Retention

and Mikolaj Przydacz1



(1)
Department of Urology, Jewish General Hospital, McGill University, Montreal, QC, Canada

 



Keywords
RetentionNeurogenic detrusor underactivityDetrusor-sphincter dyssynergiaIntermittent catheterizationClean intermittent catheterizationSterile intermittent catheterizationIndwelling catheterizationSuprapubic tubeSacral neuromodulationIntrasphincteric injections of botulinum toxin AExternal sphincterotomy



Introduction


Patients with neurogenic lower urinary tract dysfunction may suffer from urinary retention, the inability to voluntarily void urine. This condition can be acute or chronic. Acute retention of urine is defined as a painful, palpable, or percussible bladder, with the patient unable to pass any urine [1]. Chronic retention is defined as a non-painful bladder that remains palpable or percussible after the patient has passed urine. These patients may also present with incontinence due to overflow and debilitating problems such as recurrent infections resulting from chronically elevated post-void residual.

The underlying urodynamic pathology of retention includes detrusor underactivity or detrusor-sphincter dyssynergia (DSD) . Detrusor underactivity is a urodynamic observation of contractions 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 [1, 2]. In patients with relevant neurological condition, the presenting pathology can be termed as neurogenic detrusor underactivity (NDU) . This term excludes idiopathic, myogenic, and drug-induced causes of underactive detrusor [3, 4]. NDU typically occurs when neurological lesions affect sacral, infrasacral, and peripheral neural pathways regulating functions of the lower urinary tract (see Chap. 2, “Neurogenic Bladder Pathophysiology,” and Chap. 3, “Pathologies Responsible for the Development of the Neurogenic Bladder”). NDU may also appear in the acute phase of neural injury and in some general motor disorders (e.g., Parkinson disease) [5].The underlying pathophysiology of detrusor underactivity in these specific groups of patients is currently not well understood, although studies have correlated detrusor underactivity to the patient’s overall motor function [6]. Within the spectrum of detrusor underactivity, the condition in which contractions cannot be demonstrated during urodynamics is defined as an acontractile detrusor. DSD is defined as a detrusor contraction synchronous with an involuntary contraction of the urethral and/or peri-urethral striated muscle [1]. This condition is observed when neurological lesions appear between the brainstem (pontine micturition center) and the sacral spinal cord (sacral micturition center) (see Chaps. 2 and 3). Impaired coordination between detrusor and sphincter during voiding in patients without relevant neurological disorder should not be termed as DSD. In these patients, the dysfunction is more appropriately referred to as dysfunctional voiding or pelvic floor hyperactivity [7, 8].


Epidemiology


The precise incidence and prevalence of NDU and DSD are unknown given the variability in neurological disorders [5, 9]. Lack of epidemiological data is exacerbated by the requirement that NDU and DSD can be diagnosed only with a pressure-flow urodynamic study . Some studies consider only patient-reported voiding symptoms without concomitant urodynamic evaluation. Available data are limited to single cohort studies or case reports. To make matters worse, there is no agreed-upon consensus of what defines reduced contraction strength, prolonged bladder emptying, or normal voiding time span when detrusor underactivity is suspected [4]. Specific normative values need to be identified in future research [2].

The most common neurogenic causes of detrusor underactivity include diabetes, previous pelvic surgery and radiation therapy, infrasacral spinal cord injury (SCI), vertebral disk prolapse, multiple sclerosis, and Parkinson disease. Detrusor underactivity may also appear in the acute phase of cerebrovascular accident, traumatic brain injury and SCI.

DSD can occur after any trauma or disease below the pons and above the sacral cord. These mainly include: SCI, multiple sclerosis, multiple system atrophy, spinal dysraphism, and transverse myelitis [9]. DSD is more frequent in patients with a complete rather than incomplete spinal cord lesion and in such cases is more likely to be continuous [10].

Epidemiological data on related voiding symptoms and urodynamic findings of detailed disorders have been presented in Chap. 3.

Additionally, retention is the most common urological finding in infection-related neurogenic bladders. These include lumbosacral herpes zoster, genitourinary herpes simplex, tabes dorsalis, Guillain–Barré syndrome, Lyme disease, poliomyelitis, and acquired immune deficiency syndrome (AIDS) [11]. Among them, only AIDS-related voiding dysfunctions have been reliably estimated to affect 16–45% of patients with neurological complications of this disease [12]. Impaired bladder function becomes more common with disease progression [13, 14]. Neurogenic voiding dysfunction in AIDS patients portends poor prognosis. At the time of seroconversion, patients may present with acute urinary retention mainly by way of DSD [12, 15, 16]. If neural involvement progresses, NDU or acontractile detrusor may be found in up to 45% of cases.

Both NDU and DSD with related voiding symptoms significantly affect patients’ quality of life and jeopardize renal function. Clinicians should keep in mind that DSD may have more profound effects on renal function than NDU. It has been estimated that up to 50% of patients with DSD develop serious urological complications [17, 18]. High intravesical pressures during voiding lead to elevated retrograde pressures in the ureter and pelvis, hydronephrosis, renal scarring, and, ultimately, terminal renal failure. Furthermore, DSD may often occur in combination with detrusor overactivity, particularly in patients after suprasacral SCI. DSD-related complications have been shown to occur less frequently in women and patients with multiple sclerosis, perhaps due to lower detrusor pressures [7, 19, 20].


