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Year : 2012  |  Volume : 2  |  Issue : 2  |  Page : 63-69

Pathophysiology and management of urinary retention in men

1 Department of Surgery, Division of Urology, Ahmadu Bello University Teaching Hospital, Zaria, Nigeria
2 Department of Surgery, Division of Urology, Bayero University/Aminu Kano Teaching Hospital, Kano, Nigeria

Date of Web Publication3-Apr-2013

Correspondence Address:
Ahmed Muhammed
Department of Surgery, Ahmadu Bello University/Ahmadu Bello University Teaching Hospital, Zaria
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/2278-9596.110018

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Background : Urinary retention is a common problem in the elderly. The incidence increases with age so that a man in his 70s has a 10% chance and a man in his 80s has more than 30% chance of having an episode of acute urinary retention. Inadequate management of the condition can lead to unnecessary morbidity and occasionally mortality. Increasing knowledge over the years of its pathophysiology has greatly improved the management. Thus, the objective of this study is to review the current concepts in the management of urinary retention in men.
Materials and Methods: Current literature on the pathophysiology and management of urinary retention in men was reviewed. The PubMed database was searched using the key words; pathophysiology, management, urinary retention, and men.
Results: Urinary retention is a common problem in the elderly worldwide; the incidence rises with age, and by the 9th decade of life, a man has more than 30% chance of an episode of retention. There are three main pathophysiologic mechanisms: Increased urethral resistance secondary to bladder outlet obstruction, impaired bladder contractility, and loss of normal bladder sensory or motor innervations. It may be acute, acute-on-chronic, or chronic. It is now generally agreed from urodynamic studies that the traditional slow decompression of the bladder in chronic retention does not serve its aim of gradual reduction of vesical pressure; thus, the current practice is immediate and complete decompression and managing anticipated complications of postobstructive diuresis or hematuria whenever they occur.
Conclusion: Advanced age and bladder outlet obstruction secondary to benign prostatic hyperplasia remain the commonest risk factors for urinary retention. Secondary bladder dysfunction in bladder outlet obstruction, detrusor myogenic dysfunction, and alteration of bladder innervations are the major mechanisms. Immediate and complete decompression in both types of retention is the current practice.

Keywords: Management, pathophysiology, urinary retention and men

How to cite this article:
Muhammed A, Abubakar A. Pathophysiology and management of urinary retention in men. Arch Int Surg 2012;2:63-9

How to cite this URL:
Muhammed A, Abubakar A. Pathophysiology and management of urinary retention in men. Arch Int Surg [serial online] 2012 [cited 2021 Sep 16];2:63-9. Available from:

  Introduction Top

Urinary retention represents a clinical state in which the amount of urine drained or measured using ultrasound in the urinary bladder of patient who is either unable to void or the residual urine after voiding is about or greater than the bladder capacity. The International Continence Society defines chronic retention as non-painful bladder, which remains palpable or percussible after the patient has passed urine. Such patients may be incontinent. [1] Urinary retention may be acute or chronic; the acute may be spontaneous or precipitated. Precipitated acute urinary retention (AUR) has a better prognosis. [2],[3],[4] Chronic retention may be low pressure or high pressure, and the reason why a patient develops either the high-or low-pressure retention has not been elucidated. [5] AUR is painful inability to void which is usually relieved by drainage of the bladder. The mere inability to void or voiding of scanty urine associated with suprapubic pain is insufficient to make a diagnosis as other disease conditions can be associated with lower abdominal pain and reduced urine volume. Thus, a major criterion in the diagnosis of urinary retention is the drainage of large volume of urine after catheterization with relief of the pain. [3] Chronic urinary retention is not usually associated with pain and patients are still able to void or have overflow incontinence. Occasionally these patients also develop inability to void and it is termed acute-on-chronic retention. There is no consensus on the cut-off urine volume that is diagnostic of urinary retention; however, it has been suggested that drained volumes between 500 and 800 ml are typical of acute retention, while >800 ml is suggestive of either chronic or acute-on-chronic retention. In chronic retention, urine volumes above 4 L (4000 ml) have been described. [2],[3]

Urinary retention is a common urological problem seen worldwide, predominantly in the elderly. The incidence increases with age so that a man in his 70s has 10% chance and a man in his 80s has more than 30% chance of having an episode of AUR. [2],[3] The resultant functional and anatomical changes termed obstructive uropathy ranked 11 th (with the rate of 15 per million population) in terms of cause of death due to kidney and urologic diseases. It is also ranked 9 th in terms of cost of all kidney and urological diseases in the USA, as estimated by the National Institutes of Health (NIH), Kidney and Urologic Diseases Advisory Board (KUDAB) study. [6] The incidence and economic implication is not known in our setting; however, it is nonetheless a common urological problem.

