eMedicine Specialties > Emergency Medicine > Genitourinary

Urinary Incontinence

Author: Nur-Ain Nadir, MD, Clinical Assistant Instructor, Department of Emergency Medicine, State University of New York, Downstate School of Medicine
Coauthor(s): Mark A Silverberg, MD, FACEP, MMB, Assistant Professor, Assistant Residency Director, Department of Emergency Medicine, State University of New York Downstate College of Medicine; Consulting Staff, Department of Emergency Medicine, Staten Island University Hospital, Kings County Hospital, University Hospital, State University of New York Downstate at Brooklyn
Contributor Information and Disclosures

Updated: Oct 20, 2009

Introduction

Background

Urinary incontinence (UI) is defined by the International Continence Society Standardization Committee as "a condition in which involuntary loss of urine is a social or hygienic problem and is objectively demonstrable."1

Micturition, as described in Pathophysiology, is a complex process and disruption of its integration on the musculoskeletal or the neurologic level can result in urinary incontinence. Four types of urinary incontinence are defined in the Clinical Practice Guideline issued by the Agency for Health Care Policy and Research: stress, urge, mixed, and overflow. Some authors may choose to include functional incontinence as a fifth type of incontinence.2,3,4,5

For related information, see Medscape's Urinary Incontinence & OAB Resource Center.

Pathophysiology

Micturition requires coordination of several physiological processes. Somatic and autonomic nerves carry bladder volume input to the spinal cord and motor output innervating the detrusor, sphincter, and bladder musculature is adjusted accordingly. The cerebral cortex exerts a predominantly inhibitory influence, whereas the brainstem facilitates urination by coordinating urethral sphincter relaxation and detrusor muscle contraction. As the bladder fills, sympathetic tone contributes to closure of the bladder neck and relaxation of the dome of the bladder and inhibits parasympathetic tone. At the same time, somatic innervation maintains tone in the pelvic floor musculature as well as the striated periurethral muscles.

When urination occurs, sympathetic and somatic tones in the bladder and periurethral muscles diminish, resulting in decreased urethral resistance. Cholinergic parasympathetic tone increases resulting in bladder contraction. Urine flow results when bladder pressure exceeds urethral resistance. Normal bladder capacity is 300-500 mL, and the first urge to void generally occurs between bladder volumes of 150 and 300 mL.

Incontinence occurs when micturition physiology, functional toileting ability, or both have been disrupted.4 The underlying pathology varies among the different types of incontinence:

Stress incontinence

Stress incontinence is characterized by urine leakage associated with increased abdominal pressure from laughing, sneezing, coughing, climbing stairs, or other physical stressors on the abdominal cavity and, thus, the bladder.2,6,7

Two main causes of stress incontinence exist. The major cause is impaired urethral support from pelvic floor muscle weakness. The less common cause is an intrinsic sphincter deficiency usually secondary to pelvic surgeries. In either case, urethral sphincter function is impaired, resulting in urine loss at lower than usual abdominal pressures.

Urge incontinence

Urge incontinence is a result of uninhibited bladder contraction from detrusor hyperactivity.8,9 This hyperactivity can be caused by abnormalities of the CNS inhibitory pathway such as strokes or cervical stenosis. Other causes are bladder inflammation from infection, stones, or neoplasms.

Urge incontinence is characterized by a sudden strong desire to pass urine that is difficult to suppress leading to involuntary urine loss. It usually entails urgency, frequency, or nocturia. These symptoms are often referred to as the overactive bladder syndrome (OAB). Some individuals may have a pure sensory abnormality where they exhibit urinary frequency and urgency without urine loss. This is often referred to as overactive bladder dry. Elderly persons frequently experience urinary loss without the sensation of urge, but the underlying mechanism of detrusor hyperactivity is still the same.

Mixed incontinence2,4

Mixed incontinence is the coexistence of stress and urge incontinence. Although it is generally defined as detrusor overactivity and impaired urethral function, the actual pathophysiology of mixed urinary incontinence is still being investigated.

Mixed urinary incontinence is characterized by involuntary loss of urine associated with urgency as well as exertion, cough, sneeze, or any effort that increases intra-abdominal pressure. This is the most common type of incontinence in women.

