Urinary Incontinence

1. Abdallah Rimawi, MD Geriatrics Fellow SVCMC Urinary Incontinence

2. Definition Involuntary loss of urine in a sufficient amount or frequency to be a social/health problem.

3. Epidemiology UI has a prevalence 15-30% in community-residing elderly patients 50-84% among older adults in long-term care institutions 33% in older persons in acute care settings. • UI affects more than 17 million Americans, 85% of whom are women. • Estimated cost to society of $16 to 26 billion. • Race: No clear evidence of racial differences in prevalence of UI has been found. • UI is approximately twice as prevalent in older women as in older men, with 20% being women older than 45 years. In some women, stress incontinence and urge incontinence, the two most common forms of UI, may coexist.

4. Epidimiology Urge incontinence constitutes over 50% of overall incontinence in men, 10-15% in younger women, and 30-40% in older women. Stress incontinence tends to be more common in women younger than 65 years.

5. Stress vs Urge Distribution of different types of incontinence in the general population. Diagnoses other than stress, urge, and mixed are excluded. Dr. Hogne Sandvik: 1996 nobel award in biology

6. Age (years) Numbers evaluated Stress (%) Urge (%) Mixed (%) >18 1 000 50 19 31 >18 851 52 25 23 42 - 50 541 50 12 38 30 - 59 2 631 48 7 45 >60 1 955 29 10 61 Prevalence of Stress vs Urge

7. Prevalence in Females

9. Normal micturition • The normal function of the urinary bladder is to store and expel urine in a coordinated, controlled fashion. This coordinated activity is regulated by the central and peripheral nervous systems

10. Normal Urination • The process of urination involves two phases: 1) The filling and storage phase 2) The emptying phase

12. Filling Phase • Filling/ storage phase: Under Sympathetic control • the bladder begins to fill with urine from the kidneys. The bladder stretches to accommodate the increasing amounts of urine. No increase in pressure Sympathetic system relaxes Detrusor muscle • Sympathetic system closes bladder neck by constricting internal urethral sphincter • The first sensation of the urge to urinate occurs when approximately 200 ml (just under 1 cup) of urine is stored. A healthy nervous system will respond to this stretching sensation by alerting you to the urge to urinate, while also allowing the bladder to continue to fill. • The average person can hold approximately 350 to 550 ml of urine. The ability to fill and store urine properly requires a functional sphincter (the circular muscles around the opening of the bladder) and a stable, expandable bladder wall muscle (detrusor). • The filling of the urinary bladder depends on the intrinsic viscoelastic properties of the bladder and the inhibition of the parasympathetic nerves. Thus, bladder filling primarily is a passive event. • Sympathetic nerves also facilitate urine storage in the following ways: • Sympathetic nerves inhibit the parasympathetic nerves from triggering bladder contractions. • Sympathetic nerves directly cause relaxation and expansion of the detrusor muscle. • Sympathetic nerves close the bladder neck by constricting the internal urethral sphincter. This sympathetic input to the lower urinary tract is constantly active during bladder filling. • As the bladder fills, the pudendal nerve becomes excited. Stimulation of the pudendal nerve results in contraction of the external urethral sphincter. Contraction of the external sphincter, coupled with that of the internal sphincter, maintains urethral pressure (resistance) higher than normal bladder pressure. The combination of both urinary sphincters is known as the continence mechanism. • The pressure gradients within the bladder and urethra play an important functional role in normal micturition. As long as the urethral pressure is higher than that of the bladder, patients will remain continent. If the urethral pressure is abnormally low or if the intravesical pressure is abnormally high, urinary incontinence will result. • As the bladder initially fills, a small rise in pressure occurs within the bladder (intravesical pressure). When the urethral sphincter is closed, the pressure inside the urethra (intraurethral pressure) is higher than the pressure within the bladder. While the intraurethral pressure is higher than the intravesical pressure, urinary continence is maintained. • During some physical activities and with coughing, sneezing, or laughing, the pressure within the abdomen rises sharply. This rise is transmitted to both the bladder and urethra. As long as the pressure is evenly transmitted to both the bladder and urethra, urine will not leak. When the pressure transmitted to the bladder is greater than urethra, urine will leak out, resulting in stress incontinence.