  Anatomical and Physiological Properties of the Bladder Top

The bladder is a visceral organ composed of a syncytium of smooth muscles fibers and mucus membrane. The condensation of smooth muscles at the bladder neck forms the internal sphincter, while the external sphincter forms from the urogenital diaphragm around the membranous urethra.

The bladder function is controlled by sets of peripheral nerve supply, the spinal motor integration center, supraspinal center, pontine and suprapontine centers. The physiologic functional properties of the bladder are dependent on appropriate capacity, good compliance, accommodation, and sensation with voluntary control to initiate or stop action of micturition. Disruption along the above neural pathways or anatomical obstruction to the bladder outlet may lead to urinary retention.

  Pathophysiology Top

Urinary retention may be acute, acute-on-chronic, or chronic. Acute retention could be precipitated or spontaneous, while chronic retention could be low pressure or high pressure. Urinary retention commonly results from anatomical obstruction from benign prostatic hyperplasia (BPH), carcinoma of the prostate, urethral stricture; iatrogenic causes such as in intraurethral injection of bulking agents in the treatment of Intrinsic Sphincter Deficiency (ISD); and also psychogenic causes. [7],[8]

Increased outlet resistance as seen in patients with bladder outlet obstruction (BOO) is the commonest mechanism of urinary retention. Patients may manifest a range of symptoms from the resultant urinary bladder dysfunction and occasional renal insufficiency, in addition to the mechanical effect of the obstruction. There may be only mild obstructive symptoms initially, however, the patient may often not notice significant change in voiding pattern, especially with the so-called high pressure retention. Increased outlet resistance may result in bladder dilatation, hypertrophy, trabeculations, sacculations, and diverticulations. The prolonged increased residual voiding pressure eventually leads to bladder dysfunction and may manifest as detrusor instability with decreased compliance and compromise of the storage function worsening the lower urinary tract symptoms (LUTS). Such a dysfunctional bladder can suddenly decompensate, culminating in AUR, or does it insidiously with progressive distension of the bladder, resulting in chronic retention. The exact mechanisms responsible for gradual or sudden decompensation have not been elucidated. [2] Chronic retention may be high pressure (≥30 cm of H 2 O) or low pressure. The bladder becomes insensitive, hypocontractile, allowing distension beyond its capacity that may present as overflow incontinence or nocturnal enuresis. [3]

In the high-pressure retention, bladder changes may also result in functional failure of ureterotrigonal complex, resulting in vesicoureteric reflux, with the resultant back pressure on the ureters and collecting system leading to the development of hydroureters and hydronephrosis. With time, persistent elevated intrarenal pressure may lead to tubular epithelial atrophy and eventual nephron loss. The functional consequence is impaired glomerular function and eventual chronic renal failure. [5] This may further be complicated by calculi formation and recurrent urinary tract infection.

  Functional Effects of Bladder Outlet Obstruction in Animal Model Top


Initially the hypertrophic response of the bladder meets the physiological demand of outflow resistance since most parameters of tissue function remains normal. In this phase, animal models have increased frequency, smaller volumes per void, and increased voiding pressure. [9],[10] More prolonged periods of obstruction typically lead to urodynamic features of overflow incontinence. [9] Information from these anesthetized animal models does not give the clear extent the medication disrupts normal micturition patterns. Also, it cannot be concluded if the increases are due to voids or simply due to passive feeling as the limits of viscero-elastic properties of the smooth muscle bladder are met.

  Mechanisms of Outlet-Induced Bladder Dysfunction Top

Microstructure: Cell-cell communication

Alteration in cells' electrical and mechanical ways of communication is noted. Gap junctions are scanty in the bladder; intermediate or adherent type cell junction provides mechanical coupling between cells. This supports compliance and aids in coordinating the physical response of one smooth muscle to its neighbor. The intercellular projections and the changes in the electrical properties of individual cells most likely contribute to detrusor instability resulting from BOO. [11]

Effects of BOO on bladder innervation

These include obstruction-induced denervation in the form of selective degeneration of the axonal elements with findings correlating with those of impaired contractile force generation in response to electrical stimulation. [12] Other studies revealed obstruction-induced nerve growth occurs following chronic urine obstruction and these may be responsible for the irritative LUTS. [12]

Ischemia and BOO

Research findings show ischemia as a major inciting factor in the sequence of events following BOO, characterized by hypertrophy, compensation, and decompensation. [13] This was confirmed using laser Doppler flowmetry.