Overflow incontinence2,4

The major contributing factor to overflow incontinence is incomplete bladder emptying secondary to impaired detrusor contractility or bladder outlet obstruction. Factors involved in the development of overflow incontinence are physical obstruction such as pelvic organ prolapse and enlarged prostate, and neurological abnormalities, such as spinal cord injuries. It is also commonly associated with bladder neuropathy that occurs in the setting of diabetes mellitus.

Patients often complain of continuous small-volume leakage associated with weak urinary stream, dribbling, hesitancy, frequency, and nocturia.

Other less frequent causes of urinary incontinence include trauma from pelvic fracture, complications of urologic procedures, and fistulas. In the pediatric population, it includes enuresis and congenital abnormalities of the genitourinary system. Older adults can have transient incontinence from medication, decreased mobility, and fecal impaction.

Functional incontinence2

Functional incontinence is seen in patients with normal voiding systems but who have difficulty reaching the toilet because of physical or psychological impediments. Patients often present with recent symptom onset and have a good prognosis for cure if the cause is identified and treated. Functional incontinence is often secondary to reversible causes of urinary incontinence, as discussed later.

Frequency

United States

Urinary incontinence affects 10 million people in the United States and 200 million people worldwide. The cost of treating urinary incontinence in United States alone is $16.3 billion dollars, 75% of which is spent on treatment of women with this disorder. Overall prevalence of female incontinence is reported at 38%, increasing with age from 20–30% during young adult life to almost 50% in elderly women.10 Urinary incontinence affects 15-30% of the general geriatric population and 50-84% of the elderly persons in long-term care facilities.11 Urinary incontinence affects up to 7% of children older than 5 years. Incidence is 1.4% of adults aged 15-24 years and 2.9% of those aged 55-64 years.2

Mortality/Morbidity

Urinary incontinence is not really associated with any significant increase in mortality. However, patients with continual maceration of the perineal skin may be more prone to sores and thus be more likely to develop sepsis, although this has never been documented. The medical morbidity includes perineal candidal infections, cellulitis, pressure sores, constant skin irritation and moisture, urosepsis from indwelling catheters, mechanical falls and subsequent fractures from slipping on urine, and sleep deprivation from nocturia. Psychological morbidity includes poor self-esteem, social withdrawal, depression, sexual dysfunction from embarrassment, and curtailed social and recreational activities.

Race

According to one source, stress incontinence is more prevalent in Caucasian women than in African American or Hispanic women (41% vs 31% vs 30%, respectively). The incidence of urge incontinence is similar in all 3 groups (19% vs 16% vs 16%, respectively). Mixed incontinence occurs more often in African American and Caucasian women compared with Hispanic women (14% vs 15% vs 0.9%, respectively).

Sex

Female gender is a predisposing factor and mandates routine screening for urinary incontinence in all women regardless of age. Increased prevalence in women can usually be attributed to child birth – related pelvic floor damage. Anatomic genital abnormalities such as hypospadias, epispadias, and ambiguous genitalia can also contribute to incontinence.5

Age

Age is the single largest risk factor for urinary incontinence. Other risk factors for urinary incontinence include coexisting morbidity, cognitive dysfunction, functional impairment, gait abnormality, diuretic therapy, and obesity. Coexisting illness, such as cerebrovascular disease, radical pelvic surgery, or autonomic neuropathy, may increase the risk for urinary incontinence further. The occurrence of cerebrovascular disease doubles the risk for urinary incontinence in the older woman. Obesity, frailty, and diabetes are strong predictors of the occurrence of urinary incontinence. Additionally, older adults are more likely to become incontinent following the onset of UI-promoting factors such as constipation, obesity, and polyuria from uncontrolled hyperglycemia, hypercalcemia, or diuretic therapy.4,5

Clinical

History

A thorough history is essential to the evaluation of urinary incontinence. The clinical presentation of urinary incontinence, based on severity, frequency, and amount of debilitation varies from patient to patient.

Patients may be reluctant to initiate discussions about incontinence; therefore, all patients, especially those older than 65 years should be asked focused questions about voiding problems.

Nonspecific terms such as urge or nocturia should be avoided, as they may have different meanings for different patients.

