Evaluation and Management of Voiding Dysfunction and Urinary Retention
Aqsa Azam Khan
Victor W. Nitti
Introduction
Women with incomplete bladder emptying may experience a number of bothersome lower urinary tract symptoms (LUTS). These may manifest as voiding symptoms, such as urinary hesitancy, slow stream, or a sensation of incomplete bladder emptying, or storage symptoms, such as urinary frequency, urgency, nocturia, or incontinence. They may experience medical issues including urinary tract infections, and in more severe cases can have decompensation of their upper urinary tract function. In order to gain a full understanding of the various potential etiologies for incomplete bladder emptying, knowledge of the anatomy and voiding physiology is essential. In this chapter we aim to review the various etiologies for incomplete bladder emptying and voiding dysfunction in women and to review the diagnosis and management for the various conditions.
DEFINITION AND CLASSIFICATION
LUTS globally refer to the array of symptoms that may be representative of any bladder, urinary outlet, neurologic, pelvic floor, or endocrine abnormalities related to storage of urine and voiding. The International Continence Society (ICS) first developed a report of standardized definitions for LUTS in 19881 with the most recent update specifically for female pelvic floor dysfunction in 2010.2 Definitions as they pertain to retention and bladder emptying disorders are listed in Table 26.1.
Incomplete bladder emptying in women is a relatively poorly understood condition. Part of the reason for this may be due to varying classification systems and definitions to define this accurately and an overall paucity of studies.3 There is much value in understanding the terminology of lower urinary tract function in order for providers to have a common language and to develop universally applied guidelines and treatment paradigms.
PREVALENCE AND INCIDENCE
In 2005, Irwin et al.4 conducted the EPIC study, a population-based, cross-sectional telephone survey of 19,165 participants older than 18 years old in 2005 in five countries (Canada, Germany, Italy, Sweden, and the United Kingdom) using the 2002 ICS definitions for frequency, nocturia, urgency, overactive bladder (OAB), urgency urinary incontinence (UUI), stress urinary incontinence (SUI), mixed urinary incontinence (MUI), intermittency, slow stream, straining, terminal dribble, postmicturition dribble, and incomplete emptying. In their cohort, 59.2% of women reported at least one storage symptom (nocturia, urgency, frequency, UUI, MUI, SUI, other urinary incontinence) and 19.5% reported at least one voiding symptom (intermittency, slow stream, straining, terminal dribble).
Subsequently, Coyne et al.5 conducted a large international cross-sectional population-representative Internet survey of participants aged 40 years or older in the United States, United Kingdom, and Sweden which included over 15,000 women older than the age of 40 years.5 LUTS were again defined using 2002 ICS definitions and classified into storage (frequency, urgency, nocturia, incontinence [stress, urgency, mixed, coital, insensible]), voiding (weak stream, terminal dribble, hesitancy, straining, intermittency, split stream), postmicturition (incomplete emptying, postmicturition incontinence), and other (bladder pain, dysuria). The questions were asked according to a five-point Likert scale. In this cohort, women reported “sometimes” and “often” having a weak stream (20.1% and 4.4%), split stream (10.2% and 2.4%), intermittency (15.9% and 4%), hesitancy (11.8% and 2.8%), straining (5.9% and 1.4%), terminal dribble (38.3% and 14.5%), sensation of incomplete emptying (27.4% and 7.4%), and postmicturition incontinence (14.9% and 9.4%).
Studies using a postvoid residual (PVR) of 100 mL as the lower limit for voiding dysfunction in women have estimated a prevalence rate of 11%.6,7
TABLE 26.1 International Urogynecological Association/International Incontinence Society 2010 Terminology as They Pertain to Urinary Retention and Bladder Emptying Disorders | ||||||||||||||||||||||||
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LOWER URINARY TRACT PHYSIOLOGY
Many factors contribute to normal storage of urine and voiding, some which include neurologic, muscular, endocrine, and cognitive components.8 Figure 26.1 is a simplified schematic of the urinary tract and its neurologic inputs and outputs. Fowler et al.8 provide an excellent comprehensive and detailed review of lower urinary tract physiology. In order for the bladder to properly empty, it must generate a contraction that is strong enough to overcome the resistance of the outlet.9 Disorders may develop of the bladder (detrusor dysfunction) or of the outlet (bladder outlet obstruction) that may lead to incomplete bladder emptying and voiding dysfunction.
