Urinary Retention

Pathology and Management of Acute and Chronic Urinary Retention

Retention can occur in infants as a result of congenital disorders, but it is most common among men with prostatic hypertrophy, individuals with neurologic lesions, and diabetic patients with autonomic cystopathy.

Retention can be classified according to onset (acute versus chronic), site of impaired emptying (upper versus lower tract), and cause (obstruction versus impaired contractility).

Regardless of cause, retention is associated with increased incidence of urinary tract infection and risk for upper tract damage; thus, retention requires prompt diagnosis and prompt intervention. This entry provides a review of types of retention, etiologic factors, pathologic effects, assessment parameters, and treatment options.

Acute versus Chronic Retention

Acute urinary retention is characterized by the sudden onset of inability to void and is extremely painful; as a result, these patients end up in the emergency room and are sometimes misdiagnosed as having an “acute abdomen” because of the profound pain.

In patients who are unable to communicate as a result of neurologic lesions such as cerebrovascular accident, acute retention is manifest by extreme restlessness and diaphoresis. Causative factors for acute retention are typically classified as follows:

1. obstructive lesions that prevent the flow of urine, such as urethral stricture or prostate gland enlargement;
2. loss of detrusor muscle contractility caused by damage to the sensory and/or motor nerves controlling bladder function (as a result of diabetes, multiple sclerosis, and various medications); or
3. some combination of obstruction and diminished contractility. For example, antiincontinence procedures such as vaginal slings are associated with acute transient postoperative retention, which is caused in part by the effects of anesthesia and analgesics, in part by postoperative edema and temporary nerve damage, and in part by the increased urethral resistance provided by the sling.

Patients with chronic retention may inadvertently trigger an episode of acute retention by excessive alcohol intake, use of recreational drugs, or use of medications that compromise detrusor function. For example, the patient with prostatism may be placed at risk for acute retention when he is prescribed a beta blocker or a calcium-channel blocker. Table X1 highlights medications that may contribute to acute retention in the “at risk” patient.

In contrast to the dramatic onset of acute retention, chronic retention may develop over several months or even years; the most common causes are BPH and neurogenic processes such as diabetic cystopathy. Because compromised ability to empty the bladder develops gradually in these conditions, the patient may be relatively unaware of the problem.

Silent prostatism is the historical term used to describe patients who deny lower urinary tract symptoms (LUTS), despite significant postvoid residual (PVR) urine and arising blood urea nitrogen (BUN) and creatinine levels.

Chronic urinary retention may be identified “incidentally” in a routine physical examination if the patient presents with LUTS such as difficulty initiating the urinary stream, a slow or “weak” stream, and feelings of incomplete emptying.

Some patients complain of frequent, small volume voids and urinary leakage during activities associated with increased abdominal pressure, but they do not realize that the underlying problem is failure to empty the bladder effectively. Table X2 presents common lower urinary tract symptoms (LUTS).

Although chronic retention causes only “low-grade” symptoms, it can produce significant damage in terms of bladder function. For example, long-term obstruction to urine flow and the subsequent bladder distension cause denervation injury and increased collagen deposits within the bladder wall; these pathologic changes produce thickening of the bladder wall, diminished sensory awareness of bladder filling, and compromised detrusor contractility.

Relief of the obstruction may or may not “correct” the pathologic changes in bladder function, depending on the extent and duration of the obstruction and distension; if irreversible damage has occurred, the bladder will be large, “floppy,” and unable to contract effectively. Such individuals usually require long-term management with intermittent catheterization.

Alpha blockers combined with daily or twice daily catheterization may be effective for some patients with diminished voiding function. The alpha blocker helps to reduce urethral resistance, which improves bladder emptying in patients with diminished contractility; this “combination therapy” may permit the patient to manage with self-catheterization once a day, rather than four to six times a day.

Etiological Factors for Retention

Retention is frequently a multifactorial condition; however, all the etiologic factors can be broadly classified as either obstructive processes or conditions that compromise detrusor contractility. This segment focuses on the two primary “groups” of etiologic factors.

1. Obstructive Processes

Obstructive processes include any condition or lesion that interferes with the flow of urine at any point in the urinary tract, from the calyx of the kidney to the distal urethra.

Obstruction at any point causes stasis of urine above the obstruction; the urinary stasis and structural distension cause pain and infection, and untreated obstruction eventually leads to renal failure and unfortunately death.

