Stress Urinary Incontinence Women

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Stress Urinary Incontinence

Stress urinary incontinence, according to the ICS terminology committee is the symptomatic complaint of involuntary leakage on effort or exertion, or on sneezing or coughing.
The sign of involuntary urinary loss from the urethra synchronous with exertion, sneezing, or coughing.
Urodynamic diagnosis of the involuntary leakage of urine during increases in abdominal pressure in the absence of a detrusor contraction—or called urodynamic stress incontinence.

Mixed Urinary Incontinence -Urodynamic diagnosis of both involuntary leakage of urine during increases in abdominal pressure. It is related to an involuntary detrusor contraction during urodynamics and is present in approximately 40% of women with stress incontinence.

Pathophysiology of SUI -

The pathophysiology of SUI is a combination of both functional and anatomical theories of urethral mechanism and innervation

The central nervous system (CNS) controls the lower urinary tract via sympathetic, parasympathetic, and somatic nerves that coordinate the activity of the bladder, urethra, and pelvic floor muscles.
The autonomic nervous system directs the involuntary portion of lower urinary tract function, which includes sympathetic control of urine storage in the bladder and parasympathetic regulation of voiding.
The somatic nervous system is involved in the voluntary contraction of the external urinary sphincter (the rhabdosphincter), which contracts to increase urethral closing pressure. Different neurons and several neurotransmitters take part in each aspect of micturition. Sympathetic control involves the hypogastric nerve and the neurotransmitter norepinephrine (NE). Parasympathetic control involves the pelvic nerve and the neurotransmitter acetylocholine (Ach).
Somatic control includes the pudendal nerve and acetylcholine, nitric oxide, and the neurotransmitter serotonin (5-HT). Onuf’s nucleus comprises a group of somatic motor neurons in the sacral spinal cord that release 5-HT and NE.
Axons from these motor neurons traverse the pudendal nerve and innervate the striated muscle (the rhabdosphincter) that makes up the outer layer of the urethra. Urethral sphincter motor neurons have high concentrations of 5-HT and NE.
Increased activity of the sphincter motor neurons has been shown to increase contraction of the rhabdosphincter, which may improve symptoms of SUI when these are caused by weakness of or damage to the rhabdosphincter and/or the pelvic floor muscles.

The urethra is supported by a hammock, sometimes known as the urethral pelvic ligament, which is a continuation of the pubocervical fascia. This hammock extends from the arcus tendineus on one side to the arcus tendineus on the other side. It acts as a support throughout the length of the urethra.
When there are increases in abdominal pressure, the urethra is closed by the supporting hammock-like structure. It is the integrity of this structure and not where the urethra is located that is involved in the development of stress incontinence.

Petros and Ulmsten theorized that the control of urethral closure is dependent on three distinct structures: the pubourethral ligaments, attaching the urethra to the pubic bone, the suburethral vaginal hammock just described, and the pubococcygeus muscle. It is the integral play between these 3 structures that helps maintain continence during stressful activities.
The urethra is surrounded by smooth and striated muscle. The smooth and striated muscle as well as the submucosal layer provide inwardly exerted forces, which help keep the mucosal layer covered. This is described as the “intrinsic mechanism of the urethra.” Therefore, continence is a combination of both anatomic and functional aspects.
When there is excessive abdominal pressure that the urethra is unable to balance either because of anatomic function or a combination of both problems, stress incontinence will occur.

Stress incontinence occurs along a continuum.

• Hypermobility stress incontinence (HSI) is incontinence that is related to an anatomic defect or a defect in the supporting structure of the bladder.
• Intrinsic sphincter deficiency is incontinence related to the intrinsic function of the urethra.
• All women with stress incontinence probably have some degree of intrinsic sphincter deficiency because not all women with urethral mobility have stress incontinence.
• On the other end of the spectrum, it is possible to have pure intrinsic sphincter deficiency without any anatomic or hypermobility defect.
• Both aspects of function and anatomy should be considered when discussing the entity of stress urinary incontinence.