Diagnosis



History and Physical Examination


A detailed history as part of the initial evaluation is imperative. Presenting complaints associated with urinary retention usually are attributed to dysfunctional bladder emptying. Thus, most patients complain of voiding problems (hesitancy; straining; poor, prolonged and intermittent flow; terminal dribble) and post-micturition symptoms (sensation of incomplete emptying, post-micturition dribble), terms for which have been developed and defined by the International Continence Society (ICS) .



  • Hesitancy—the term is used when an individual describes difficulty in initiating micturition, resulting in a delay in the onset of voiding after the individual is ready to pass urine.


  • Straining to void—the term describes the muscular effort used to either initiate, maintain, or improve the urinary stream.


  • Slow stream—reported by the individual as his or her perception of reduced urine flow, usually compared to previous performance or in comparison to others.


  • Intermittent stream (intermittency)—the term is used when the individual describes urine flow, which stops and starts, on one or more occasions, during micturition.


  • Terminal dribble—the term is used when an individual describes a prolonged final part of micturition, when the flow has slowed to a trickle/dribble.


  • Feeling of incomplete emptying—a self-explanatory term for a feeling experienced by the individual after passing urine.


  • Post-micturition dribble —the term is used when an individual describes the involuntary loss of urine immediately after he or she has finished passing urine, usually after leaving the toilet in men, or after rising from the toilet in women.

The interview should elicit information regarding initiation of micturition (reflex, strain, Credé) and investigate whether performed by individuals themselves or with caretakers. Patients may also present with complete lack of voiding (usually accompanied by abdominal pain) or incontinence (due to overflow). In patients already catheterized, the duration of each catheter use before change and performed catheterization technique should be recorded. Reassessment of bladder-emptying technique is also important. Patients should be asked about other urological complaints, in particular storage problems (urgency, frequency, nocturia), as both NDU and DSD may sometimes present with mixed storage and voiding symptoms [21]. Clinician should also evaluate the presence of bladder sensation. The onset of complaints should be carefully investigated and classified as acute or chronic. In patients with chronic retention, symptom onset may be gradual and it can go unnoticed by caregivers or by patients with limited bladder sensation or who are severely cognitively impaired and cannot report symptoms [22]. Previous history of urinary retention or episodes of catheterization should be elicited. Possible progression of the voiding dysfunction should be clarified (stable or changing complaints), as it has been shown that DSD tends to worsen over time, and there is a correlation between neurological status and clinical findings [7]. Similarly, the prevalence of detrusor underactivity may increase with age, and studies report that it is more common in men. Up to 48% of elderly non-neurogenic patients may show underactive detrusor [5]. Potential myogenic causes of detrusor underactivity should also be excluded [4]. This include impaired bladder perfusion (chronic ischemia is commonly seen in patients with atherosclerosis and microvascular diseases), bladder fibrosis, and age-related degradation [21]. Special attention should be given to diabetic patients, as reported symptoms usually result from integrative mechanism, i.e., both myogenic and neurogenic damage [23]. In elderly male patients, reported voiding symptoms may be associated with bladder outflow obstruction (BOO) mainly due to benign prostatic hyperplasia. However, it is not possible to differentiate NDU, DSD, and BOO without urodynamic study [21]. Studies have shown that there is a poor correlation between symptoms and urodynamic diagnosis in this specific group of patients [24, 25]. Accurate assessment of symptoms indicating possible complications or other causes of retention (hematuria, dysuria, fever) should be conducted to rule out comorbid pathology such as malignancy, urolithiasis, or urinary tract infection. Neurological symptoms related to underlying neurological pathology should also be documented with onset, severity, evolution, and any treatment.

It is important to analyze how reported complaints affect the patient’s quality of life. Patients should be asked about the degree of hardship the symptoms cause and whether they influence their daily activities, social life, and work productivity.

As patients with neurourological complaints may also suffer from neurogenic bowel and sexual dysfunction, bowel and sexual histories are important [26, 27]. Bowel history should elicit information regarding pattern and frequency of defecation; rectal sensation; desire to defecate; and possible episodes of fecal incontinence, constipation or defecation initiation (digitation, suppository use) [28]. Sexual history should investigate symptoms of genital or sexual dysfunction; presence of sensation in genital area; lack of desire (loss of libido); difficulty in achieving orgasm; dyspareunia in women; and erectile dysfunction or ejaculation problems (premature, delayed, retrograde, anejaculation) in men.

Retention and other voiding problems may be aggravated by different comorbidities. Apart from underlying neurological disorder, other causes of urinary retention can be categorized as obstructive, infectious/inflammatory, or pharmacologic [11]. The most common obstructive pathology in men is benign prostatic hyperplasia [29, 30]. Furthermore, end-stage BOO may also lead to significant detrusor underactivity. Other obstructive causes include prostate cancer, phimosis, paraphimosis, and external-constricting devices applied to the penis. In women, obstructive retention often involves pelvic organ prolapse such as cystocele, rectocele, or uterine prolapse. In both sexes, urethral strictures, stones, and foreign bodies, as well as bladder tumors with blood clots can directly block the flow of urine [31]. Benign or malignant pelvic masses as well as fecal impaction and gastrointestinal or retroperitoneal masses may lead to external compression of the bladder neck. Infectious/inflammatory causes of urinary retention include sex-specific and general pathologies. In males, acute prostatitis and prostatic abscess may cause urine retention. In females, painful vulvovaginal lesions and vulvovaginitis can vitally impair voiding. Urethritis (from a urinary tract infection or sexually transmitted infection) as well as genital herpes (with local inflammation and painful urination) may lead to urine retention in both sexes. Numerous pharmacologic agents have direct or indirect effects on the lower urinary tract and can decrease detrusor contractility [3, 30, 32]. Both prescribed and over-the-counter drugs may worsen voiding symptoms and lead to retention. Drugs with antimuscarinic properties, such as tricyclic antidepressants, may compete with acetylcholine at muscarinic receptors, resulting in bladder relaxation. Nonsteroidal anti-inflammatory drugs have shown to doubly increase the risk of urinary retention [33]. Calcium channel antagonists may also occasionally precipitate retention in individuals who have presumably been rendered more vulnerable as a result of predisposing risk factors [3]. It has been shown that polypharmacy significantly increases the risk of urinary retention [34]. Table 8.1 lists medications associated with voiding difficulties [3, 30, 32]. Other causes may include any prior urinary tract trauma or surgery, post-partum complications (e.g., obstetric anal sphincter injury, peri-urethral lacerations, wound breakdown), as well as de novo post-partum urinary symptoms.