In a rat model, Zhao, et al. demonstrated that ischemia-reperfusion temporarily mimicked the effect of BOO and the two had similar effects on the tissue proteolysis believed to be involved in BOO-induced muscle dysfunction. [14] An increase in mRNA and protein levels of inducible nitric oxide (NO) synthase was demonstrated soon following partial obstruction, showing that the metabolic effect of bladder musculature is enhanced through vasodilatory effects of substances, e.g., NO. With time, this ultimately fails and hypoxic effects on smooth muscles and nerves result in bladder dysfunction.

Role of growth factors and proto-oncogens

An increase in the expression of basophilic growth factors and a decrease in that of transforming growth factor beta-1 were noted following acute obstruction in rabbits. This is reversed with relief of obstruction. [15] Also, there is increase in transcripts for proto-oncogens, c-myc, cfos, Her-Ras, linked to hyperplastic and hypertrophic process occurring after obstruction. [13]

  Effect of BOO on Extracellular Matrix Top

Ultrastructural examination of obstructed human bladder in aging humans reveals that collagen in particular is deposited between the hypertrophic smooth muscles cells, widening the space between the individual muscle cells. Hyperelastosis is also seen in some instances, which explains the poor compliance in elderly with BOO. [11] Mesenchymal cells in the serosa are thought to transform to myofibroblast capable of synthesizing collagen and fetal type of smooth muscle cells. Kinotam noted predominantly type 1 collagen in comparison to more distensible type III. [14] Altered collagen deposition is believed to affect passive mechanical processes of the bladder. Also, the ratio of subtypes is more important than the total volume of collagen deposited. In addition to connective tissue hyperplasia, urothelial and smooth muscle hyperplasia was demonstrated based on the estimate of DNA content and the level of H 3 -thymidine in obstructed rats and rabbits, [13],[15],[16] though most studies revealed predominantly smooth muscle hypertrophy as a cause for the increase in bladder mass.

  Contractility Top

In general, electrically induced contractions appear to be more sensitive to the effect of obstruction than cabachol-or KCl-induced contraction query. [14] More prolonged severe obstruction leads to diminished contraction. In obstructed bladder with detrusor instability, unlike normal bladder, atropine resistance has being demonstrated. [8],[14] Unlike in animals, the contribution from non-adrenergic and non-cholinergic innervations remains controversial, and their presence in pathologic condition suggests an induction. [12]

  Etiology of Contractile Dysfunction Top

This includes alteration in cytocontractile proteins, [16] which may be linked to induced hypocontractility. Changes in intracellular calcium ion concentration paralleling the altered contractile response following BOO are nearly identical to those seen following inhibition of Ca 2+ release from intracellular stores. [13],[17],[18] There are also changes in smooth muscle metabolism following the hypertrophy, with decreased ATP availability for metabolism as a result of a shift to anaerobic metabolism. [17],[19],[20],[21],[22] Kato, et al.[22] noted no change in ATP with mild obstruction as against severe obstruction with ischemia where increased voiding pressure and prolonged act of micturition and lowered ATP production creates avenue for impaired contractile function.

  Patient's Evaluation Top

This must be prompt, systematic, and thorough to ensure a proper diagnosis and initiation of the appropriate treatment. Initial evaluation is aimed at characterizing the type of obstruction as either acute or chronic retention. Following emergency presentation in AUR, priority must be to relieve retention, and prevention or control of sepsis with correction of possible fluid and electrolyte derangements.

Appropriate history should include characterization of the voiding symptoms including continence, the duration and onset, past voiding symptoms, and history of hematuria. Symptoms in patients with BOO are variable, with a relatively poor correlation between individual symptoms and the presence of BOO. [23] In fact, only about half of men judged to be clinically obstructed on a clinical basis will have urodynamic evidence of outlet obstruction. [24] Therefore, while symptom scores provide a useful tool for guiding management strategies and follow-up responses to therapies, they are generally not predictive of outlet obstruction or impaired contractility. History of any form of sexual dysfunction, weight loss, generalized body weakness, and anorexia may suggest prostate cancer. Neurological evaluation is crucial to exclude neurogenic bladder. Past medical history may unveil hypertension, diabetes, and other significant co-morbid conditions. It should be established if the acute retention is precipitated (prolonged postponement of micturition, ingestion of large volume of fluids, or diuretic abuse) or spontaneous. Precipitated retention has a better prognosis following trial without catheter (TWOC). [3],[25]

On examination, patients with acute retention are usually in severe pains and restless, while those with chronic retention are calm. Facial puffiness, pedal edema, anemia, acidotic breath, and elevated blood pressure may be found in patients with impaired renal function.

