Voiding Dysfunction

Introduction


Female voiding dysfunction is poorly understood and has no official definition. The term can be used to describe any number of voiding difficulties. According to the International Continence Society, “normal voiding is achieved by a voluntarily initiated continuous detrusor contraction that leads to complete bladder emptying within a normal time span, and in the absence of obstruction.” Therefore, female voiding dysfunction can be presumed to be any condition that falls outside this definition.


Voiding dysfunction affects as many as 62% of women being referred to a urogynecologist or urologist for lower urinary tract symptoms (LUTS). The prevalence increases with age, and many women are asymptomatic. Often, urinary urgency and frequency are the only symptoms, and women are treated for urinary tract infections or overactive bladder without diagnosis of the voiding dysfunction.


Physiology of urine storage and voiding


The normal storage and emptying of urine depend on co-ordinated control at the level of the brainstem, spinal cord and peripheral nerves. The pontine micturition center controls voluntary voiding by co-ordinating relaxation of the urethral sphincter and contraction of the detrusor (bladder wall) muscle. This center receives inhibitory input from suprapontine centers including the cerebral cortex, cerebellum and basal ganglia, and stimulatory input from the anterior pons and posterior hypothalamus. It then relays efferent input to the bladder and urethral sphincter. There is another micturition center in the sacral spinal cord at the level of S2–4. This center allows for bladder contraction without pontine or suprapontine input. The lower urinary tract gets its peripheral innervation from the pelvic, hypogastric and pudendal nerves. The bladder receives parasympathetic efferent innervation from S2–4 via the pelvic nerve; the bladder and urethra get sympathetic efferent innervation from T10–L2 via the hypogastric nerve; and the striated external urethral sphincter receives sympathetic innervation from S2–4 via the pudendal nerve.


Bladder filling and distension cause firing of sensory afferent nerves, which travel up the spinal cord to the pontine micturition center. If it is time to void, this center will relay that message via efferent output down the spinal cord to the pelvic plexus at spinal cord segments S2–4. From there, the pelvic nerve stimulates the detrusor muscle to contract. This is co-ordinated with the pudendal nerve signaling the urethral sphincter to relax and allow the passage of urine. If, on the other hand, it is not an appropriate time to void, suprapontine centers will send inhibitory input to the pontine micturition center and prevent voiding until the time is appropriate.


Patient evaluation


Patient history should focus on symptoms related to the lower urinary tract. Symptoms of voiding dysfunction include urinary urgency, frequency, hesitancy, a sense of incomplete bladder emptying, straining to void, decreased force of stream, and urinary retention. A complete medical and surgical history will often identify the underlying etiology. Relevant history includes symptoms of pelvic organ prolapse, neurologic symptoms, medical history such as diabetes mellitus, history of stroke or other neurologic injury, and surgical history, including surgery for incontinence or prolapse, any pelvic surgery, especially radical hysterectomy or colectomy, and neurologic or orthopedic spine surgery.


On exam, particular attention should be paid to the pelvis. The urethra should be examined for any lesions, such as obstructing masses. The vagina should be examined for prolapse of the anterior vaginal wall, vaginal apex or cervix, and the posterior vaginal wall, all of which can obstruct the urethra. On bimanual exam, the presence of any pelvic masses, such as leiomyomas, should be determined. Cervical and lower uterine myomas may sometimes lead to obstruction of the bladder outlet.


Urinary symptoms can often be the presenting symptoms of neurologic disease in young women. It is therefore crucial to perform a thorough neurologic evaluation of all patients with LUTS. The neurologic history focuses on mental status changes, upper and lower extremity weakness or sensory defects, as well as gait. Physical examination assesses these same functions. The Mini Mental Status Examination is a reliable tool for the evaluation of mental status. Having the patient extend and flex the hip, knee and ankle and invert and evert the foot tests muscle strength of the lower extremities. These tests assess sacral spinal cord integrity. Patellar, ankle and plantar deep tendon reflexes are also tested. Upper motor neuron lesions may be associated with hyper-reflexia, whereas lower motor neuron lesions may demonstrate diminished reflexes. Light touch and pinprick are used to test sensory function along the sacral dermatomes on the perineum and thighs. The anal reflex can assess the function of spinal cord segments L5–S5. When this reflex is intact, stroking the skin adjacent to the anus will elicit a reflex contraction of the external anal sphincter muscle. This reflex can be difficult to evaluate and is not always present in neurologically intact individuals. Cerebellar function can be evaluated by observing the patient’s gait or by testing finger-to-nose or heel-to-shin co-ordination. In addition to inhibiting the pontine micturition center, the cerebellum also maintains pelvic floor tone.

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Jun 6, 2016 | Posted by in GYNECOLOGY | Comments Off on Voiding Dysfunction

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