Obstructive processes can be classified either by type (congenital, neoplastic, structural/functional, inflammatory, and miscellaneous) or by site (upper tract versus lower tract) (Table X3).

1.1    Classification by Type

Congenital lesions include obvious and serious anomalies such as myelomeningocele as well as occult lesions of variable severity, such as posterior urethral valves or vesicourethral reflux. Any lesion that produces significant obstruction to urinary flow places the child at risk for urinary tract infections, hydronephrosis, and permanent renal damage.

Neoplastic lesions include Wilm’s tumor, renal cell or transitional cell carcinoma, ureteral carcinoma, multiple myeloma, and metastatic lesions; these tumors represent a dual threat, in that the malignancy itself is a threat to life, and the obstruction to urine flow presents an additional threat to life and health.

Common structural and functional lesions include ureteral and renal calculi, urethral strictures, BPH Opens in new window, pelvic organ prolapse Opens in new window, and even pregnancy and severe constipation Opens in new window. Uncommon conditions producing functional obstruction include neurologic lesions resulting in detrusor sphincter dyssynergia, such as spinal cord injury. Finally, inflammatory conditions such as endometriosis and tuberculosis are uncommon causes of urinary tract obstruction.

1.2     Classification by Site

Retention can also be classified according to site. This approach is helpful because the pathologic features and management of upper tract obstruction differ from those of lower tract obstruction.

1.2.1     Upper tract obstruction

Upper tract obstruction most commonly occurs at the ureteropelvic junction (UPJI), in neonates and children as well as adults.

In neonates, obstruction at the UPJ is typically the result of abnormal development of the UPJ during embryonic life; the UPJ begins development as a solid structure but then undergoes canalization to form a hollow channel. Incomplete canalization results in a narrow channel, abnormal resistance to urine flow, and increased vulnerability to obstructive lesions such as calculi.

Obstruction at the UPJ can also be caused by aberrant blood vessels that distort the anatomy of the renal pelvis and proximal ureter, by tumors, and by renal calculi. Patients with conditions producing partial UPJ obstruction are at high risk for complete obstruction from renal calculi, which are more likely to form because the increased resistance to urine flow produces varying degrees of stasis and infection, which are risk factors for calculi formation.

Untreated obstruction of the UPJ results in progressive hydronephrosis and hydroureter, atrophy of the renal parenchyma, and compromised renal function. The degree to which obstruction negatively affects renal function is affected by the severity of the obstruction (the degree to which urine flow is blocked), the duration of the obstruction, and whether or not infection occurs.

In a completely obstructed kidney, tissue damage is evident within 7 days; however, if the obstruction is relieved within 14 days following onset, return to normal or preobstructive function is probable.

If complete obstruction persists for 21 days without relief, only 50% of renal function is likely to return. Interestingly, the damage progresses from distal to proximal; histologic changes are first noted in the distal nephron and advance steadily to eventually involve the glomerulus.

The pathologic changes include reduction in arterial flow and impaired venous drainage; the ischemia and congestion contribute significantly to the renal tissue damage. When the obstructive process is complicated by infection, the associated inflammation further intensifies the rate and severity of the pathologic process.

1.2.2    Lower tract obstruction

Obstruction occurring at the level of the bladder neck or urethra is classified as lower tract obstruction; the most common causes of obstruction in men are pathologic conditions of the prostate, and urethral stricture.

Strictures can be caused by a variety of conditions, including radiation therapy for genitourinary cancer and surgical procedures such as radical prostatectomy; the reported incidence of stricture following radical prostatectomy is as high as 25%. Additional causes of stricture include straddle injuries, pelvic fractures, and sexually transmitted diseases. The stricture gradually obstructs the urethra, causing increased pressure proximal to the obstruction; the rising pressures proximal to the lesion may cause gradual thinning of the urethral walls, formation of urethral diverticula, and “pocking” of urine resulting in infection.

In women, lower urinary tract obstruction is most commonly caused by pelvic organ prolapse Opens in new window and cystocele or by antiincontinence procedures (such as urethral sling procedures); rarely, obstruction is caused by urethral stricture or pelvic neoplasms.

Pelvic organ prolapse Opens in new window causes outlet obstruction either by altering the angle of the urethrovesical junction or by directly compressing the urethra. Antiincontinence procedures cause outlet obstruction by “oversuspending” or “overcompromising” the urethra.