Table 8.1
Pharmacologic agents associated with urinary retention and voiding symptoms [3, 30, 32]























































Class

Drugs

Antiarrhythmics

Disopyramide, procainamide, quinidine

Anticholinergics (selected)

Atropine, belladonna alkaloids, benztropine, biperdin, darifenacin, dicyclomine, disopyramide, fesoterodine, flavoxate, glycopyrrolate, hyoscyamine, ipratropium bromide, oxybutynin, propantheline, scopolamine, solifenacin, tolterodine, trihexyphenidyl

Antidepressants

Amitriptyline, amoxapine, clomipramine, desipramine, doxepin, duloxetine, imipramine, maprotiline, nortriptyline, paroxetine

Antihistamines (selected)

Brompheniramine, chlorpheniramine, cyproheptadine, diphenhydramine, hydroxyzine, meclizine, promethazine

Antihypertensives

Hydralazine, nifedipine

Antiparkinsonian agents

Amantadine, benztropine, bromocriptine, levodopa, trihexyphenidyl

Antipsychotics

Chlorpromazine, clozapine, fluphenazine, haloperidol, prochlorperazine, quetiapine, thioridazine, thiothixene

Antiulcer agents

Cimetidine, ranitidine

Calcium channel antagonists

Amlodipine, diltiazem, felodipine, nifedipine, verapamil

Chemotherapeutic agents

Vincristine, cisplatin

Hormonal agents

Estrogen, progesterone, testosterone

Muscle relaxants

Baclofen, cyclobenzaprine, diazepam

Sympathomimetics (alpha-adrenergic agents)

Ephedrine, phenylephrine, phenylpropanolamine, pseudoephedrine

Sympathomimetics (beta-adrenergic agents)

Isoproterenol, metaproterenol, terbutaline

Miscellaneous

Amphetamines, carbamazepine, dopamine, mercurial diuretics, nonsteroidal anti-inflammatory drugs (e.g., indomethacin), opioid analgesics (e.g., morphine, hydromorphone, oxycodone)

A well-conducted medical history should be completed with an assessment of the patient’s social situation. Accessibility to care, toileting, catheters, and other supplies may be limited by financial constraints or other social factors. Family or caregiver support should be queried and the patient’s independence should be evaluated.

A proper history should not only aim to diagnose the cause and nature of bladder dysfunction but also to identify associated complications of neurogenic lower urinary tract dysfunction. The consequences of urinary retention depend on the chronicity of the problem and the degree of urine retention. In patients with acute complete obstruction, metabolic disturbances, including acidosis, azotemia, and hyperkalemia, can be life-threatening. Increased intravesical and intraureteral pressures can dramatically reduce the glomerular filtration rate and renal blood flow. Rupture of the urinary tract is also possible. In patients with chronic retention, hydronephrosis, renal failure, recurrent urinary tract infections, or urolithiasis may be observed during initial consultation (see Chaps. 1015).

In addition to medical history , a comprehensive physical examination should be performed. It consists of examining the abdomen, back, and loins, as well as pelvic and genital organs. Abdominal examination should include percussion and palpation of the bladder [11]. A bladder may be percussible if it contains at least 150 mL of urine and it should be palpable with more than 200 mL [30, 35]. Bladder tone and pain should be assessed. Further exam may also reveal abdominal or flank masses or fullness, suggesting malignancy or fecal impaction. Clinicians should evaluate sensation within sacral dermatomes (special consideration for S2–S4 dermatomes) and perianal area (see Chap. 4, “Medical History and Physical Examination,” Fig. 4.​1), spinal cord-mediated reflexes (see Chap. 4, Table 4.​3), as well as anal sphincter tone and voluntary contractions. The urethra should be examined for the presence of obstructing masses, diverticula, cysts, or breakdowns. The external genitalia are evaluated for evidence of injury, pathological masses, or local irritation contributing to painful urination or urine retention. In men, prostate size should be assessed. In women, a pelvic exam should analyze pelvic organ prolapse that can cause bladder outflow obstruction. A bimanual exam may help to evaluate uterine size, position, and support, as well as rule out any palpable pathological masses. Inspection of the vagina and surrounding perineal skin may reveal atrophy, lesions, or scars associated with prior surgery, as well as urine-related skin breakdown. Tenderness of the levator muscles may suggest pelvic floor hypertonicity associated with dysfunctional voiding. Urethral hypermobility and the presence of stress urinary incontinence (spontaneous or induced by Valsalva or cough) should be assessed.

The clinician should carefully examine hand function, in particular functional ability of the thumb and index or middle finger, as patients with retention usually require intermittent catheterization.

Clinicians should also assess the patient’s mental status, cognition, mode of ambulation, mobility, gait, balance, coordination, weakness, and spasticity.