The abdomen should be examined for suprapubic swelling and tenderness. A tensely distended swelling in the suprapubic region could be acute, acute-on-chronic, or high-pressure chronic retention. In low-pressure chronic retention, bladder outline may be vaguely palpable because of the flaccid bladder, but the area is dull to percussion. Urethral discharge or palpable indurations plus features of epididymo-orchitis are suggestive of urethral stricture. Perianal and perineal sensations as well as anal sphincteric tone and bulbocarvenosal reflex test the integrity of the sensory and motor efferent fibers in the pudendal nerves. Prostate may be enlarged with benign or malignant features. Lower limb motor and sensory evaluation including deep tendon and plantar reflexes are the important components of genitourinary neurological examinations.

  Investigations Top

The basic laboratory investigation includes serum urea, electrolytes, and creatinine, urine analysis, urine microscopy and culture, blood sugar, and Prostate Specific Antigen (PSA). Patients in chronic retention with elevated urea and creatinine risk postobstructive diuresis. These patients also risk postobstructive hematuria and further deterioration of the renal impairment. Abdominopelvic ultrasound will measure residual urine in chronic retention in addition to unveiling some of the complications following chronic retention, such as hydronephrosis, bladder stone, and loss of corticomedullary differentiation associated with impaired kidney function. Transrectal ultrasound assesses the prostate size, echogenicity, and integrity of the capsule. Urethrocystoscopy and urodynamic studies may all be indicated.

  Treatment Top

Treatment begins with prompt bladder drainage via urethral catheterization; if this fails then drainage should be via suprapubic cystostomy. In patients with deranged renal function, close monitoring for postobstructive diuresis, hematuria from hyperemia or rupture of distended veins, and the risk of further progression of the impaired kidney function is important. To reduce the risk of these complications, some schools of thought advocate that bladder should be decompressed slowly in all patients with chronic urinary retention. In theory, slow decompression should relieve the sudden engorgement of the bladder mucosa and the development of petechial hemorrhages. In practice, however, slow decompression is extremely difficult to achieve; the first few milliliters of urine withdrawn from a bladder which is totally inelastic will reduce the pressure at a considerable rate. [21] The traditional slow decompression of the bladder by gradually releasing a gate clip on the drainage tube, or by removing small quantities of urine at regular intervals, does not achieve its aim of gradual reduction in intravesical pressure [21] because firstly withdrawal of as little as 50 ml of urine from a tensely distended inelastic bladder leads to close to 50% reduction in vesical pressure; secondly, prolonged drainage of stagnant urine at high pressure with an indwelling catheter predisposes to urinary tract infection which could worsen the already compromised renal function; and thirdly it is time consuming and labor intensive. [4],[6],[7],[13] Recently, Perry, et al.[21] suggested slow decompression of the bladder with a suprapubic intravenous fluid giving set; however, it is also susceptible to the same disadvantages enumerated above. George and co-workers have shown from isotope renography that there is a dramatic change in isotope washout from the upper urinary tract as the bladder pressure diminishes, and there seems no justification for delaying this improvement by slow decompression. [21]

These patients should have intravenous line in situ with strict input and output monitoring; it is necessary to monitor the serum and urinary electrolytes every 6-12 h to appropriately replace the sodium and potassium intravenously, preventing hyponatremia and hypokalemia.

These patients can be started on intravenous fluid 0.45% NaCl at a 2-hourly rate, replacing half the previous 2 h urine output once there is an evidence of hemodynamic instability. Once the patient's urea and creatinine have normalized, then all intravenous fluid therapies can be stopped. However, there is experimental evidence that maintaining dogs in a volume-replete-expanded state during obstruction helped them achieve their preobstruction baseline serum creatinine after relief of obstruction. [22]