An uncommon cause of outlet obstruction is pseudodyssynergia caused by dysfunctional voiding patterns; in this situation, the patient unconsciously contracts the pelvic floor muscles during voiding, which creates obstruction to bladder emptying (“dyssynergia” contraction of the sphincter muscles during bladder contraction).

1.2.3    Impact of outlet obstruction

Obstruction at the level of the urethra or bladder neck has a very negative impact on bladder wall structure and function. Investigations based on Gosling’s pioneering research provide convincing evidence of the following sequelae of lower urinary tract obstruction: increased deposit of collagen within the bladder wall; reduced production of and response to acetylcholinesterase (which results in increased bladder contractility resulting from increased levels of acetylcholine), and electrical potential).

In addition, studies indicate that obstruction causes a reorganization of the spinal micturition reflex, which results in hypertrophy of the afferent and efferent neurons, an increase in C-fiber neurons, and increased production of nerve growth fiber.

These changes may explain why men with prostatic obstruction develop symptoms of overactive bladder that are not always relieved by performance of transurethral resection of the prostate (TURP).

Severe prolonged obstruction and the resulting bladder distension cause denervation, a thickened bladder wall, and loss of contractility. Once these changes have occurred, it is usually too late to “undo” the damage; relieving the obstruction does not necessarily restore normal detrusor function, and the patient may require intermittent catheterization and/or alpha-adrenergic antagonists (alpha blockers) on a long-term basis to provide effective emptying.

1.2.4    Effects of lower tract obstruction on upper tract

The upper tracts are normally protected against problems within the lower tract. Even when the bladder is grossly distended, the ureterovesical valves initially prevent the retrograde flow of urine (reflux). However, when distension is prolonged, the position and configuration of the ureterovesical valves are gradually distorted; the progressive distortion reduces the resistance to retrograde flow and permits urine to reflux into the ureters and kidneys.

Prolonged bladder distension also causes major changes in the structure and function of the ureters; they initially hypertrophy in an attempt to overcome the resistance to urine flow, which causes them to become tortuous and elongated.

Eventually, the ureters become so stretched and dilated that they lose their tone and capacity for peristalsis; in addition, the tortuous and elongated ureters may become angled in a way that causes them to “self-obstruct.” The end result of compromised ureteral function is back pressure on the renal pelvis and calyces.

Normal renal pressures are almost zero; however, as ureteral pressures rise, pressures within the renal pelvis and calyces rise also, resulting in dilation of the calyces and renal pelvis. The renal pelvis initially hypertrophies in an attempt to overcome the obstruction, but persistent obstruction results in total loss of tone and contractility. Table X4 highlights the progression of renal damage caused by persistent obstruction.

1.2.5     Clinical Presentation

Clinical presentation varies, depending on the rate at which the obstruction develops and the “preobstruction” voiding patterns. For the patient with postprostatectomy incontinence, early obstruction (from stricture formation) produces a marked improvement in bladder control; the patient is usually pleased and typically interprets these symptoms as “progress.”

Over a relatively short time, however, the patient develops the classic symptoms of lower urinary tract obstruction: straining to void, progressive weakening of the urinary stream, hesitancy, intermittency, postvoid dribble, daytime frequency (voiding more often than every 2 hours), and nocturia (beign awakened by the urge to void more than once per night in people younger than 65 years of age and more than twice per night in people older than 65 years of age). Urgency and urge incontinence Opens in new window may also occur, and hematuria may be noted if the obstruction is complicated by urinary tract infection.

Depending on the etiology and severity, obstructed voiding may lead to acute or chronic urinary retention. For example, postprostatectomy stricture formation can produce complete obstruction and acute retention over the course of 1 to 2 days if the patient fails to seek assistance on initial onset of voiding difficulty.

Upper tract damage is manifest by flank pain that frequently radiates along the course of the ureter, hamaturia, pyuria, fever, chills, and malaise. If the hydronephrosis is severe enough to produce uremia, the patient will also exhibit nausea, weight loss, and pallor.

2. Retention Caused by Compromised Detrusor Contractility

The second primary etiologic factor for urinary retention is loss of detrusor contractility. This can occur as a result of damage to the parasympathetic nerves innervating the bladder or as a result of direct damage to the detrusor muscle.