13. Emptying Phase • Emptying phase: requires the ability of the detrusor muscle to appropriately contract to force urine out of the bladder. At the same time, your body must be able to relax the sphincter to allow the urine to pass out of the body.

14. Normal micturition cycle

15. Central Control • Brain • The brain is the master control of the entire urinary system. • The micturition control center is located in the frontal lobe. • Sends inhibitory signals to the detrusor muscle Via the Pons and spine to prevent the bladder from emptying (contracting) until a socially acceptable time and place to urinate is available. • Certain lesions or diseases of the brain, including stroke, cancer, or dementia, result in loss of control of the normal micturition reflex. • The signal transmitted by the brain is routed through 2 intermediate stops (the brainstem and the sacral spinal cord) prior to reaching the bladder.

16. Brain  Pons • PONS • Pons: a major relay center between the brain and the bladder. • Contains the pontine micturition center (PMC) which coordinates the urethral sphincter relaxation and detrusor contraction to facilitate urination. • The PMC is Exitatory in nature and causes urination unless inhibited by the brain. The PMC functions as a relay switch in the voiding pathway. Stimulation of the PMC causes the urethral sphincters to open while facilitating the detrusor to contract and expel the urine. • Usually the brain takes over the control of the pons at age 3-4 years, which is why most children undergo toilet training at this age.

17. Sequence of normal events When Bladder becomes full, the stretch receptors of the detrusor muscle send a signal to the pons (via the spinal cord), which in turn notifies the brain. Patients perceive this signal (bladder fullness) as a sudden desire to go to the bathroom. Under normal situations, the brain sends an inhibitory signal to the pons to inhibit the bladder from contracting until a bathroom is found. • When the PMC is deactivated, the urge to urinate disappears, allowing the patient to delay urination until locating a suitable bathroom. When urination is appropriate, the brain sends excitatory signals to the pons, allowing the urinary sphincters to open and the detrusor to empty.

18. Brain  Pons Spinal cord • Spinal cord • The spinal cord connects the brainstem and the lumbosacral spine. • The spinal cord functions as a long communication pathway between the brainstem and the sacral spinal cord. When the sacral cord receives the sensory information from the bladder, this signal travels up the spinal cord to the pons and then ultimately to the brain. The brain interprets this signal and sends a reply via the pons that travels down the spinal cord to the sacral cord where the bladder receives it.

19. Spinal cord Trauma • An intact spinal cord is critical for normal micturition. If the spinal cord is severely injured or severed, the affected individual will exhibit constant urinary leakage because of uncontrollable bladder spasms, a condition called detrusor hyperreflexia. • If complete spinal cord transection has occurred, the patient will demonstrate symptoms of urinary frequency, urgency, and urge incontinence but will be unable to empty his or her bladder completely. This occurs because the urinary bladder and the sphincter are both overactive, a condition termed detrusor sphincter dyssynergia with detrusor hyperreflexia

20. Sacral spinal cord • The sacral spinal cord is the terminal portion of the spinal cord at the lower back in the lumbar area. This is a specialized area of the spinal cord known as the sacral reflex center. It is responsible for bladder contractions. The sacral reflex center is the primitive voiding center. • If the sacral cord becomes severely injured (eg, spinal tumor, herniated disc), the bladder may not function. Affected patients may develop urinary retention, termed detrusor areflexia. The detrusor will be unable to contract, so the patient will not be able to urinate and urinary retention will occur.

21. Physiology PNS Sympathetic system (Epinepherine & Norepinepherine): Normally controls the bladder and internal urethral sphincter Accommodation: an increase the bladder capacity without raising bladder pressure Keeps the internal urinary sphincter tightly closed. relaxes bladder dome inhibits parasympathetic system The sympathetic activity also inhibits the micturition reflex is inhibited.