 FIGURE 26.1 Physiology of voiding. (Reprinted by permission from Springer: Nitti V, Khan A. Retention and bladder-emptying disorders. In: Heesakkers J, Chapple C, De Ridder D, et al, eds. Practical functional urology. Switzerland: Springer International Publishing, 2016:353-370, reprinted with permission [License Number 4933271299074].) |
Storage: The primary controller of urinary storage is the sympathetic nervous system, which uses activation of β3-adrenergic receptors on the detrusor to promote bladder smooth muscle relaxation and α1-receptors to contract the urethral smooth muscle. The effects on the outlet are reinforced by the somatic motor neurons which pass through the pudendal nerve to innervate the external urethral sphincter striated muscle and allow for a maintained contraction of these muscles.
Voiding: With increased bladder filling, the afferent messaging increases in intensity via pelvic nerves. This in turn stimulates the spinobulbospinal reflux pathway which then activates the pontine micturition center (PMC). The PMC then “flips the switch” and will simultaneously activate the parasympathetic nervous system while reflexively inhibiting the sympathetic and somatic fibers. This allows for relaxation of the outlet (the bladder neck and urethral sphincter) followed by stimulation of the detrusor muscarinic receptors by acetylcholine release. Subsequently, the bladder is able to contract through an open bladder outlet. Ongoing work is being done to learn about the roles of less studied pathways, such as periaqueductal gray matter and cognitive brain centers.
PATHOPHYSIOLOGY
There are many potential causes for incomplete bladder emptying and voiding dysfunction in women (Table 26.2). These causes can further be classified by whether it is due to dysfunction of the bladder (detrusor underactivity) or dysfunction of the bladder outlet (bladder outlet obstruction).
Bladder: Detrusor Underactivity
Primary dysfunction of the bladder now referred to as “detrusor underactivity” is defined as “a contraction of reduced strength and/or duration, resulting in prolonged bladder emptying and/or a failure to achieve complete bladder emptying within a normal time span.”10 Detrusor underactivity has replaced terms such as “impaired detrusor contractility,” “detrusor areflexia,” “hypotonic bladder,” “underactive bladder (UAB),” and “detrusor/bladder failure.” The causes for detrusor underactivity are variable and may stem from a variety of causes such as neurologic, pharmacologic, or myogenic etiologies. The clinical syndrome that occurs with detrusor underactivity is difficult to define due to the variability and nonspecific nature of symptoms associated with this condition, unlike with the clinical syndrome that accompanies OAB, but has been gaining attention by the medical community as of recently. One suggested definition by Osman et al.11 of the clinical syndrome of UAB as “reduced sensation of the need to void (the opposite of urgency) that may be associated with frequency and nocturia or reduced voiding frequency often with a feeling of incomplete bladder emptying and incontinence that may predominate at nighttime.” A study by Gammie et al.12 analyzing their urodynamic database over 28 years identified several symptoms and signs that correlated with detrusor underactivity. Urodynamic criteria to be considered as having detrusor underactivity included a PdetQmax <20 cm H2O, Qmax <15 mL/s, <90% bladder volume emptying, and excluding any clinical obstruction. Women with detrusor underactivity compared to women with normal
pressure-flow studies had higher rates of decreased urinary stream, interrupted urinary stream, hesitancy, incomplete bladder emptying, palpable bladder, absent and/or decreased sensation, enuresis, and impaired mobility. Most recently in 2018, the ICS Working Group on UAB released a terminology report in which they define UAB symptoms as being “characterized by a slow urinary stream, hesitancy and straining to void, with or without a feeling of incomplete bladder emptying sometimes with storage symptoms,” maintaining their prior ICS definitions for abnormal urodynamic detrusor activity for detrusor underactivity or acontractile detrusor.13 They further state that UAB occurs in association with diverse pathophysiologies and based on current knowledge there is no single distinguishing symptom.
pressure-flow studies had higher rates of decreased urinary stream, interrupted urinary stream, hesitancy, incomplete bladder emptying, palpable bladder, absent and/or decreased sensation, enuresis, and impaired mobility. Most recently in 2018, the ICS Working Group on UAB released a terminology report in which they define UAB symptoms as being “characterized by a slow urinary stream, hesitancy and straining to void, with or without a feeling of incomplete bladder emptying sometimes with storage symptoms,” maintaining their prior ICS definitions for abnormal urodynamic detrusor activity for detrusor underactivity or acontractile detrusor.13 They further state that UAB occurs in association with diverse pathophysiologies and based on current knowledge there is no single distinguishing symptom.