Bladder Diary and Questionnaires


Because reported complaints need to be objectively established, specific or generic questionnaires should be employed (note the discussion of questionnaires for SCI patients in Chap. 4, and the discussion of generic questionnaires and those for patients with multiple sclerosis in Chap. 7, “Incontinence Due to Neurogenic Detrusor Overactivity”). A voiding diary can be helpful in clarifying the frequency and severity of patient’s symptoms (see the discussion of voiding diaries in Chap. 5, “Testing”). In patients suffering from retention, a catheterization diary, used in the same manner as the voiding diary, may be more valuable [36]. Recorded parameters include time and volume of urine obtained at catheterization, as well as the same values obtained for any voids between catheterizations. When sensation is preserved, episodes of urgency may also be noted. Obtained quantities may help in characterizing the patient’s compliance to bladder management regimes. When catheterization volumes exceed the volume at which filling pressures become unsafe for the upper urinary tract, appropriate management needs to be implemented. Moreover, careful record of catheterizations can show fluctuations in diuresis and could be used to determine the optimal catheterization frequency to adopt.


Urinalysis and Urine Culture


Infectious and inflammatory pathologies may cause or aggravate reported voiding problems in neurologically impaired individuals. Therefore, a urinalysis is recommended in patients suffering from retention [37, 38]. It may also reveal hematuria, proteinuria, or glycosuria, indicating possible complications of neurogenic bladder or important comorbidities that may lead to urine retention. As described in Chap. 5, a dipstick analysis may be more useful to exclude than to prove urinary tract infection, and if any evidence of infection is detected, urine culture with antibiotic sensitivity is required. Of note, asymptomatic bacteriuria should not be routinely treated (see Chap. 5—section “Urinalysis/Urine Culture”) [17]. In already catheterized patients, samples from leg bags should not be analyzed. Well-obtained urine specimens are samples taken from a freshly inserted intermittent sterile catheter and those taken from a catheter port [39].


Uroflowmetry


In patients who still void, non-invasive uroflowmetry should be conducted to objectively document the voiding pattern and the initial ability of bladder empting. It also serves as an valuable method to monitor treatment results [17]. Obtained findings may include a low flow rate, decreased peak flow rate, prolonged and intermittent flow, hesitancy, low voided volume , and prolonged voiding time (Fig. 8.1) [40]. However, these findings are not specific, because they may also be seen in NDU, DSD, or structural abnormalities [41].

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Fig. 8.1
(a) Detrusor-sphincter dyssynergia. (b) Valsalva voiding curve: patients with areflexic or hypocontractile bladder void with Valsalva maneuver that is represented as an intermittent and irregular curve (From Storme and McCammon [40], with permission)


Post-void Residual


Clinicians emphasize that post-void residual (PVR) urine volume should be assessed in all patients suspected of urinary retention [22]. Elevated PVR predisposes to incontinence, urinary tract infections, bladder stones, and renal dysfunction [42]. An elevated PVR indicates dysfunctional voiding, but it cannot be used to discern whether this is caused by poor detrusor contractility (underactive detrusor) or by obstruction (DSD, structural abnormalities). However, measurement of PVR may reveal the necessity of immediate introduction of bladder catheterization (if not already implemented). The PVR volume at which the patient’s bladder-emptying technique should be changed is related to the overall bladder capacity and remains a matter of dispute [43]. It is currently recommended to introduce patients to catheterization techniques when a PVR volume consistently exceeds 100 mL and patients present with related symptoms [44, 45]. On the other hand, chronic urinary retention was traditionally defined as a PVR >300 mL [46]. Available data suggest that ultrasound measurement of PVR is preferable to catheterization, and portable scanners can be easily used in daily clinical practice as a convenient non-invasive tool [4751].


Renal Evaluation


In patients with significantly elevated post-void residual, history of previous retention, or with risk factors for chronic kidney disease, renal evaluation is recommended. Basic laboratory and imaging studies are necessary to monitor kidney function. Measuring serum creatinine, blood urea nitrogen, and electrolytes levels, as well as calculating the glomerular filtration rate, help to assess renal function. Creatinine clearance provides more precise data but requires a 24-h urine collection to assess creatinine excretion. Incomplete collection can result in underestimation of renal function. Renal scintigraphy with assessment of glomerular filtration rate is recommended when renal function is poor, muscle mass reduced, or if the function of each kidney has to be assessed separately in high-risk patients [43]. A renal ultrasound is a valuable tool for the general assessment of kidney structure and may reveal hydronephrosis, abnormal masses , scarring, stones, and other structural changes affecting the parenchyma (see Chap. 5, Figs. 5.​2, 5.​3, and 5.​4).


Bladder Ultrasound


Bladder ultrasound helps to detect stones and any possible tumor, indicating other causes of urinary retention or already developed complications of neurogenic bladder.


Other Investigations


Additional tests may help in proper diagnosis. Their utilization depends on clinical presentation. Evaluation of serum blood glucose and prostate-specific antigen can be considered based on the patient’s history, symptoms, and signs. Contrast cystourethrography may be helpful in outlining the bladder neck and urethra, as well as vesicoureteral reflux. Direct visualization of the urethra and bladder via urethrocystoscopy may be useful to detect strictures, tumors, stones, or inflammation, and should be especially considered in patients with recurrent urinary tract infections [17]. Advanced imaging techniques (computed tomography, magnetic resonance imaging) should be performed when pelvic, abdominal, or retroperitoneal mass, as well as other malignancy causing external bladder neck compression is suspected [11].


