise and tighten the urethro-vesical junction. Synthetic materials.

TVT

TVT

TVT

TVT

T.O.T

3. Kelly’s placation with anterior colporrhaphy Indicated when repair of cystocoele is planned by anterior colporrhaphy Associated with 60-70% success rate but fall to 30% after 5 years Less morbidity than any other abdominal procedure.

vaginal urethroplastic techniques Types of urethroplastic tenhniques are: (Kelly’s sutures) plication of the fascia around the urethrovesical junction. Kennedy, pacey’s and Nichols operation.

Kelly’s sutures

Other surgical procedures 4. Periuretheral injection of collagen. This is a short term treatment, but long term results are only 30% after 5 years 5. Needle suspension Peyrera and Stamey procedures are not used nowadays (30% cure rate after 5 years).

Needle suspension procedures Pereyra operation and its modifications.

Treatment of detrusor overactivity 1. Behavioural: Bladder retraining tend to increase the interval between voids and inhibit symptoms of urgency. However it is time consuming & require cooperative patients 2. Medical treatment a. Anticholinergic drugs: they reduce the vesical pressure and increase the bladder volume. - Oxybutinine 2.5mg twice daily - Tolterodine or detrusitol (drug of choice) as it has less side effects, 2mg twice daily b. Imipramine often used for enuresis and c. Antidiuretic hormone as Desmopressin often used for nocturia