22. Parasympathetic • The parasympathetic nervous system functions in a manner opposite to that of the sympathetic nervous system • stimulates the detrusor muscle to contract the bladder • Causes internal and external urethral sphincter relaxation and opening • Inhibits the pudendal nerve which opens the external sphincter • Causes initiation of micturition and emptying of the urinary bladder

23. Somatic • Regulates action of voluntary muscles • Contraction of external urethral sphincter The somatic nervous system regulates the actions of the muscles under voluntary control. Such as muscles of the external urinary sphincter and the pelvic diaphragm. . suprasacral-infrapontine spinal cord trauma can cause overstimulation of the pudendal nerve that results in urinary retention.

25. Urinary Incontinence

26. Requirements for storage • Accomodation – increase in volume with decrease in pressure • Closed outlet • Appropriate sensation of fullness • Absence of involuntary bladder contractions

27. Requirements for emptying • Good contractility • Lack of anatomic obstruction • Coordination of bladder and outlet

28. Requirements for continence • Mobility • Manual dexterity • Cognitive ability to recognize and react to bladder filling • The motivation to stay dry

29. Sudden/Temporary incontinence etiology • Urinary tract infection or prostate infection/inflammation • Stool impaction causing pressure on the bladder • Side effects of medications (such as diuretics, tranquilizers, some cough and cold remedies, certain antihistamines for allergies, and antidepressants) • Polyurea due to poorly controlled diabetes • Pregnancy • Short-term bedrest -- for example, when recovering from surgery • Mental confusion • Usually reversable once treated or removed

30. Long term incontinence: • Spinal injuries • Urinary tract anatomical abnormalities • Neurological conditions like multiple sclerosis or stroke • Weakness of the sphincter, the circular muscles of the bladder responsible for opening and closing it; this can happen following prostate surgery in men, or vaginal surgery in women • Pelvic prolapse in women -- falling or sliding of the bladder, urethra, or rectum into the vaginal space, often related to having had multiple pregnancies and deliveries • Large prostate in men • Depression or Alzheimer’s disease • Nerve or muscle damage after pelvic radiation • Bladder cancer • Bladder spasms

31. Types of Urinary Incontinence • Stress incontinence - loss of urine with increased intraabdominal pressure without detrusor contraction. Most common form of UI in women • Urge incontinence - (true, detrusor overactivity, or reflex) is precipitous loss of urine, preceded by a strong urge to void, with increased intravesical pressure and detrusor contraction. • Continuous incontinence - is involuntary loss of urine at all times and in all positions. • Overflow incontinence - results from detrusor underactivity, bladder outlet obstruction, or both. Leakage is small in volume but continual. In men, it can be the result of an enlarged prostate.

32. Stress incontinence • Stress incontinence is an involuntary loss of urine that occurs during physical activity, such as coughing, sneezing, laughing, or exercise. • Stress incontinence is a bladder storage problem in which the strength of the urethral sphincter is diminished, and the sphincter is not able to prevent urine flow when there is increased pressure from the abdomen. • Stress incontinence may occur as a result of weakened pelvic muscles that support the bladder and urethra, or because of malfunction of the urethral sphincter. Prior trauma to the urethral area, neurological injury, and some medications may weaken the urethra. Stress incontinence can worsen during the week before your menstrual period. At that time, lowered estrogen levels might lead to lower muscular pressure around the urethra, increasing chances of leakage. The incidence of stress incontinence increases following menopause.

33. Stress incontinence • Sphincter weakness may occur in men following prostate surgery or in women after pelvic surgery. Stress incontinence is often seen in women who have had multiple pregnancies and vaginal childbirths, or who have pelvic prolapse (protrusion of the bladder, urethra, or rectal wall into the vaginal space), with cystocele, cystourethrocele, or rectocele. • Studies have documented that about 50% of all women have occasional urinary incontinence, and as many as 10% have frequent incontinence. Nearly 20% of women over age 75 experience daily urinary incontinence. • Stress urinary incontinence is the most common type of urinary incontinence in women. Risk factors for stress incontinence include female sex, advancing age, childbirth, smoking, and obesity. Conditions that cause chronic coughing, such as chronic bronchitis and asthma, may also increase the risk of stress incontinence.