  Postobstructive Diuresis Top

This refers to the marked polyuria (3 L/day or more than 200 ml/h on three consecutive measurements) and natriuresis that occurs after the relief of BOO, bilateral ureteral obstruction (BUO), or obstruction of a solitary kidney. The causes of the diuresis are multifactorial: from retained urea, sodium, and water during the obstruction, an impaired concentrating ability of renal tubules due to loss of the corticomedullary concentration gradient, effect of circulating hormones, especially atrial natriuretic peptide, [2],[26] and occasionally caused by iatrogenic infusion of sodium-rich intravenous fluids. The mean drained urine volume is 1.5 L with a range 800-4200 ml. O'Reilly, et al.[5] reported a mean residual urine volume of 2.4 L in 36 patients, while Abrams, et al.[27] and Bishop [15] reported 1.4 L and 1.43 L, respectively, in 55 patients each. The reported incidence of postobstructive diuresis has a wide variation ranging from as low as 0.5% and to as high as 78%. [8],[15] O'Reilly, et al. had reported 78% incidence of postobstructive diuresis, while Bishop [28] reported diuresis in 27 of the 47 patients (57%) with elevated plasma creatinine (>120 μmol/L). While all the patients studied by O'Reilly, et al. had elevated plasma creatinine, only 57% developed postobstructive diuresis following rapid bladder decompression. Thus, postobstructive diuresis has not been shown to correlate with the degree of plasma creatinine elevation or the extent of renal impairment. Studies that directly compared slow versus rapid bladder decompression found no significant difference in the incidence of complications. [29],[30],[31],[32],[33]

  Postobstructive Hematuria Top

In some instances, this may be heavy requiring bladder irrigation with normal saline and blood transfusion. Bleeding which occurs within an hour or two of emptying the bladder will almost certainly be caused by the sudden hyperemia which develops in the bladder mucosa from the large veins that become grossly distended as a result of the sudden release of pressure or rupture of these veins, [32] though rarely, from acute tubular necrosis in the kidney. Postobstructive hematuria is thought to be a common complication, and advocates of slow bladder decompression are quick to site the sudden decompression of the bladder and subsequent engorgement of the vesical veins and their rupture to be responsible. [33] However, they fail to put into account the contribution of urinary tract infection and trauma of catheterization. Studies have shown that the incidence of hematuria is low and is often variable; when it does occur, it is usually mild, inconsequential, resolves within 24-48 h, and rarely requires blood transfusion. [34],[35] The largest study that specifically looked at the incidence of hematuria following rapid bladder decompression was by Glahn, et al.[32] in which they studied 300 patients and they found only a 16% incidence of hematuria.

  Persistent Elevation of Urea and Creatinine Top

For the patient whose urea and creatinine are persistently elevated, i.e., not steadily declining after decompression of the bladder, or they decline but then plateau at a value above normal, a repeat renal ultrasound will provide valuable information when compared to the original (pre-relief) study. [35] Persistence of the hydronephrosis on renal ultrasonography may signify concomitant obstruction of the ureters above the level of the bladder. In this situation, further study of the ureters with cystoscopy and retrograde ureteropyeloscopy is indicated. Depending on the results of these studies, computed tomography (CT) scan may be needed to further delineate any extrinsic compression. A persistent elevation of urea and creatinine despite resolution of the hydronephrosis seen on the initial sonogram may mean the patient has reached baseline and will not improve further.

  Outcome and Subsequent Management Top

This depends on the type of retention, cause of the obstruction, and the extent and duration of retention. In BPH, a TWOC is successful in majority of patients with precipitated retention; however, only a quarter are successful in those with spontaneous retention and 50% of these will have a recurrence of retention in a week, 60% in 1 month, and 70% in a year. [3],[34] The current use of highly selective alpha-adrenergic blockers at least 24 h before TWOC and maintained thereafter has increased the number of successful trials of voiding. This is aimed at either delaying the need for prostatectomy or avoiding it altogether. [30],[33]

Following prostatectomy, patients often have improved peak flow rate and International Prostate Symptoms Score (IPSS), but the persistence of uninhibited bladder contraction in 25% may be accounted for postoperative urgency. [36] This suggests bladder-induced disorders do not readily completely reverse in some cases. Also, improvements in IPSS and flow rate are less when prostatectomy is delayed as in low-pressure chronic retention (decompensated state) as opposed to early interventions in patient with similar symptoms [24] in which complete return to normal is more likely. Postobstructive diuresis and postobstructive hematuria resolve spontaneously in majority of patients, with only a few requiring aggressive management. Those with end-stage renal failure will require renal replacement therapy.