Urodynamics


Because symptoms lack adequate precision, urodynamic study is of value in the final diagnosis. It allows distinguishing between NDU (impaired contractility with low pressure-low flow) and DSD (functional obstruction with high pressure-low flow). Only urodynamic study can offer more detailed information about the underlying mechanism of neurogenic lower urinary tract dysfunction. Urodynamic study should be performed according to widely adopted and reliable recommendations. These include Good Urodynamic Practices and Terms 2016: Urodynamics, uroflowmetry, cystometry, and pressure-flow study, developed by the ICS and Urodynamic studies in adults: AUA/SUFU guideline, developed by the American Urological Association and the Society of Urodynamics, Female Pelvic Medicine & Urogenital Reconstruction [52, 53].


Patients with Retention Due to Neurogenic Detrusor Underactivity

The main urodynamic finding is detrusor underactivity defined as a detrusor contraction of reduced strength and/or duration resulting in prolonged bladder emptying and/or a failure to achieve complete bladder emptying [1]. When no detrusor contraction is noted, an acontractile detrusor may be identified. Presented abnormalities are isolated to the voiding phase of urodynamic study. Nevertheless, neurological patients suffering from retention may also present with abnormalities of storage phase, including reduced sensation and increased cystometric capacity.


Detrusor Underactivity

Urodynamic investigation of detrusor underactivity is characterized by a poor maximum flow rate (Qmax) and an abnormal flow pattern, associated with a poorly sustained, low-amplitude detrusor contraction (Figs. 8.2 and 8.3) [54, 55]. However, there are currently no universally accepted urodynamic parameters to define presented abnormalities [4]. The ICS does not define specific cutoffs or state any preference for any certain method of evaluation. Standardized assessment is characterized by lack of normative data, thus highly subjective. Several conceptions have been proposed to describe the relationship between detrusor pressure (Pdet) and urinary flow (Q) when detrusor underactivity is suspected. For day-to-day clinical practice, some experts proposed simple criteria of detrusor underactivity defined as [46]:

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Fig. 8.2
Urodynamic tracing of a female with difficulty urinating due to detrusor underactivity. Permission to void denoted by red arrow. The patient was noted to apply external pressure to her suprapubic region, or Crede, to assist with voiding. Thus, a subtle rise in the abdominal pressure is noted with Crede maneuver which is also reflected in the vesical pressure tracing. Qmax of 21 mL/s is not representative of her flow curve as she does a Crede maneuver to achieve that result. Average flow rate is considerably lower and more representative of her altered voiding function. Electromyography (EMG) shows appropriate relaxation as voiding starts, though increased EMG activity during void may reflect straining (From Bacsu et al. [55], with permission)


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Fig. 8.3
Urodynamic tracing of a male who is 4 years post-radical prostatectomy with incomplete bladder emptying and elevated residual. Permission to void given twice, and noted with increases in both abdominal and vesical catheters and corresponding small volume voids. Detrustor pressure (Pdet) does not rise substantially with his void, and a prolonged flow curve is noted. Qmax is 10 mL/s with Pdet @Qmax of 14 cm H2O. His BCI (PdetQmax + 5 Qmax) is 64 (<100), which represents detrusor underactivity. He also was catheterized for 90 mL at the end of the study (From Bacsu et al. [55], with permission)





$$ {\displaystyle \begin{array}{l}\mathrm{Pdet}@\mathrm{Qmax}<30-45\ \mathrm{cm}\ {\mathrm{H}}_2\mathrm{O}\ \mathrm{with}\hfill \\ {}\mathrm{Qmax}<10-15 \mathrm{mL}/\mathrm{s}\hfill \end{array}} $$
Pdet @Qmax—detrusor pressure at maximum flow rate, Qmax—maximum flow rate.

As female bladders generate lower pressures during voiding, some studies consider female detrusor underactivity when detrusor pressure at Qmax is less than 10 cm H2O [25]. To objectify bladder contractility, mathematical equations have been developed. These mainly include bladder contractility index (BCI) [56], the Watts factor [57], and the linearized passive urethral resistance relation (linPURR) [58]. Among them, BCI seems to be the most useful for daily clinical practice. It is simple, quick to calculate, and easily reproducible. BCI is based on detrusor pressure at maximum flow rate (Pdet @Qmax) and maximum flow rate (Qmax):



$$ \mathrm{BCI}=\mathrm{Pdet}@\mathrm{Qmax}+5\ \mathrm{Qmax} $$

In men, BCI > 150 suggests strong contractility; BCI 100–150 suggests normal contractility; and BCI < 100 suggests weak contractility. Complete absence of detrusor contraction may be termed as acontractile bladder (Fig. 8.4) [55, 57]. Because the equation was primarily developed for men with bladder outflow obstruction, Tan modified the BCI calculation and proposed a new formula of contraction strength for women, known as the projected isovolumetric detrusor pressure (PIP) [59]:



$$ \mathrm{PIP}=\mathrm{Pdet}@\mathrm{Qmax}+\mathrm{Qmax} $$


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Fig. 8.4
Urodynamic tracing of a female with acontractile detrusor and inability to void due to multiple sclerosis . Urodynamics revealed delayed first sensation (537 mL) and cystometric capacity of 733 mL. No incontinence was observed during filling. Despite having large cystometric capacity and desire, with permission, to void (at red arrow), she did not mount any detrusor contraction. An increase in vesical pressure is noted through this long filling curve suggestive of somewhat altered compliance. Given that this occurs over a volume of over 700 mL, the impact of this pressure change can be mitigated by an appropriate catheterization schedule. Urodynamic catheters were removed after the patient was unable to void with reasonable attempts of urination. After the catheter was removed, she urinated only 11 mL. Detrusor acontractility is diagnosed during her attempt to void (From Bacsu et al. [55], with permission)

With this modified formula, normal contractility in the female was defined as PIP = 30–75 [59]. In efforts to better clarify detrusor underactivity, further calculations have been proposed that can be helpful in assessing more complicated patients; these should be studied in the professional urodynamic literature [60, 61].