34. Stress incontinence treatment • Goal of nonsurgical treatment is to increase internal sphincter tone. Mild to moderate stress incontinence may be effectively treated with exercise therapy, medications, or both. • The most common cause of stress incontinence in older women is urethral hypermobility: In up to 60% of women with stress incontinence, pelvic floor (Kegel) exercises can result in better control of the bladder when coughing, laughing, sneezing, or exercising.1These exercises should be performed 10-20 times, 3 times a day • Medication may be used to tighten the bladder and prevent urine leakage, but its effectiveness varies. • Electrical stimulation can be used to reduce both stress incontinence and urge incontinence

35. Treatment stress incontinence • Surgical intervention • Surgery elevates the bladder neck and brings the proximal urethra back into the abdomen; the 1-year success rate is 80-95%. Surgery to add support for the bladder neck is usually needed for severe stress incontinence that does not respond to medication or exercise.

36. Treatment stress incontinence • Medications: • Alpha-adrenergic agonists (pseudoephedrine) are used especially for women on estrogen; they increase the internal sphincter tone and bladder outflow resistance. Use with caution in patients with hypertension or arrhythmia. • Estrogen cream to the vagina or oral estrogen tablets : may be helpful in improving periurethral and vaginal tissue thickness and quality. • Treat precipitating conditions (atrophic vaginitis, cough). • Incontinence pads may be used to absorb the small amount of urine that usually leaks during stress.

37. Urge incontinence • Alternate Names : Detrusor Hyperreflexia, Detrusor Instability, Overactive Bladder, Spasmodic Bladder, Unstable Bladder • Bladder muscle contracts inappropriately, regardless of the amount of urine that is in the bladder. Population: May occur in anyone at any age, but it is more common in women and elderly. Second only to stress incontinence as the most common cause of urinary incontinence (involuntary loss of urine). Approximately 1% to 2% of adult females are affected by urge incontinence. • In men, urge incontinence may be due to secondary bladder injuries caused by benign prostatic Mechanism PVC: "Premature Vesicular Contraction" Overly sensitive bladder Urge to void is perceived Inhibition of detrussor contraction is ineffective

38. Etiology urge incontinence Etiologies:Urge incontinence may result from neurological injuries (such as spinal cord injury or stroke), neurological diseases (such as multiple sclerosis), infection, bladder cancer, bladder stones, bladder inflammation, or bladder outlet obstruction. The majority of cases are classified as idiopathic -- a specific cause cannot be identified Signs and Symptoms Irresistable urge to void Urge preceeded by various stimulation : Posture change, Hear or feel water ,Laugh or cough Urine volume lost :Few drops to entire bladder contents Urine loss timing:Begins seconds after trigger

39. Urge incontinence Diagnostics Rule out neurological or infectious etiology Sterile in-out catheterization or Ultrasound measurement of post-void residual

40. Urge incontinence treatment • Treat symptomatically if no known cause • Pelvic Muscle Rehabilitation : improves muscle tone and prevent urine leakage. • Daily Kegel exercises (contracting and relaxing the pelvic floor muscles) • Biofeedback • Vaginal weight training: Small weights are held within the vagina by tightening the vaginal muscles. • Pelvic floor or nerve electrical stimulation. Mild, painless electrical impulses are used to stimulate the pelvic muscles and/or nerves to help relieve the symptoms of overactive bladder and urge incontinence. • Behavioral Therapies • Bladder training teaches people how to resist the urge to urinate. • Toileting assistance uses routine or scheduled toileting and prompted voiding to empty the bladder regularly to prevent leaking. • Surgery • Surgical procedures of the bladder may be performed for people who do not respond to any other treatment

41. Treatment urge incontinence • Medication :aimed at relaxing the involuntary contraction of the bladder and improving bladder function • anticholinergic agents (propantheline) • antispasmodic medications (oxybutynin, tolterodine, flavoxate) • tricyclic antidepressants (imipramine, doxepin) • calcium channel blockers (tolterodine) • beta agonist (terbutaline) • Oxybutynin (Ditropan) and tolterodine (Detrol) :antispasmodic medications that relax the smooth muscle of the bladder. These are the most commonly used medications for urge incontinence • Side effects of oxybutynin and tolterodine are minimal, with the most common being dry mouth and constipation. However, these medications cannot be used by patients with narrow angle glaucoma. • Anticholinergic medications block inappropriate contractions of the bladder. They were widely used in the past to treat urge incontinence because they are relatively inexpensive yet effective. Oxybutynin and tolterodine have virtually replaced the use of these medications because they have fewer side effects. • Tricyclic antidepressants have also been used to treat urge incontinence because of their ability to inhibit or "paralyze" the bladder smooth muscle. Possible side effects include fatigue, dry mouth, dizziness, blurred vision, nausea and insomnia