TABLE 26.2 Causes of Incomplete Bladder Emptying in Women | ||||||||||||||||||||||||||
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Neuropathic causes: Certain infections, such as HIV, herpes simplex virus, postinfectious polyneuritis causing Guillain-Barre, and tertiary syphilis have been found to cause neurologic dysfunction leading to impaired detrusor function.14 Diabetic neuropathy may affect innervation to the detrusor leading to dulled sensory input and altered smooth muscle function.15 Parkinson disease (PD) typically causes detrusor overactivity but has been found to present with detrusor underactivity or acontractility.16 Patients that have suffered hemorrhagic or cerebellar infarcts have also demonstrated these findings.17 Damage to the subsacral lower motor neurons which exit from the lumbosacral vertebrae may occur through a variety of conditions, some which include trauma, multiple sclerosis, pelvic surgeries, disc herniation, spinal stenosis, myelodysplasia, and spinal arteriovenous malformations.
Pharmacologic causes: The impact of certain medications on the bladder may lead to poor detrusor function or poor relaxation of the bladder outlet. Although antimuscarinics are used for management of LUTS, they can have an effect in some in which the detrusor function is inhibited enough to lead to incomplete bladder emptying. Opioids can have similar effects on the bladder. The study discussed previously by Gammie et al.12 also found a higher rate of detrusor underactivity on those on antidepressants. α-Agonists, such as phenylephrine, pseudoephedrine,18 and clonidine, can lead to poor relaxation of the bladder neck.
Myogenic causes: Normal aging has been found to be associated with morphologic changes to the detrusor muscle in which there are decreased ratios of detrusor muscle to collagen.19 Loss of bladder contractility and voiding efficiency with increasing ages has been demonstrated on urodynamic studies.20 The insula, which is the region of the brain responsible for sensing visceral sensations, has shown diminished response to bladder filling on magnetic resonance imaging (MRI) in asymptomatic aging people.21
Overdistension can lead to reversible and irreversible changes to the detrusor smooth muscle contractile function.22,23 Bladder outlet obstruction may lead to chronic overdistension that results in reduced blood flow and ischemic damage to detrusor myovesical plexuses and subsequent denervation.24 There has also been an association found between childbirth and possible overdistension injury. Labor exceeding 700 minutes has shown to have increased risk for postpartum voiding dysfunction,25 and persistent postpartum urinary retention has an estimated 0.05% incidence in a study that analyzed 8,000 consecutive births.26 Independent risk factors associated with postpartum urinary retention are cesarean section birth and third- or fourth-degree perineal tearing.27
Postoperative urinary retention (PUR) following regional or general anesthesia has been reported in several surgical specialties. Urinary retention and urinary tract infection in patients who underwent hip fracture repair were reported in 39.3% and 24%, respectively,28 which may have implications for hardware placed in those cases. Factors predictive of PUR include preoperative obstructive symptoms, age older than 50 years, male gender, spinal/epidural anesthesia, greater than 750 mL intraoperative fluids, anesthesia time greater than 2 hours, prolonged postoperative analgesia, and bladder volume greater than 270 mL upon entry to the postanesthesia care unit.29,30 Extensive pelvic surgeries such as radical hysterectomy may lead to some degree of denervation that may also impact bladder function.31
Bladder Outlet Obstruction
Bladder outlet obstruction may be due to a fixed anatomic obstruction, or, less obviously, a failure of the outlet to relax resulting in a functional obstruction not due to a structural abnormality. Chronic outlet obstruction has shown association with many morphologic changes of the bladder, including changes to the extracellular matrix, mitochondria, smooth muscle enzymes, and electrical gap junctions.22,32 It can lead to a rapid growth and hypertrophy of the smooth muscle of the bladder with an increase in collagenous connective tissue33 but decreased myosin concentrations resulting in a diminished contractility of the bladder.33,34 It has also been postulated that obstruction may lead to ischemia, which in turn can impact all the components of the bladder that comprise its viscoelastic properties such as the epithelium, connective tissue, vasculature, and smooth muscle. Ultimately, this may lead to acute muscle dysfunction.33 It is theorized that the degree of muscle dysfunction is related to the degree of hypertrophy of the tissue and not so much the duration of the obstruction.35 The bladder has shown remarkable regenerative abilities, however, and has shown recovery following some cases of obstruction in as short as 14 days after unobstruction.36
Fixed obstruction
There are many potential sources of fixed obstruction that may lead to incomplete bladder emptying in women, including distortion of the normal anatomy, vaginal, uterine, or urethral pathologies, or iatrogenic sources.