Common causes of denervation damage include diabetic cystopathy, multiple sclerosis, chronic alcoholism, and sacral level cord lesions. Diabetic cystopathy is particularly common but is frequently unrecognized in the early phases, which are characterized by diminished sensory awareness of bladder filling and reduced detrusor contractility.

These pathologic changes result in less frequent voiding and elevated postvoid residual volumes. The lack of sensory awareness means that the patient fails to realize that anything is wrong until severe distension has occurred; at this point, the denervation damage is complicated by further loss of contractility caused by “stretch” damage to the muscle fibers of the detrusor.

To prevent permanent bladder damage, providers must monitor bladder function among individuals with diabetics, especially those with other forms of neuropathy; early indicators of diabetic cystopathy include weak or prolonged urinary stream, recurrent urinary tract infections, and elevated posvoid residual volumes.

Direct damage to the detrusor muscle is most likely to occur as a result of severe acute retention that causes overstretching of the muscle fibers; common causative factors include surgery, especially pelvic procedures, and acute neurologic lesions or processes.

Risk factors for retention in surgical patients include anesthetic agents, intraoperative fluid administration, sympathetic stimulation caused by pain, sympathomimetic medications, and patient sedation; strategies to minimize the risk of significant bladder distension include reduction of intraoperative fluid volume, pain control, administration of alpha-adrenergic anatagonists, careful monitoring for evidence of distension (especially in patients who are sedated or have undergone spinal anesthesia), and prompt catheterization for patients with evidence of retention.

Acute neurologic lesions or processes (such as spinal cord injury, transverse myelitis, or cerebrovascular accident) may also result in acute severe retention, caused by sudden loss of both sensory awareness and bladder contractility; these patients must be closely monitored for evidence of retention, and most require short-term management with an indwelling catheter (or routine intermittent catheterization).

Failure to recognize and effectively manage acute retention causes either acute or progressive loss of detrusor contractility and a corresponding increase in bladder distension and retention of urine. As noted earlier, medications such as anticholinergics can contribute to the severity of the retention and can precipitate acute retention in the patient with compromised detrusor contractility.

Assessment of the Patient with Known or Suspected Retention

Assessment of the patient with urinary retention is discussed under the following parameters.

1. History

The history should focus on the onset of voiding difficulties and any associated events (such as prostatectomy), conditions known to contribute to urinary retention (such as diabetes, multiple sclerosis, or Parkinson’s disease), any history of upper tract disease, all prescription and over-the-counter medication, and the type of severity of lower urinary tract symptoms (LUTS).

In assessing the impact of lower urinary tract symptoms, it is very helpful to use a validated tool such as the American Urological Association (AUA) Symptom Score Opens in new window (also known as the International Prostate Symptom Score). The nurse should also assess the patient’s cognitive status, ambulatory status, and general well-being and functional ability; for patients with cognitive or functional impairment, it is critical to assess the patient’s living arrangements and support system.

2. Voiding Diary

A voiding diary Opens in new window is extremely helpful in assessing the patient’s diurnal and nocturnal voiding frequency, the frequency and severity of any urinary leakage, and the type and volume of fluid intake. The voiding diary does not accurately reflect functional bladder capacity in the patient with significant retention; determination of functional capacity in these patients requires measurement of both voided volume and PVR (the two volumes are added together).

3. Physical Examination

A careful physical examination is a critical element in the assessment of an individual with known or suspected urinary retention. In beginning the exam, the clinician should be alert to systemic indicators of acute retention, such as diaphoresis, restlessness, and elevated heart and respiratory rates; this is particularly important when assessing patients with altered sensation or impaired ability to communicate.

For example, bladder distension in the patient with a spinal cord lesion above the level of T6 can result in a life-threatening complication known as autonomic dysreflexia—a condition caused by extreme sympathetic nervous system stimulation and can be triggered by a number of conditions, including fecal impaction Opens in new window, pressure ulcers, bladder distension, or bladder filling during urologic procedures such as cystoscopy or urodynamics; urologic procedures are the most common triggering event.

The most significant indicator of autonomic dysreflexia is a rapid rise in blood pressure to life-threatening levels; associated signs and symptoms include flushing, mucous membrane congestion, and blurred vision above the level of the lesion and pallor, goose bumps, increased spasticity, penile erection, and bowel and bladder spasms below the level of the lesion. The primary element of effective management is elimination of the triggering condition, such as irrigation or replacement of an obstructed urethral catheter; in addition, the patient may require a rapid-acting antihypertensive, such as sublingual nifedipine (10 mg) or glyceryl trinitrate spray.