Risk Factors for Stress Urinary Incontinence:

• Being female
• Childbirth
• Coughing over a long period of time (such as chronic bronchitis and asthma)
• Aging
• Obesity
• Smoking

Patient History:

• Presence or absence, incidence, severity, bother and effect on quality of life of urgency incontinence or stress incontinence.
• Other LUTS should also be assessed.
• Presence or absence of dysuria and hematuria.
• Whether occult neurologic disease could be present.
• Obstetric and gynecologic history, previous surgery/radiotherapy, bowel symptoms, and drug history.
• Other medical issues

Physical Examination and Evaluation:

• Focused physical examination requires abdominal and pelvic examination, as well as basic neurologic examination.
• Assessment of bladder emptying is necessary and done by palpating the lower abdomen.
• Patient use of a bladder diary to determine the number of incontinence episodes, activities which prompt urine leakage, and the frequency, timing, and amount of voiding that takes place throughout a 3- to 7-day period
• Urinalysis in all patients.

Nonsurgical treatment options for SUI include:

• Behavioral therapies 
• Pelvic floor muscle rehabilitation (PFMR)
• Drug therapies, including α-adrenergic agonists, β-antagonists, β-agonists, serotonin and norepinephrine reuptake inhibitors, and estrogen
• Vaginal occlusive or supporting devices, urethral plugs, electric simulation can be used as a way of rehabilitating pelvic floor muscles; magnetic stimulation has also been used in this mode.

Although surgery is the single most effective treatment for SUI there is a 40% to 50% chance that women can avoid an operation and be satisfied with the outcome by going through PFMT.

Early surgical intervention is more appropriate for patients with significant associated prolapse (beyond the hymenal ring) that may be corrected at the same time, those who are highly motivated to be completely dry or who have high levels of physical stress due to lifestyle or occupation, those with relatively severe SUI, and especially those with good pelvic floor function on initial examination.

Surgical treatment options for SUI include:

• Surgical bulking agents
• A variety of suspension techniques
• Sling procedures
• Retropubic operations to restore urethral support
• Artificial urinary sphincters
• Bladder Outlet reconstruction
• Myoplasty
• Indwelling catheter
• Bladder neck closure
• Urinary diversion

The treatment of patients with mixed urgency and SUI often involves a combination of antimuscarinic therapy and surgery.

Urethral slings are currently the procedure of choice for the surgical correction of female stress urinary incontinence.

Medical therapy for Mixed Urinary Incontinence is associated with significant resolution of the urgency component in only two thirds of patients.
This therapy does not address the bladder outlet and would not be expected to achieve complete dryness.
Surgery may cure or aggravate the urgency symptoms and lead to de novo urgency.
This aspect of anti-incontinence surgery is unpredictable and a major cause of patient dissatisfaction.

References:

• Abrams P, Artibani W, Cardozo L, et al: Reviewing the ICS 2002 terminology report: the ongoing debate. Neurourol Urodyn 2009; 28(4):287.
• Abrams P, Cardozo L, Fall M, et al: The standardisation of terminology of lower urinary tract function: report from the Standardisation Sub-committee of the International Continence Society. Neurourol Urodyn 2002; 21(2):167-178.
• Abrams P, Cardozo L, Khoury S, Wein A, ed. Incontinence, 4th ed. Plymouth (MA): Health Publications Ltd; 2009.
• de Groat WC and Yoshimuran N. Annu Rev Pharmacol Toxicol. 2001;41:691-721.
• DeLancey JO. Am J Obstet Gynecol. 1994;170:1713-1720.
• Fantl JA et al. JAMA. 1991;265:609-613.
• Goode et al. JAMA. 2003;290(3):345-352.
• Petros PE and Ulmsten UI. Int Urogynecol J Pelvic Floor Dysfunct. 1997;8(2):74-80.
• Thor KB and Katofiasc MA. J Pharmacol Exp Ther. 1995;274:1014-1024.
• Sexton CC, Coyne KS, Kopp Z, et al: The overlap of storage, voiding and postmicturition symptoms and implications for treatment seeking in the USA, UK and Sweden: EpiLUTS. BJU Int 2009; 103(Suppl. 3):12-23.
• Stephenson TP, Mundy AT: The urge syndrome. In: Mundy AT, Stephenson TP, Wien AJ, ed. Urodynamics: principles, practice and application, 2nd ed. New York: Churchill Livingstone; 1994:263-276.