Chapter 16 IDIOPATHIC URINARY RETENTION IN THE FEMALE
Urinary retention describes the inability to void voluntarily with a bladder volume exceeding the expected bladder capacity. More attention has been placed on male urinary retention caused by benign prostatic hypertrophy than urinary retention in women. Causes of incomplete bladder emptying in women are as variable and numerous as in men, but the presumed infrequency and difficulty in diagnosis accounts for less focus on them.1 The largest body of medical literature on causes of female urinary retention, even in the past decade, assumes a psychogenic or hysterical basis to the problem.2 The exact incidence of female urinary retention is unknown, but proper workup ensures that psychogenic retention is a diagnosis of exclusion and not an assumption. Excellent reviews of causes, workup, and management of urinary retention in females were published by Nitti and Raz1 and Smith and coworkers.3 Classically cited causes of urinary retention include neurologic, pharmacologic, anatomic, myopathic, functional, and psychogenic origins.
There are no quantitative definitions for bladder volumes associated with urinary retention. Instead, it is the effects of the urinary retention on the female patient that is of clinical concern. Diagnosis and management are not directed at addressing a specific volume or postvoid residual (PVR) volume; instead, the focus is on treating the effects of urinary retention. The symptomatic female patient may present with abdominal discomfort, irritative voiding symptoms, recurrent urinary tract infections, and incontinence and may eventually suffer from the sequelae of long-term retention, upper tract deterioration.
Instead of describing all of the causes of urinary retention in women, we focus on the area of idiopathic urinary retention, a group of causes that was previously gathered under the term psychogenic retention. The following sections provide an overview of common causes of urinary retention, discuss the history and basis of idiopathic retention, and describe the diagnostic tools and treatment options for the management of pseudomyotonia, a term coined by Fowler in 1986.
Reviews have classified urinary retention as transient or established (i.e., requiring a more comprehensive workup). Transient causes include immobility (especially postoperative), constipation or fecal impaction, medications, urinary tract infections, delirium, endocrine abnormalities, and psychological problems. After the underlying cause is treated or the offending agent is removed, there is usually a return to normal voiding.1,3 Common causes of established urinary retention are listed in Box 16-1.
Disruption in neural pathways and non-neurogenic causes can cause bladder outlet obstruction and decreased bladder contractility, leading to urinary retention. Normal voiding requires the coordinated contraction by the detrusor of adequate magnitude and concomitant lowering of resistance at the smooth and striated sphincters, with an absence of obstruction.4 The pontine micturition center controls voiding by stimulating parasympathetic fibers at S2 to S4, causing a detrusor contraction and inhibiting sympathetic fibers (T11 to L2) and somatic fibers of the pudendal nerve (S2 to S4). This causes relaxation of the bladder neck and proximal urethra and the external urethral sphincter, respectively.3
Detrusor–external sphincter dyssynergia (DESD) is a neurogenic cause of bladder outlet obstruction resulting from a suprasacral spinal cord lesion. DESD is associated with myelitis, spinal cord injury (i.e., upper motor neuron), and multiple sclerosis. Video urodynamics studies (VUDS) demonstrate detrusor hyperreflexia, high detrusor pressures, an increase in external sphincter activity, and small voided volumes. The ideal treatment for DESD is anticholinergics with clean intermittent catheterization (CIC).1,5
Multiple sclerosis is a focal demyelinating disease with a predilection for women between the ages of 20 and 50 years. Multiple sclerosis is associated with upper motor neuron and lower motor neuron lesions and therefore causes bladder outlet obstruction and decreased bladder contractility. Between 50% and 90% of patients with multiple sclerosis complain of voiding symptoms, usually urinary retention.6 Detrusor hyperreflexia is the most common findings on VUDS, with areflexia identified in up to 40% and DESD in up to 66%.7 The most important factors predisposing a multiple sclerosis patient to complications are high detrusor filling pressure (>40 cm H2O) and an indwelling Foley catheter.8 Management includes anticholinergics with or without CIC and behavioral therapy.9
Cauda equina syndrome is caused by distal spinal cord injury, intervertebral disk protrusion, myelodysplasia, neoplasms, and vascular malformations, leading to decreased bladder contractility. It is associated with a complex of lower back pain, sciatica, saddle anesthesia, lower extremity weakness, sexual dysfunction, and bowel or bladder dysfunction. Urinary retention and straining are the most common urologic presentation. Diagnosis is made by computed tomography, magnetic resonance imaging (MRI), or myelography.1,3 VUDS indicate an areflexic bladder, variable detrusor pressures, and sphincter denervation on electromyography.10 The extent of sensory deficit in the perineal or saddle area is the most significant negative predictor of bladder function recovery.11 Recovery of bladder function occurs over 3 to 4 years in 25% of patients with prompt surgical intervention.3
Pelvic plexus injury is most common during abdominoperineal resection, radical hysterectomy, proctocolectomy, and low anterior resection after injury or malignant extension to pelvic, hypogastric, and pudendal nerves. Findings of VUDS are similar to those for cauda equina syndrome. Urinary retention usually resolves within months, with one third of patients having permanent voiding dysfunction. Urodynamically, permanent voiding dysfunction is characterized by fixed, residual, striated sphincter tone and an open, nonfunctional smooth sphincter. CIC is the management of choice until normal voiding returns.1,12
Multiple infectious, endocrine, and nutritional abnormalities cause peripheral neuropathy and decreased bladder contractility, leading to urinary retention. The classic example is diabetic cystopathy, but others include pernicious anemia, alcoholic neuropathy, tabes dorsalis, herpes zoster infection, Guillain-Barré syndrome, and Shy-Drager syndrome. Diabetic cystopathy often has insidious loss or impairment of bladder sensation, with progressive increase in bladder volumes and hypocontractility.13–16 Management combines behavioral modification (e.g., timed voiding, Credé voiding) and CIC to facilitate emptying.1
There are many non-neurogenic causes of bladder outlet obstruction and decreased bladder contractility that lead to urinary retention in the female patient (see Box 16-1). Most obstruction is classified as anatomic and functional. Anatomic obstruction includes primary bladder neck obstruction, inflammatory processes, prolapse, neoplasm, gynecologic, iatrogenic, and other causes. Functional obstruction is usually described in terms of dysfunctional voiding and external sphincter spasticity.