4. Diagnostic Studies

Essential studies in the evaluation of a patient with suspected urinary retention include PVR urine measurement and urinalysis; serum BUN and creatinine are also obtained when there is any concern regarding upper tract function, such as the patient with high PVR measurements or evidence of long-standing retention. Invasive tests, such as urodynamic studies and renal scans, are typically reserved for more complex cases in which advanced diagnostic data are required to direct treatment. Table X5 highlights common diagnostic studies and findings.

• Postvoid Residual Measurement. PVR measurement helps to confirma the diagnosis of retention and is accepted as a standard element in the assessment of a patient with LUTS or with conditions associated with retention (such as prostatic hypertrophy, pelvic organ prolapse, or neurologic lesions).

• PVR can be obtained either via in-and-out catheterization or via portable bladder ultrasound. To ensure accuracy, the PVR measurement must be completed within several minutes of voiding, especially in the well-hydrated or overhydrated patient; documentation should include the time and volume of voided urine as well as the time and volume of PVR measurement. Because there are individual variations in completeness of bladder emptying throughout the day or with activity, PVR measurement are ideally repeated two to three times to ensure a complete and accurate “picture” of the patient’s voiding patterns and ability to empty the bladder. The exception to this guideline is an initial PVR measure exceeding 500 mL, which is always indicative of significant retention.
• Urinalysis. Patients with retention and urinary stasis are at increased risk for urinary tract infection; therefore, the assessment of these individuals should always include urinalysis (dipstick and microscopy). Microscopy to rule out pyuria is a particularly important component of the initial assessment. If the dipstick and microscopic findings are indicative of infection, culture and sensitivity should be obtained to direct treatment. Patients with infected urine who are scheduled for urinary tract instrumentation (such as cystoscopy) should receive an intravenous aminoglycoside 30 minutes before instrumentation to prevent urosepsis. In addition to urinalysis, men who present with irritative voiding symptoms (frequency and urgency) should have urine cytology studies conducted to rule out bladder cancer.

• Uroflow and Urodynamic Studies. Uroflow testing is extremely beneficial in screening for problems with emptying; it may be performed separately or in conjunction with urodynamic testing. It is important to ensure that the patient has a relatively full bladder, because low voided volumes (less than 150 mL) can produce false-positive readings (that is, a flow pattern that mimics obstruction or impaired contractility). Uroflow studies can usually distinguish between normal and impaired emptying, but they cannot reliably determine the specific etiologic factors (obstruction versus impaired contractility).
  
  
  Urodynamic testing is frequently indicated for patients with retention, because this is the only study that can accurately and reproducibly determine whether the retention is caused by obstruction, impaired contractility, or a combination of both factors. Obstruction is manifest by a poor or intermittent stream in combination with high detrusor pressures (greater thatn 40 cm H₂O), whereas impaired contractility presents as a diminished or intermittent stream in combination with low detrusor pressures (less than 30 cm H₂O). There is an argument for routinely obtaining urodynamic studies in men with BPH who are suspected of having some degree of impaired contractility, because TURP in these patients is unlikely to improve symptoms or urinary flow rate and may actually make the patient worse.

• Imaging Studies. Imaging studies are typically reserved for selected patients and are chosen based on the type of data needed. For example, retrograde urethrogram is commonly performed when urethral stricture is suspected, to confirm location and length of the stricture. Similarly, ultrasound can be used to assess renal and prostate size and the presence of bladder trabeculation (an indicator of prolonged obstruction). Finally, a radionucleotide scan may be done to assess renal function. Table X5 outlines the various diagnostic studies that may be undertaken in the evaluation of a patient with known or suspected retention.

Management of the Patient with Acute or Chronic Retention

Primary management options for the patient with urinary retention include behavioral strategies, short-term (or long-term) indwelling catheterization, clean intermittent catheterization, alpha-adrenergic blocking agents, and surgical procedures to correct any obstructing lesions. The specific therapy for a given patient is determined by the particular etiologic factors and by patient/caregiver abilities and preferences.

For men with retention caused by BPH, the treatment choices have changed significantly over the last decade; the development of new pharmacologic agents and noninvasive surgical procedures has reduced the number of patients treated with standard surgical procedures (such as TURP) by more than 60%. The specific options now available for treatment of BPH are discussed in greater detail in this webpage.