Reduced Bladder Sensation

Sensation of bladder filling is purely subjective and therefore depends on a cooperative and informed patient for reliability. Bladder sensation is reduced if it is diminished throughout bladder filling. Bladder sensation may also be completely absent. Many neurologically impaired patients may present with alternations of first sensation of bladder filling, first desire to void, and/or strong desire to void. It has been shown that up to 71% of patients after SCI or with myelodysplasia may experience impaired sensation compared to 30% of non-neuropathic patients [62]. Among individuals with altered sensation, up to 40% of neurological patients may report complete absence of sensation compared to 3% of non-neuropathic patients. Interestingly, further testing of non-neuropathic patients with impaired bladder sensation can reveal unrecognized underlying neurological pathology such as diabetic polyneuropathy, multiple sclerosis, or peripheral neuropathy after multiple pelvic surgery. Clinicians should bear in mind that the assessment of bladder sensation is highly subjective and should be taken with caution, as some patients may report a sensation of bladder filling even when the bladder is not being filled [63, 64]. Proposed intervals of bladder volumes referring to normal bladder sensations are included in Chap. 7, “Incontinence Due to Neurogenic Detrusor Overactivity,” in the section “Urodynamics.”


Increased Cystometric Capacity

Normal cystometric capacity is generally defined as 300–550 mL with larger values obtained in men compared to women [65]. Both detrusor underactivity and reduced bladder sensation significantly contribute to increased cystometric capacity. In daily clinical practice, the combination of detrusor underactivity with reduced bladder sensation and increased cystometric capacity is most often seen in patients with diabetic cystopathy (Fig. 8.5) [66].

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Fig. 8.5
Cystometrogram of a patient with diabetic cystopathy showing a hypocontractile large capacity bladder; maximum cystometric capacity was never reached. Vesical pressure and abdominal pressure were equalized at the start of the study with a corresponding detrusor pressure of zero. Filling was discontinued at a volume of 1500 cc. This bladder is highly compliant without evidence of detrusor overactivity (From Smith et al. [66], with permission)


Patients with Retention Due to Detrusor-Sphincter Dyssynergia

DSD is a urodynamic observation of a detrusor contraction synchronous with an involuntary contraction of the urethral and/or peri-urethral striated muscle [1]. It is diagnosed during the voiding phase of urodynamics. DSD may lead to prolonged detrusor contractions, structural bladder damage, vesicoureteral reflux, and upper urinary tract damage. As DSD occurs in lesions between the brainstem and the sacral spinal cord, patients may also present with concomitant neurogenic detrusor overactivity (NDO) and involuntary control of micturition.

In healthy individuals, there is a slight gradual increase in sphincter electromyogram (EMG) activity during bladder filling [67]. The EMG signal should stay relatively quiet and consistent [68]. During voiding, the first recorded event of this phase is a sudden and complete relaxation of the striated sphincteric muscles, shown by complete electrical silence of the EMG [67]. This is followed almost immediately by a rise in detrusor pressure as the bladder and proximal urethra become isobaric. The EMG signal then resumes once the bladder is empty. The sphincter complex is also coordinated during sudden increases in abdominal pressure. Coughing or Valsalva maneuvers elicit reflex contraction of the sphincter manifested as an increase in EMG activity [67].

In patients with DSD, relaxation of the striated sphincteric muscles during voiding is absent and coexists with detrusor contraction (Fig. 8.6) [67]. Diagnosis of DSD by EMG requires elevated EMG activity during detrusor contraction, in the absence of Valsalva and Crede maneuvers [8, 69]. These maneuvers would be detected as a rise in abdominal pressure (Pabd). Additional fluoroscopy has proven invaluable in the diagnosis because a urodynamist can see a dilation of the urethra to the level of the striated sphincter (spinning top urethra), no passing contrast through the area of the striated sphincter, and/or intermittent contractions of the striated sphincter.

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Fig. 8.6
(a) Increased electromyography activity causing urethral obstruction . (b) Open bladder neck with poor flow past-urethral sphincter (From Harris et al. [67] with permission)

Two classifications of DSD have been proposed. Blaivas et al. suggested that DSD should be classified according to the pattern of external urethral sphincter electromyographic activity, whereas Yalla et al. proposed classification according to the bladder pressure and resulting flow [7072]. In order to simplify this condition for daily clinical practice, DSD can also be characterized as intermittent (Fig. 8.7) [68] or continuous (Fig. 8.8) [68] according to the consistency of the sphincter contraction during the detrusor contraction [10]. The initial description of DSD and the chronology of events still remain a matter of dispute. Studies have shown that urethral sphincter may contract before, after, or at the same time as detrusor [7, 71, 73].

A440047_1_En_8_Fig7_HTML.gif


Fig. 8.7
Detrusor-sphincter dyssynergia. Intermittent involuntary contraction of the striated sphincter during the involuntary detrusor contraction (From Borawski [68], with permission)


A440047_1_En_8_Fig8_HTML.gif


Fig. 8.8
Detrusor-sphincter dyssynergia. An involuntary contraction of the striated sphincter that continues throughout the involuntary detrusor contraction (From Borawski [68], with permission)

Readers should be aware that the diagnosis of DSD with EMG is poorly standardized with variance in the type of electrodes (needle, patch) and their placement [8, 69]. Patch electrodes are frequently used due to easier placement, better tolerance, and greater patient mobility [69].