Relevant questions include the following:12,13

  • Duration of complaint
  • Conditions at onset (pregnancy, postpartum, surgery, trauma)
  • Patterns (nocturnal vs diurnal)
  • Precipitants (cough, sneeze, position change, sound of running water)
  • Frequency/severity/quantity
    • Number of pads
    • Voiding diary
    • Amount of urine can distinguish between overflow incontinence and detrusor overactivity.
  • Concomitant symptoms
    • Fecal incontinence
    • Pelvic organ prolapse
    • Vaginal splinting for bowel movements
    • Urinary hesitancy, frequency, urgency, dysuria
    • Incomplete emptying, poor stream
    • Pelvic pressure/pain
    • Chronic constipation
    • Sacral backache
  • Medical conditions
    • Cancer, radiation
    • Diabetes
    • Neurologic disease
    • Surgeries (pelvic, urologic, spinal, CNS)
    • Postmenopausal hypoestrogenism
    • Benign prostatic hyperplasia
    • Chronic urinary tract infection (UTI), stones
    • Prolonged labor, multiparity, obstetric lacerations, large babies
    • Connective tissue disease
    • Chronic obstructive pulmonary disease (COPD)
    • Obesity
    • Congestive heart failure (CHF), hypertension
    • Medications side effects (eg, anticholinergics, calcium channel blockers, diuretics, sedatives, alpha-agonists, alpha-antagonists, alcohol)
  • Social history (living conditions, activities, history of smoking, alcohol and caffeine use)

Physical

A comprehensive examination is necessary to detect contributory factors and any underlying serious medical conditions. Evaluations should always consider neurologic conditions such as multiple sclerosis, cord lesions, and neoplasms of the bladder and prostate, especially if risk factors exist.13

  • Neurologic
    • Check for perineal sensation, resting and volitional tone of anal sphincter, anal wink, and bulbocavernous reflex.
    • Assess cognitive status, motor strength and tone, vibration, and peripheral sensation especially in the lower extremities.
  • Abdomen
    • Examine for masses, distended bladder after voiding, hernia, and signs of fluid overload.
    • Examine flank for tenderness. Examine back for deformity, dimpling, or hair tuft.
  • Pelvic
    • All women require a pelvic examination. Examine the vaginal mucosa for atrophy, narrowed introitus, vault stenosis, and inflammation.
    • Evaluate the anterior and posterior vaginal walls. Check for rectocele by pushing the speculum to support only the anterior vaginal wall while the patient coughs.
    • Perform a bimanual examination to detect masses.
    • Assess for adequate pelvic support by removing the top blade of the speculum and holding the bottom blade firmly against the posterior vaginal wall for support.
  • Cotton swab test12
    • This examination evaluates urethral mobility.
    • Place a sterile cotton swab through the urethra into the bladder. Pull the swab back until resistance is met, which indicates entry into the urethra. At this point, ask the patient to strain maximally.
    • A change of angle greater than 30 degrees indicates urethral hypermobility.
    • A positive finding does not confer a specific diagnosis, and older women have a high false-negative rate.
  • Stress testing12
    • This test evaluates stress-induced leakage when the bladder is full.
    • Ask the patient to cough forcefully or strain vigorously. Instantaneous urine leak is highly suggestive of stress incontinence, whereas delayed leakage is suggestive of stress-induced detrusor overactivity.
    • This test is very sensitive but can be misleading in inhibited patients and in those with low bladder volume.

Causes

Urinary incontinence (UI) can have many etiologies, some of which can be transient while others are of a more permanent nature. Some of these etiologies can also be life-threatening as discussed later.

Transient urinary incontinence

Transient urinary incontinence is often seen in both elderly and hospitalized patients. The mnemonic DIAPPERS is a good way to remember most of the reversible causes of incontinence.14

  • D: Delirium or acute confusion
  • I: Infection (symptomatic UTI)
  • A: Atrophic vaginitis or urethritis
  • P: Pharmaceutical agents
  • P: Psychological disorders (depression, behavioral disturbances)
  • E: Excess urine output (due to excess fluid intake, alcoholic or caffeinated beverages, diuretics, peripheral edema, congestive heart failure, or metabolic disorders such as hyperglycemia or hypercalcemia)
  • R: Restricted mobility (limits ability to reach a bathroom in time)
  • S: Stool impaction

Other systemic illnesses should also be considered in the differential diagnosis of urinary incontinence. These include vesicovaginal/vesicocutaneous fistula, bladder cancer or bladder stones, prostate cancer, leading to obstructive symptoms and overflow incontinence.