1. Behavioral Strategies

Behavioral management may be of benefit for the patient with mild retention resulting from impaired bladder contractility; this approach involves strategies such as fluid management (avoidance of diuretic fluids and even spacing of fluid intake), routine scheduled voiding to prevent increased bladder distension, and “double voiding” (voiding, waiting 1 to 2 minutes, and then attempting to void again before leaving the bathroom).

Biofeedback may be beneficial for selected individuals with pseudo-detrusor-sphincter dyssynergia caused by dysfunctional voiding patterns; visual feedback of pelvic muscle activity is frequently very helpful in teaching the individual to relax the pelvic floor muscles to permit bladder emptying. However, effective use of biofeedback requires a motivated person with normal or near-normal innervations of the pelvic floor.

2. Pharmacologic Management Options

There are limited options for pharmacologic management of urinary retention. Alpha-adrenergic antagonists may be of benefit for patients whose retention is caused or exacerbated by excessive urethral tone or by prostatic hyperplasia; these agents reduce urethral resistance by blocking sympathetic receptors at the bladder neck. They are most commonly used for patients with BPH.

Cholinergic agents such as bethanechol are theoretically of benefit in the management of retention, particularly when the retention is caused by impaired contractility; however, these agents have proven relatively ineffective in clinical practice and are therefore not commonly used. No pharmacologic agent can relieve upper tract obstruction; however, these patients frequently require analgesics for pain control and antibiotics for management of infection.

3. Surgical Management Options

Surgical procedures are of benefit in selected cases, for diagnosis, primary correction of an obstructive lesion, or to establish urinary drainage above the point of obstruction.

Cystoscopy should be performed whenever direct visualization of the urethra, bladder neck, or bladder is indicated; specific situations in which cystoscopy is beneficial include suspected urethral trauma or stricture and signs and symptoms of bladder cancer, such as hematuria. (Patients with hematuria should also have urine cytology studies performed.)

Surgery can also be used to treat selected cases of retention; for example, strictureplasty or dilatation may relieve or reduce obstruction caused by urethral stricture, surgical repair of pelvic organ prolapse and cystocele corrects any associated obstruction in women (the alternative to surgery is use of a pessary), and TURP or alternative prostatic ablation procedures may be of benefit for patients with BPH. (Acute retention in men with BPH is typically treated medically, because TURP in this situation is associated with significant morbidity, that is, bleeding, pyelonephritis, and sepsis.) Ureteral reimplantation is the procedure of choice for persistent vesicoureteral reflux.

Finally, surgical procedures may be required to establish drainage proximal to an uncorrectable obstructive lesion; the specific procedure depends on the level of obstruction. For example, placement of a ureteral stent (or construction of a ureterostomy) may be required to maintain ureteral patency in the patient with ureteral stricture or ureteral compression, and nephrostomy tube placement may be required for the patient with uncorrectable ureteral obstruction. The goal of surgical intervention is to restore drainage promptly, because this may allow reversal of renal damage; if renal function does not improve, the kidney remains infected, and the patient is symptomatic, nephrectomy may be required.

Summary

Urinary retention is defined as the inability to empty the bladder completely. The most common cause of retention is in men with prostatism; retention is also common among diabetic patients and is often overlooked.

Pathologic factors contributing to retention at the level of the bladder include bladder outlet obstruction, diminished bladder contractility, or a combination of both. Retention may also occur in the upper tract, as a result of obstructive lesions in the bladder, ureter, or kidney. In both cases, these may be acquired or congenital.

Whatever the cause, some general principles guide assessment and treatment: maintaining renal and bladder health, preventing infections, and maintaining quality of life. Upper tract obstructions are always managed surgically. Retention caused by lower tract obstruction may be managed surgically but may also be amenable to a variety of conservative strategies such as intermittent catherization, alpha-blockers, and biofeedback.

Retention caused by loss of contractility is managed by behavioral therapies (such as double voiding and timed voiding), alpha blockers, and/or catheterization.

Nursing management of patients with retention is critical and involves education regarding medications (and monitoring for efficacy and for adverse effects), empathetic and thorough instruction in clean intermittent catheterization, measures to prevent or promptly manage urinary tract infections, follow-up and evaluation of the total individualized treatment plan, and ongoing attention to development and implementation of a management plan that preserves both renal health and the patient’s quality of life.