Distorted anatomy: There may be abnormal or distorted anatomy that leads to obstruction of the bladder neck or urethra. Some examples of this include an ectopic ureterocele or pelvic organ prolapse. Bladder prolapse in some may lead to kinking of the urethra or there may be extrinsic compression from a large rectocele or enterocele.37
Vaginal or uterine pathology: Conditions such as a Skene gland cyst or abscess, Bartholin gland cyst, retroverted or fibroid uterus, or impacted pregnant uterus may also be sources of extrinsic compression on the urethra. Vaginal malignancies or large pelvic malignancies may also cause extrinsic compression.38,39
Urethral pathology: Anatomic abnormalities or malignancies of the urethra may act as a fixed obstruction. These include conditions such as urethral diverticulum, urethral caruncle,40 urethral prolapse, urethral stricture, meatal stenosis, or urethral carcinoma. Urethral stricture are estimated to have a prevalence of less than 1% in women who present with voiding complaints,41 although they are likely underreported. They may be affiliated with a history of trauma, lichen sclerosis, or transurethral surgeries such as urethral dilations.
Iatrogenic: The most common cause for female bladder outlet obstruction in women is anti-incontinence surgery. Data evaluating PUR have estimated a 2% incidence of obstruction following SUI surgery.42 This may be an underestimation, however, as it is possible that many women have significant obstructive symptoms due to a subclinical obstruction without significant voiding dysfunction.43,44 There are varying rates of obstruction depending on which procedure was performed, with reports from greatest to least of 33% after autologous slings, 22% after Burch colposuspension, 20% following retropubic slings, and 7% and 4% for transvaginal needle suspension and tension-free vaginal tape, respectively.45 Risk factors for obstruction following an anti-incontinence surgery include concomitant pelvic organ prolapse, prior history of anti-incontinence surgery, and preoperative urodynamics findings of a PVR greater than 100 mL, peak flow of less than 20 mL/s, or detrusor acontractility.44
Functional obstruction
A functional obstruction occurs due to a failure of relaxation or coordination of the bladder outlet rather than a fixed and structural obstruction. This may occur at the level of the bladder neck or at the urethral sphincter.
Primary bladder neck obstruction (PBNO): Failure of the bladder neck to open adequately during voiding is referred to as PBNO. This diagnosis is based on two general requirements, which are a lack of anatomic obstruction and lack of increased striated sphincter activity during voiding,46 and is postulated to be due to either underlying neurologic pathology47 or a failure of mesenchymal elements to properly degrade with subsequent incorporation of connective tissue and hypertrophy of smooth muscle in the region.48 Recently, there has been an increased recognition of this condition in women,49,50 although overall there is a paucity of literature and little estimation as to the prevalence of this condition.
Dysfunctional voiding: Poor relaxation of the urethral sphincter and/or pelvic floor in the absence of a neurologic etiology is referred to as dysfunctional voiding. In children, this was coined by Dr. Frank Hinman Jr as the “nonneurogenic neurogenic bladder,”51,52 and sometimes is also called Hinman syndrome. This condition is thought to develop early in childhood and thought to resolve in most cases after puberty.52 One theory on its development is a habitual pelvic floor and/or urethral sphincter contraction during micturition in young children with pelvic floor discomfort, such as from constipation or possibly abuse, or in response to urinary urgency.53 This condition has also been noted in adults, possibly as a compensatory response to detrusor overactivity which leads to habitual urethral sphincter contraction throughout voiding, and is often is associated with a myriad of bothersome storage and voiding symptoms.52 This dysfunctional voiding is diagnosed when the patient is noted to have variable contractions throughout their void which prevents them from emptying normally.
Fowler syndrome: First described in 1988,54 Fowler syndrome differs from dysfunctional voiding or detrusor sphincter dyssynergia because these patients are often in retention but asymptomatic at the time of diagnosis.55 This presents in typically postmenarche young females in the second and third decades of life with chronic inhibition of the detrusor due to a long-standing poorly relaxing external urethral sphincter.55 An association was made in the original paper with Fowler syndrome and polycystic ovarian syndrome because 14 of the 22 women had this condition while also demonstrating abnormal electromyography (EMG) activity suggesting a possible hormonal contribution,54 but as of yet, there is poor data to support this claim.55
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