Neurological causes

From an emergency medicine perspective, neurological causes can be associated with increased morbidity and mortality and therefore should not be missed.14

  • Cortical lesions like strokes, tumors, aneurysms, or hemorrhages can lead to inappropriate voiding secondary to depressed social awareness, decreased sensation, and/or inappropriate urethral sphincter relaxation.
  • Spinal cord lesions can alter sympathetic and parasympathetic tone resulting in urinary incontinence.
  • Peripheral nerve disease such as diabetic peripheral neuropathy can cause urinary incontinence through a contractile dysfunction of the bladder.
  • Metastatic carcinoma can cause epidural spinal cord compression. Back pain is the initial symptom in most cases. Almost 20% of cases involve the lumbosacral spine. If the sacral cord is involved, urinary incontinence or retention can be expected. Urinary incontinence symptoms represent an unfavorable prognostic in this patient population. Early diagnosis and treatment of spinal cord compression is extremely important. Paraplegia or quadriplegia can develop within hours or days after the first neurologic deficit appears.
  • S2-S5 nerve root injury (herniation) can causes bladder dysfunction. Cauda equina syndrome can be seen with a large centrally protruding disk. Symptoms include bilateral leg pain and weakness, saddle anesthesia and urinary retention, or incontinence or fecal retention or incontinence. It is important to recognize this syndrome early because there is a high risk for chronic neurologic deficits if treatment is delayed.
  • Hemi-cauda equina syndrome (from a herniated lumbar disk) can also manifest as urinary incontinence. It presents with unilateral leg pain, unilateral sensory deficit in the S1-S5 dermatomes, and UI or urinary retention. These patients require urgent neurosurgical consultation for emergency surgery.
  • Multiple sclerosis should be considered in any patient without evidence of urinary tract infection who has a history of episodic or rapid onset of urinary symptoms. Urinary incontinence symptoms may be alone or may be accompanied by other vague neurological symptoms.

Pharmacologic causes

Many medications directly or indirectly contribute to urinary incontinence. They must always be considered as the cause of new-onset urinary incontinence, especially in elderly persons where polypharmacy is often encountered.13,14

  • Medications with anticholinergic properties or side effects including antipsychotics and antidepressants can cause urinary retention and thus overflow incontinence.
  • Alpha-adrenergic agonists can cause urinary retention and thus overflow urinary incontinence.
  • Alpha-antagonist cause urethral relaxation and thus urinary incontinence.
  • Diuretics can overwhelm bladder capacity causing urinary incontinence in elderly persons.
  • Calcium channel blockers decrease smooth muscle contractility in the bladder causing urinary retention with overflow incontinence.
  • Sedative-hypnotics can cause functional urinary incontinence by causing immobility secondary to sedation.
  • ACE inhibitors can exacerbate urinary incontinence by effects of diuresis as well as side effect of cough with relaxation of pelvic floor musculature.
  • Anti-parkinson medications can cause urinary urgency and constipation.

More on Urinary Incontinence

Overview: Urinary Incontinence
Differential Diagnoses & Workup: Urinary Incontinence
Treatment & Medication: Urinary Incontinence
Follow-up: Urinary Incontinence
References

References

  1. Bates P, Bradley WF, Glen E, Griffiths D, Melchior H, Rowan D, et al. The standardization of terminology of lower urinary tract function. J Urol. 1979;121:551-554. [Medline].

  2. Nazir T, Khan Z, Barber HR. Urinary incontinence. Clin Obstet Gynecol. Dec 1996;39(4):906-11. [Medline].

  3. Chutka DS, Fleming KC, Evans MP. Urinary incontinence in the elderly population. Mayo Clin Proc. Jan 1996;71(1):93-101. [Medline].

  4. Gibbs CF, Johnson TM 2nd, Ouslander JG. Office management of geriatric urinary incontinence. Am J Med. 2007;120(3):211-220. [Medline].

  5. Wilson MM. Urinary incontinence: selected current concepts. Med Clin North Am. Sep 2006;90(5):825-36. [Medline].

  6. [Guideline] American College of Obstetricians and Gynecologists. Urinary incontinence in women. 1533-1545. Obstet Gynecol. 2005;105(6):1533-1545. [Medline].

  7. [Guideline] Rogers RG. Clinical practice: urinary stress incontinence in women. N Engl J Med. 2008;358:1029-1036. [Medline].