Primary bladder neck obstruction was introduced in 1933 by Marion17 as a diagnosis of exclusion. Typically, these women present with irritative voiding symptoms and are given a trial of anticholinergics or antispasmodics; the course is eventual progression to periodic urinary retention or high PVR urine volumes. The exact cause is unknown, but the advent of video urodynamic testing has made diagnosis more accurate. The hallmark of primary bladder neck obstruction is incomplete opening or funneling of the bladder neck in the setting of sustained detrusor contraction of normal or high amplitude. There is resultant poor or nonexistent flow but a synergic external urethral sphincter. Management is medical and surgical. Terazosin has been used with improvement in flow rate and reduction of PVR volumes. Surgical options include transurethral incision of the bladder neck and Y-V-plasty of the bladder neck. Care is taken to avoid injury to the external sphincter, which can lead to stress urinary incontinence.1,3,18–20
Inflammatory processes, such as bladder neck fibrosis, urethral stricture, meatal stenosis, urethral caruncle, Skene’s gland cyst or abscess, and urethral diverticulum, are associated with anatomic obstruction. Management usually involves treatment of the offending infection and surgical excision of obstructing lesions.
Patients with pelvic prolapse (e.g., uterine, cystocele, enterocele, rectocele) usually present with incomplete emptying, lower urinary tract symptoms, and recurrent urinary tract infections with or without stress urinary incontinence. They may describe positional changes or the need to reduce the prolapse to void. Bladder outlet obstruction is caused by kinking or compression of the urethra during voiding. VUDS are useful in making the diagnosis. After the initial diagnosis, a pessary or packing should be used to reduce the prolapse and confirm the diagnosis. This helps predict the outcome of prolapse repair. Treatment of symptomatic prolapse is usually surgical.1,21 In cases of significant morbidity or age, a pessary alone may be used.
There are multiple neoplastic, obstetric, and gynecologic causes of bladder outlet obstruction in women. Urethral carcinoma is the only urologic malignancy more frequent in women (0.2%), although it remains rare. Patients present with bleeding and develop irritative and obstructive symptoms. Treatment ranges from local excision to anterior exenteration with complementary radiation therapy.22 Gynecologic neoplasms and masses usually cause urinary retention by external compression or direct invasion. A retroverted, impacted uterus that occurs in the first trimester of pregnancy is associated with urinary retention. Gravid females are usually managed with manual dislodging of the uterus or a pessary until voiding resumes.1
The most common iatrogenic cause of urinary retention is surgical correction of stress urinary incontinence. The published incidence ranges from 2.5% to 24%, which may be underestimated. The irritative or obstructive voiding symptoms and recurrent urinary tract infections that result may be overlooked if the patient demonstrates normal emptying. The placement of sutures is the key factor determining a procedure’s likelihood of causing obstruction. For example, sutures placed too medially cause urethral deviation or periurethral scarring; those placed too distally can cause kinking, leading to stress urinary incontinence; and tying sutures too tightly leads to hypersuspension, closing the bladder neck.1 Newer mid-urethral slings can cause bladder outlet obstruction if the urethra is injured or the tape is placed under tension. The diagnosis is made by a patient’s history before the procedure, physical examination, VUDS, endoscopy, and imaging. Urethrolysis is the treatment of choice. However, several studies have not correlated urodynamics and successful voiding after urethrolysis.23–25
Other iatrogenic causes of bladder outlet obstruction include a history of recurrent urethral dilation and postoperative urethral strictures. Urethral dilation leads to postdilatation bleeding or urine extravasation into periurethral tissue, causing scarring of the urethral wall and periurethral fibrosis.26 This is diagnosed with VUDS and managed with transurethral resection or incision. Urethral strictures are rare in women, but they are seen endoscopically after urethral surgery and prior instrumentation. They are usually managed with periodic selfcatheterization, permanent CIC, transurethral incision, or urethral reconstruction.1
Dysfunctional voiding and external sphincter spasticity are non-neurogenic functional causes of bladder outlet obstruction. Both conditions have been associated with inappropriate electromyographic activity during micturition with decreased urinary flow27 and with high pressure increases in the urethral pressure profile. Dysfunctional voiding is referred to as pseudo-dyssynergia (which mimics DESD), because it is a learned be-havior that can be treated and cured. Treatment combines timed voiding, biofeedback, and anticholinergics.1 External sphincter spasticity, characterized by “spasticity of the external sphincter and pelvic floor”28 results from introital or vaginal infections, Skene’s gland abscesses, adnexal disease, or cystitis. Pudendal nerve block improves voiding. VUDS reveal a bladder with intact sensation without the ability to contract due to cortical inhibition from the spastic pelvic floor.21 After managing painful or inflammatory lesions, treatment involves pharmacologic agents, including muscle relaxants and α-blockers. α-Blockers relax the bladder neck and urethra and enhance pelvic ganglionic transmission, which improves detrusor contraction. α-Blockers also treat the urinary retention that develops from transient spasticity.1,26,28