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Key Clinical Questions

  • image How should you evaluate urinary and fecal incontinence in the hospital or rehabilitation setting?

  • image How do you treat urinary and/or fecal incontinence?

  • image What are the important elements of incontinence management in transitions of care?

  • image What are the treatment options for urinary retention in hospitalized patients?

  • image What are the guidelines for urinary catheter use and management in hospitalized patients?

It has been estimated that 22% to 35% of patients on general medical wards have UI and 10% have FI. In the hospital setting, both UI and FI may coexist with urinary retention (UR). Incontinence may cause skin breakdown and pressure ulcers, and UI may cause increased use of indwelling catheters, and falls. Catheter-associated urinary tract infection (CAUTI) accounts for up to 70% to 80% of all hospital health care acquired infections (HAIs). Hospital-acquired CAUTI, a “never event,” is both a marker of insufficient quality performance and negatively impacts reimbursement. The duration of catheter use is strong risk factor for CAUTI in hospital settings. Poor quality incontinence management also increases costs from absorbent and containment products and increased use of already limited resources (eg, nursing and aide time), and may lead to increased caregiver burden after discharge.


  • Although continence care is often delegated to nursing staff, failure to recognize, evaluate, and treat incontinence and UR as significant “hazards of hospitalization,” especially in older patients, may increase morbidity, length of stay, and functional impairment, even up to 30 days postdischarge.


Normal micturition and defecation involve similar neural control and muscular coordination. Continence results from effective storage during filling and efficient emptying during the voiding phase or defecation phase. Efferent nerves arising from the sacral micturition center at S2-S4 mediate bladder muscle (detrusor) contraction via muscarinic receptors. Sympathetic, adrenergic nerves arising from T11-L2 sustain contraction of smooth muscle in the proximal urethral and internal anal sphincters. The distal urethral sphincter and the external anal sphincter are voluntarily controlled via somatic cholinergic nicotinic nerves arising from the sacral micturition center. Urethral and anal closures are also maintained through contraction and support from striated muscle and fascial elements in the pelvic floor. A micturition center in the pons linked to subcortical and frontal centers that inhibit urgency and voiding controls coordination of bladder filling and emptying. Less is known about neurological control of defecation, although similar mechanisms have been proposed that coordinate relaxation of the external anal sphincter with the change of the ano-rectal angle with valsalva. Normal defecation also depends on stool consistency (affected by diet and colonic transit time), rectal compliance and sensation (ability to retain stool in the rectum and delay defecation until socially appropriate), and integrity of the internal and external anal sphincters and the puborectalis muscles.



Especially relevant in the hospital setting, urinary and ...

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