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Urological Care of the Spinal Cord–Injured Patient

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Urological Care of the Spinal Cord–Injured Patient WJ350312_323-331.qxd 4/22/08 4:52 AM Page 323 J Wound Ostomy Continence Nurs. 2008;35(3):323-331. Published by Lippincott Williams & Wilkins CONTINENCE CARE CE Urological Care of the Spinal Cord–Injured Patient Nancy Fonte Spinal cord injury (SCI) is a catastrophic occurrence affecting the (47.5%). Falls are the second most frequent cause of SCI lives of 11,000 people in the United States every year. Urologic (22%), and violence, primarily from gunshot wounds, ac- complications account for much of the morbidity associated with count for 13% of all these injuries. Recently, the propor- SCI and as much as 15% of the associated mortality. Spinal tion of sports-related injuries has declined to 8.9%. The cord–injured patients are required to digest a plethora of self- majority of all those injured are men (79%), and the aver- management information during the emotionally and psycho- age age at the time of injury is 37.6 years.2 logically distressing period immediately following their injury. As a vital resource in the SCI patients’ recovery process, it is crucial ■ Continence Physiology for the WOC nurse to have knowledge of the specialized needs of this population. This article reviews the effects of SCI on blad- The term continence denotes the ability to store urine der function, discusses potential complications of the neurogenic until an acceptable opportunity for urination occurs. bladder, and provides an overview of management options to Normal bladder function involves a cycle of filling, stor- assist the patient in adaptation and restoration of quality of life. age, and a conscious desire and decision to void.3 This entire cycle relies on control of the detrusor (bladder) ■ Introduction muscle and competence of the sphincter mechanism. The initial desire to void occurs when the bladder is Spinal cord injury (SCI) affects approximately 11,000 people filled with an amount of urine ranging approximately in the United States each year.1 The level and extent of spinal from 250 to 450 mL.4 As the bladder distends, afferent cord damage determines the extent and severity of sensory nerves in the lamina propria (submucosal layer) of the and motor deficits, as well as the impact on respiratory, bladder wall transmit messages to multiple modulatory lower urinary tract, sexual, and bowel function. Since only area within the brain. These areas, in turn, inhibit mic- 1% of persons with an SCI experience complete neurologi- turition until the individual makes a conscious decision cal recovery, the goal of care is rehabilitation to maximal to urinate.5 The pons contains a specialized group of functional independence and preservation of quality of life neurons known as the pontine micturition center, which within the context of their SCI-related impairments.2 Even coordinates the micturition reflex.6 During bladder fill- with an aggressive rehabilitation program, persons with SCI ing, the detrusor muscle remains relaxed and the smooth are at considerable risk for complications such as pressure ul- and striated muscles of the urethral sphincter mecha- cers and urinary tract complications associated with neuro- nism maintain tone, ensuring a closed bladder outlet. genic bladder. Urologic complications account for the With voiding, the detrusor muscle contracts and the ure- majority of morbidity rates and 10% to 15% of deaths in this thral sphincter muscles relax, ensuring nonobstructed population.1 Managing urinary elimination is one of the urinary outflow.7 Efferent signals from the central brain many adaptation challenges the spinal cord–injured person and brainstem are transmitted to the bladder via the au- must master. How well they are assisted through the process tonomic nervous system. The autonomic nervous sys- will help achieve the restoration of their quality of life. The tem regulates autonomic body functions, such as the WOC nurse has specialized knowledge in urological compli- heartbeat, bowel, and urinary tract contraction; it is di- cations and acts as an essential health care team member vided into the sympathetic and the parasympathetic during and after the rehabilitation process. Ⅲ Nancy Fonte, BSN, RN, CWOCN, AtlantiCare, Home Health, ■ Causes Egg Harbor Township, New Jersey. Corresponding author: Nancy Fonte, BSN, RN, CWOCN, AtlantiCare, The Spinal Cord Injury Information Network reports that Home Health, 6550 Delilah Road, Suite 304, Egg Harbor Township, motor vehicle accidents are the most frequent cause of SCI NJ, 08234. ([email protected]). Copyright © 2008 by the Wound, Ostomy and Continence Nurses Society J WOCN ■ May/June 2008 323 WJ350312_323-331.qxd 4/22/08 4:52 AM Page 324 324 Fonte J WOCN ■ May/June 2008 nerves.8 