  8. Mills W, Grennland JE, McMurray G. Studies of the pathophysiology of idiopathic detrusor instability: the physiologic properties of detrusor smooth muscle and its pattern of instability. J Urol. Feb 2000;163(2):646-51.

  9. Wein AJ, Rackley RR. Overactive bladder: a better understanding of pathophysiology, diagnosis and management. J Urol. 2006;175 (3 pt 2):s5-10. [Medline].

  10. Anger JT, et al. The prevalence of urinary incontinence among community dwelling adult women: results from the National Health and Nutrition Examination Survey. J Urol. 2006;175:601. [Medline].

  11. Fultz NH, Herzog AR. Epidemiology of urinary symptoms in the geriatric population. Urol Clin North Am. Feb 1996;23(1):1-10. [Medline].

  12. Dupont MC, Albo ME, Raz S. Diagnosis of stress urinary incontinence. An overview. Urol Clin North Am. Aug 1996;23(3):407-15. [Medline].

  13. Erdem N, Chu FM. Management of overactive bladder and urge urinary incontinence in the elderly patient. Am J Med. Mar 2006;119(3 Suppl 1):29-36. [Medline].

  14. Curtis LA, Dolan TS, Cespedes RD. Acute urinary retention and urinary incontinence. Emerg Med Clin North Am. 2001;19(3):591-619. [Medline].

  15. Patel AK, Chapple CR. Urodynamics in the management of female stress incontinence--which test and when?. Curr Opin Urol. Jul 2008;18(4:359-64. [Medline].

  16. Barry WD. Selecting medications for treatment of urinary incontinence. Am Fam Physician. 2005;71(2):315-22,329.

  17. Alhasso AA, McKinlay J, Patrick K, Stewart L. Anticholinergic drugs versus non-drug active therapies for overactive bladder syndrome in adults. Cochrane Database Syst Rev. 2006;18 (4):CD003193. [Medline].

  18. Herbison GP, Arnold EP. Sacral neuromodulation with implanted devices for urinary storage and voiding dysfunction in adults. Cochrane Database Syst Rev. Apr 15 2009;CD004202. [Medline].

  19. Shamliyan TA, Kane RL, Wyman J, Wilt TJ. Systematic review: randomized, controlled trials of nonsurgical treatments for urinary incontinence in women. Ann Intern Med. Mar 2008;148(6):459-73. [Medline].

  20. Duthie J, Wilson DI, Herbison GP, Wilson D. Botulinum toxin injections for adults with overactive bladder syndrome. Cochrane Database Syst Rev. Jul 18 2007;(3):CD005493. [Medline].

Further Reading

Keywords

urinary incontinence, UI, involuntary urine loss, stress incontinence, urge incontinence, mixed incontinence, overflow incontinence, urine leakage, urine loss

Contributor Information and Disclosures

Author

Nur-Ain Nadir, MD, Clinical Assistant Instructor, Department of Emergency Medicine, State University of New York, Downstate School of Medicine
Nur-Ain Nadir, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, Emergency Medicine Residents Association, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

Mark A Silverberg, MD, FACEP, MMB, Assistant Professor, Assistant Residency Director, Department of Emergency Medicine, State University of New York Downstate College of Medicine; Consulting Staff, Department of Emergency Medicine, Staten Island University Hospital, Kings County Hospital, University Hospital, State University of New York Downstate at Brooklyn
Mark A Silverberg, MD, FACEP, MMB is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, Council of Emergency Medicine Residency Directors, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Medical Editor

Peter MC DeBlieux, MD, Professor of Clinical Medicine and Pediatrics, Section of Pulmonary and Critical Care Medicine, Program Director, Department of Emergency Medicine, Louisiana State University Health Sciences Center
Peter MC DeBlieux, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, Radiological Society of North America, and Society of Critical Care Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Richard H Sinert, DO, Associate Professor of Emergency Medicine, Clinical Assistant Professor of Medicine, Research Director, State University of New York College of Medicine; Consulting Staff, Department of Emergency Medicine, Kings County Hospital Center
Richard H Sinert, DO is a member of the following medical societies: American College of Physicians and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Erik D Schraga, MD, Consulting Staff, Department of Emergency Medicine, Mills-Peninsula Emergency Medical Associates; Consulting Staff, Permanente Medical Group, Kaiser Permanente, Santa Clara Medical Center
Disclosure: Nothing to disclose.

 
 
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