It is important to note that some volitional behaviors such as recruitment of pelvic floor due to pain or discomfort, Valsalva/Crede maneuvers, or any other source of artifact (fluid on patch, etc.) may mimic DSD [67]. If an unexpected increase in EMG signal was noted without any identifiable artifact, video imaging should be employed. Fluoroscopy can significantly help in the diagnosis of DSD and in the determination of vesicoureteral reflux [8, 17]. Furthermore, it is more sensitive in leakage detection than direct observation. Diagnostic discrepancy between EMG and fluoroscopy ranges from 40 to 46% [8, 69]. Male patients are more often diagnosed by means of EMG, whereas female patients are more often referred to video imaging [8, 69]. It has been suggested that the diagnosis of DSD in males by video imaging may be impaired due to anatomical bladder outflow obstruction (prostate), whereas in females diagnosis by EMG may be impaired due to increased electrode artifact [9]. A combination of EMG and fluoroscopy seems to be the best option but with limited availability [8, 69]. Moreover, it has been suggested that the clinician should be present during the urodynamic study to increase the accuracy of the diagnosis [9, 69].

A rare finding in neurologically impaired patients is a discoordination between bladder neck relaxation and detrusor contraction. This abnormality is also referred to as bladder neck dyssynergia, detrusor-internal sphincter dyssynergia, smooth sphincter dyssynergia, and proximal sphincter dyssynergia [7]. Similarly to DSD, this primary bladder neck obstruction leads to high detrusor pressure with low urinary flow rate. Non-neurogenic causes of the reported discoordination include benign prostatic hyperplasia and urethral stricture in males, and obstruction from pelvic organ prolapse, urethral stricture, previous anti-incontinence surgery, or urethral diverticulum in females [67]. Pelvic floor dysfunction is another possible cause seen in both sexes. Such discoordination does not cause a significant increase in EMG activity during voiding, as seen in tracing of patients with DSD or dysfunctional voiding (the EMG only reflects changes in the external urethral sphincter). Bladder neck dyssynergia can be diagnosed only by simultaneous imaging of the bladder outlet during voiding. Fluoroscopy of the pressure-flow study will show a failure of bladder neck opening (closed bladder neck and no bladder neck funneling) with a relaxation of the striated sphincter. Just for the record, patients with DSD will present with opened bladder neck without concurrent relaxation of the external sphincter [7, 74].

Clinicians should remember that in the absence of a neurological abnormality, impaired coordination of detrusor contraction and sphincter relaxation is more appropriately referred to as dysfunctional voiding or pelvic floor hyperactivity (see Chap. 2). Dysfunctional voiding is defined as an intermittent and/or fluctuating flow rate due to involuntary intermittent contractions of the peri-urethral striated muscle during voiding in neurologically normal individuals [1].

As patients with DSD are at high risk for multiple complications, including renal failure, and the disorder often worsens over time, routine lifelong follow-up monitoring should be offered to this specific group [7, 17, 70, 75]. It has been shown that patients with complete sensory and/or motor deficit have worse prognosis of DSD than those with incomplete deficits [75].


Treatment



Treatment of Patients with Retention Due to NDU



Intermittent Catheterization

Intermittent catheterization (IC) is a method of bladder emptying at a specified time frequency by inserting a catheter into the bladder, draining the bladder, and then removing the catheter [76]. This technique does not require an intact sacral micturition reflex to be present. IC is considered to be a safe and effective treatment modality of neurogenic bladder dysfunction for short- and long-term use [7779]. Nowadays, IC should be recommended as the first choice of treatment for those with inability to empty the bladder adequately and safely , particularly if the patient is physically and mentally willing to perform the task or has a caregiver who is able to assist [80]. Threshold volumes for initiating IC are not standardized and remain a matter of dispute [54]. Experts proposed than a PVR volume consistently more than 100 mL in symptomatic patients should prompt the start of IC [45]. IC should be immediately implemented in patients with PVR-related recurrent urinary tract infections, overflow urinary incontinence, or upper tract damage [21].

IC can be done either by the patient (intermittent self-catheterization, or ISC) or by a caregiver. Neurological disorders , including poor manual dexterity (in particular insufficient hand skills), weakness, tremor, rigidity, spasticity, disturbed perineal sensation, impaired visual acuity, cognitive impairment, or paraplegia, can affect the ability of a patient to perform self-catheterization [43]. Elderly patients should not be disqualified from self-techniques, as studies have shown that they have abilities similar to the general population in learning IC [81]. Thus, they should be offered IC preferentially over indwelling catheterization whenever possible. Furthermore, ISC is associated with reduced depression and lower discontinuation rates compared with assisted IC [82, 83]. General contraindications for IC include [54, 76]:



  • abnormal urethral anatomy (strictures, false passages, bladder neck obstruction)


  • small bladder capacity (<200 mL)


  • little motivation or inability or unwillingness to adhere to the catheterization time schedule


  • high fluid intake regimen (may require frequent catheterization, which may not be practical)


  • adverse reaction to passing a catheter into the genital area multiple times a day or prohibitive body habitus or psychological lack of acceptance (patient’s acceptance is required for long-term compliance)


  • tendency to develop autonomic dysreflexia with bladder filling despite treatment


  • caregiver who is unwilling to perform catheterization (relative contraindication)

Such limitations should be carefully assessed before starting IC.