Sympathetic outflow regulating lower urinary during bladder filling; it typically occurs in injuries that tract function originates from neurons in the 10th tho- affect spinal segments C2 to S1. Failure to store because racic to the 2nd lumbar vertebrae. Efferent signals are of the outlet usually occurs with lower injuries affecting transmitted via the hypogastric nerve; sympathetic sig- the lumbosacral vertebrae, spinal segments S2–4. Failure nals promote urinary storage via detrusor relaxation and to empty because of the outlet may be caused by detru- contraction of smooth muscle within the proximal ure- sor-sphincter dyssynergia (DSD) in SCI. Detrusor-sphincter thra. The primary neurotransmitter responsible for these dyssynergia is defined as impaired coordination between effects is norepinephrine. Parasympathetic signals regu- detrusor muscle contraction and relaxation of the stri- lating lower urinary tract function originate from neu- ated sphincter during micturition. As a result, the detru- rons in the second, third, and fourth sacral segments. sor muscle and striated sphincter contract at the same Activation of the parasympathetic nerves results in mic- time, functionally obstructing the bladder outlet. These turition (bladder evacuation) via direct stimulation of problems may present at different points following SCI. the detrusor muscle and indirectly via opening of the Therefore, ongoing assessment and changes in bladder urethral sphincter mechanism.9 Acetylcholine is the pri- management extends well beyond the initial rehabilita- mary neurotransmitter mediating parasympathetic ac- tion period.9 tivity in the lower urinary tract. The somatic nervous system innervates the skeletal muscles of the body. ■ Complications of the Neurogenic Bladder Efferent nerves originating from neurons in sacral spinal segments 2 through 4 travel via the pudendal nerve to Multiple complications can occur when normal innerva- innervate the striated muscle of the urethral sphincter tion to the bladder and urinary sphincter is impaired. mechanism (rhabdosphincter), the periurethral striated Common complications include urinary incontinence, muscle, and the pelvic floor muscles.8 urinary tract infection (UTI), upper urinary tract distress, urinary calculi, autonomic dysreflexia, and bladder ■ Neurogenic Bladder and SCI cancer. Spinal cord injury adversely affects detrusor muscle func- Urinary Tract Infection tion and urethral sphincter, resulting in neurogenic blad- Urinary tract infection is the most common urological der dysfunction.6 Within minutes after initial injury, the complication for the SCI patient. Sepsis, frequently caused spinal cord swells to fill the spinal canal at the injury by UTIs, is a leading cause of mortality among patients level. This swelling inhibits blood flow and oxygenation with SCI.2 Urinary tract infections increase the number of to the spinal cord tissue. Axons and neural cells are dam- hospital admissions and length of a hospital stay and lead aged. Bleeding may occur in the central gray matter, pos- to loss of therapy time.13 The SCI-related factors that con- sibly spreading to other areas of the spinal cord. These tribute to UTI risk in persons with SCI include (1) incom- events cause a condition known as spinal shock, lasting plete bladder emptying, (2) low bladder wall compliance, from several hours to several weeks. During spinal shock, and (3) insertion of an indwelling catheter. even undamaged areas of the spinal cord become tem- Incomplete bladder emptying with micturition allows porarily disabled, causing inhibition of all reflexes and urine to remain in the bladder and act as a medium for function below the level of injury and creating an acon- bacterial growth. In patients with DSD, contraction of the tractile detrusor.10 The return of reflex activity, such as striated muscles of the sphincter mechanism creates tur- the bulbocavernosus reflex, marks the end of spinal bulence during micturition allowing urine to move from shock and may be followed by hyperreflexia, hypertonic- the more bacteria-laden distal urethra to the usually ster- ity clonus, and neurogenic detrusor overactivity.11 The ile proximal urethra, increasing the risk of colonization extent and the type of damage to the voiding cycle are and UTI.5 determined by the location, completeness, and vascular Low bladder wall compliance also predisposes to extension of the lesion. Vascular extension refers to is- upper UTI (pyelonephritis) and urosepsis by creating sta- chemic damage to the spinal cord beyond the orthopedic sis affecting the entire urinary tract. It is caused by level of injury. A complete injury produces both sensory chronic bladder outlet obstruction with deposition of ex- and motor loss; with an incomplete injury, the person cess collagen in the bladder wall (seen on x-ray as trabec-
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