42. Overflow incontinence • Overflow Incontinence Overflow incontinence is the uncontrollable leakage of small amounts of urine, usually caused by some type of blockage or by weak contractions of the bladder muscles. When urine flow is blocked or the bladder muscles can no longer contract, the bladder becomes overfilled and enlarged. Pressure in the bladder increases until small amounts of urine dribble out. • In men, an enlarged prostate can block the opening into the urethra from the bladder. Less commonly, blockage is caused by narrowing of the bladder neck or the urethra (urethral stricture), which may occur after prostate surgery. In men and women, constipation can cause overflow incontinence if stool fills the rectum to the point of putting pressure on the bladder neck and urethra. A number of drugs that affect the brain or spinal cord or that interfere with nerve messages, such as anticholinergic drugs and opioids, may impair bladder contractions and cause overflow incontinence. Nerve damage that paralyzes the bladder (neurogenic bladder) can also cause overflow incontinence. Diabetes mellitus can also cause a form of neurogenic bladder and overflow incontinence.

43. Overflow S/S Signs and Symptoms Palpable distended bladder post voiding Post-void residual >200 cc Have patient void Insert Urinary Catheter and record urine volume Normally less than 50 cc

44. Overflow Diagnosis and management Diagnosis :Ultrasound assess bladder volume Uroflowmetry (urodynamics) Management: General • Correct underlying outflow obstruction • Intermittent Self Catheterization • Double Voiding • Crede's Maneuver

45. Overflow medications Medical Management: 1) Betanachol (Urecholine) Mechanism : Cholinergic agonist with Parasympathetic stimulation contracts detrussor Indications: Non-obstructive bladder atony Contraindications : Hyperthyroidism , Peptic Ulcer Disease , Asthma 2) Alpha-Adrenergic blockade Prazosin (Minipress) ,Terazosin (Hytrin) Mechanism Decreases bladder neck and urethral tone Indications :Benign Prostatic Hypertrophy ,Sphincter Hyperspasticity

46. Overflow Outlet obstruction • These patients have difficulty emptying their bladders; therefore, the goal is to improve bladder drainage. Follow conservative management by modifying fluid excretion and prompted voiding. • Do a renal sono to find cause and proceed • Medications include alpha-adrenergic antagonists; prazosin decreases internal sphincter tone and can improve the flow of urine. Use antiandrogens and luteinizing hormone-releasing hormone (LHRH) analog if atonic bladder-cholinergics (eg, bethanechol) are ineffective in treating UI. • Self-catheterization or a Foley catheter is used, especially in cases of neurogenic bladder. • Urethral strictures may require dilation or surgery, especially if the prostate is enlarged.

47. Overflow Underactive detrusor • Initial goals are to reduce residual volume, eliminate hydronephrosis, and prevent urosepsis. Insert an indwelling or intermittent catheter to decompress the bladder (for 2 wk). • Identify and reverse potential causes of impaired detrusor function (eg, fecal impaction, medications).

48. Female Pelvic muscles

49. Intense urge to void: Detrusor overactivity/Urge incontinence Loss with cough/laugh/bending: stress incontinence Continuous leakage: Detrusor underactivity/overflow incontinence Types of UI

50. History • Obtaining a thorough history is the most important step in the evaluation of UI. • Onset • During pregnancy • Postpartum • Surgery or trauma • Frequency/severity/amount • Number of pads • Voiding diary • A small amount of urine usually is seen in overflow incontinence or outlet incompetence, and moderate flow in detrusor overactivity. • Patterns (eg, nocturnal versus diurnal) • Precipitants • Medications • Cough • Position changes