IC can be carried out with sterile or clean technique . The sterile (non-touch) variant involves using a sterile single-use catheter along with sterile gloves, gown, and mask; disinfectant wipes or swaps; and sterile drainage tray or closed collection bag. Healthcare professionals in hospital settings mainly use this technique. Clean technique uses either a sterile single-use catheter or a clean reused catheter and a clean container with clean gloves or hands washed with soap and water. Patient population using single-use hydrophilic catheters have an estimated incidence of urinary tract infection between 40 and 60%, compared with the observed prevalence of urinary tract infection for multiple use of 70–80% [8487]. Clean technique has been widely adopted in community settings, as it is less time consuming and easier to perform, as well as decreases the cost of IC [88]. Nevertheless, the overall clinical evidence remains insufficient for powerful decision-making and it is not possible to state that one catheter method is better than another [77, 78, 89]. An updated systematic Cochrane review on strategies for catheter use emphasized that the evidence base is weak [90]. Currently, clean IC is most commonly used, and experts suggest that the sterile technique cannot be considered as a routine procedure [28, 91]. Sterile IC may be used in patients with recurrent urinary tract infections occurring with clean IC, and aseptic IC is an alternative to sterile IC [54, 76, 89, 92]. In addition, readers should be aware that decreased frequency of urinary tract infections with sterile technique is counterbalanced by significantly increasing cost compared with clean catheterization [89].

Suitable catheter material is an important factor for successful outcomes. Several types of catheter are currently available including [79]:



  • uncoated polyvinyl chloride


  • uncoated polyvinyl chloride with a separate lubricant applied manually


  • gel-coated polyvinyl chloride (prelubricated with gel by the manufacturer)


  • hydrophilic-coated (needing activation by manually adding water)


  • ready-to-use hydrophilic-coated (coating already contains water)

There are multiple products available with different features designed to make IC easier, depending on various circumstances (Fig. 8.9) [93]. A recently published systematic review with meta-analysis demonstrated advantages of hydrophilic-coated catheters in decreasing risk of urinary tract infection and urethral trauma, as well as improving patient’s satisfaction. Prelubricated catheters has been shown to be superior to conventional polyvinyl chloride catheters [89]. Moreover, it is noteworthy that catheter type may be important for patient compliance with treatment. Patient satisfaction is crucial, as it influences adherence to the IC regimen. Studies have shown greater degree of satisfaction with hydrophilic and prelubricated catheters , given their advantages of convenience, comfort, and ease of insertion when compared to conventional polyvinyl chloride [89, 9498]. Therefore, acceptance might be maximized by starting all new patients on hydrophilic catheters [84].

A440047_1_En_8_Fig9_HTML.jpg


Fig. 8.9
Display of the multiple products available with different features designed to make intermittent catheterization easier, depending on various circumstances (Continence Products Advisor [93], courtesy of the International Continence Society (ICS), with permission)

In order to improve outcomes and prevent complications, proper education and support are required, both during initial teaching and future follow-up. A well-trained and experienced clinician, usually a specialized nurse, has a vital role in teaching proper self-catheterization technique, exploring possible barriers, and maintaining compliance with long-term management [99]. Well-structured training programs for patients have been shown to improve outcomes [81] and acceptance of treatment [100102]. Patient education has been further described in Chap. 17, Proper Education of Patients Suffering from Neurogenic Bladder.

The frequency of catheterization depends on specific clinical presentation, including bladder volume, fluid intake, and PVR volume, as well as urodynamic parameters (compliance, detrusor pressure) [43]. Adequate frequency ranges from occasional IC to complete dependency on IC for bladder emptying [54]. Experts recommend that complete urinary retention should be managed with four to six catheterizations per 24 h [43]. Some individuals may need to awake from sleep at night to catheterize. If bladder volumes at catheterization consistently exceed 500 mL, it has been proposed to increase frequency of IC and adjust fluid intake, as well as to consider alternative method of bladder management [54, 76]. On the other hand, clinicians should be aware that more than six catheterizations per day is usually considered excessive and may have negative impact on patient compliance with treatment [42]. The catheter size most often used is between 12–16 Fr [28]. Patients who leak urine between catheterization require special attention. Possible causes of this situation include urinary tract infections, progression of neurological disease, emerging new problems of bladder or sphincter, as well as inadequate fluid intake. Those who are able to void but empty their bladder incompletely will need to use the catheter one to three times per 24 h after voiding [43].

Complications of IC include bacteriuria and urinary tract infection, urethritis, epididymoorchitis, epididymitis, prostatitis, urethral trauma/hematuria, urethral false passages, urethral stricture, autonomic dysreflexia (in those with injuries at T6 and above), and bladder stones [76]. Complications may increase in the long term [78]. However, it has to be emphasized that it is sometimes difficult to attribute causality because developing complications can potentially be caused by the underlying bladder dysfunction [79]. Complication rates are reduced with self-catheterization technique compared with assisted IC [86, 103, 104]. In individuals with recurrent urinary tract infections who perform IC, clinicians should reassess catheterization technique as well as consider change of catheter type, or start antibiotic prophylaxis [105]. Asymptomatic bacteriuria is a common finding in patients performing IC. It has been estimated that the incidence of bacteriuria is 1–3% per catheterization, and 1–4 episodes of bacteriuria occur for 100 days of clean IC [106]. After 30 days, almost all patients will develop this condition [107, 108]. Just for the record, asymptomatic bacteriuria should not be routinely treated except in pregnant women and individuals before surgical procedures within the urinary tract (see Chap. 10, “Urinary Tract Infection”).

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Jan 13, 2018 | Posted by in NEUROLOGY | Comments Off on Retention

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