  Conclusion Top

Advanced age and BOO secondary to BPH remain the commonest risk factors for urinary retention. Secondary bladder dysfunction in BOO, detrusor myogenic dysfunction, and alteration of bladder innervations are the major mechanisms. Immediate and complete decompression in both types of retention is the current practice.

  References Top

1.Abrams P, Cardozo L, Fall M, Griffiths D, Rosier P, Ulmsten U, et al. The standardisation of terminology in lower urinary tract function: Report from the standardisation sub-committee of the International Continence Society. Urology 2003;61:37-49.  Back to cited text no. 1
2.Kaplan SA, Wein AJ, Staskin DR, Roehrborn CG, Steers WD. Urinary retention and post-void residual urine in men: Separating truth from tradition. J Urol 2008;180:47-54.  Back to cited text no. 2
3.Mitchell JP. Management of chronic urinary retention. Br Med J (Clin Res Ed) 1984;289:515-6.  Back to cited text no. 3
4.Young TV, Mitchell JP. Distension of the bladder leading to vascular compression and massive oedema. Br J Urol 1968;40:248-50.  Back to cited text no. 4
5.O'Reilly PH, Brooman PJ, Farah NB, Mason GC. High pressure chronic retention. Incidence, aetiology and sinister implications. Br J Urol 1986;58:644-6.  Back to cited text no. 5
6.Meigs JB, Barry MJ, Giovannucci E, Rimm EB, Stampfer MJ, Kawachi I. Incidence rates and risk factors for acute urinary retention: The health professionals follow up study. J Urol 1999;162:376-82.  Back to cited text no. 6
7.Jacobsen SJ, Jacobson DJ, Girman CJ, Roberts RO, Rhodes T, Guess HA, et al. Natural history of prostatism: Risk factors for acute urinary retention. J Urol 1997;158:481-7.  Back to cited text no. 7
8.Tanagho EA, Bella AJ, Lue TF. Neuropathic bladder disorders. In: Smith's general urology, 17 th edn. Tanagho EA, McAninch JW, eds. San Francisco. Lange Medical Books/McGraw-Hill, 2008: 438-53.  Back to cited text no. 8
9.Mostwin JL, Karim OM, Van Koeveringe G. The guinea pig model of gradual urethral obstruction. J Urol 1991;145:854-8.  Back to cited text no. 9
10.Steers WD, De Groat WC. Effect of bladder outlet obstruction on micturition reflex pathways in the rat. J Urol 1988;140:864-71.  Back to cited text no. 10
11.Elbadawi A, Yalla S, Resnick NM. Structural basis of geriatric voiding dysfunction. IV. Bladder outlet obstruction. J Urol 1993;150:1681-95.  Back to cited text no. 11
12.Perlberg S, Caine M. Adrenergic response of bladder muscle in prostatic obstruction. Its relation to detrusor instability. Invest Urol 1982;20:524-7.  Back to cited text no. 12
13.Levin RM, Monson FC, Haugaard N, Buttyan R, Hudson A, Roelofs M, et al. Genetic and cellular characteristics of bladder outlet obstruction. Urol Clin North Am 1995;22:263-83.  Back to cited text no. 13
14.Zhao Y, Levin S, Wein AJ, Levin RM. Correlation of ischemia/reperfusion or partial outlet obstruction -induced spectrin proteolysis by calpain with contractile dysfunction in rabbit bladder. Urology 1997;49:293-300.  Back to cited text no. 14
15.Kim KM, Kogan BA, Massad CA, Huang YC. Collagen and elastin in the obstructed fetal bladder. J Urol 1991;146:528-31.  Back to cited text no. 15
16.Uvelius B, Persson L, Mattiason A. Smooth muscle hypertrophy and hyperplasia in the rat detrusor after short-time infravesical obstruction. J Urol 1984;131:173-6.  Back to cited text no. 16
17.Buttyan R, Jacobs BZ, Blaivas JG, Levin RM. Early molecular response to rabbit bladder outlet obstruction. Neurourol Urodyn 1992;11:225-38.  Back to cited text no. 17
18.Saito M, Hypolite JA, Wein AJ, Levin RM. Effect of partial outflow obstruction on rat detrusor contractility and intracellular free calcium concentration. Neurourol Urodyn 1994;13:297-305.  Back to cited text no. 18
19.van Koeveringe GA, Mostwin JL, van Mastrigt R, van Koeveringe BJ. Effect of partial urethral obstruction of force development of the guinea pig bladder. Neurourol Urodyn 1993;12:555-71.  Back to cited text no. 19
20.Wang ZE, Gopalakurup SK, Levin RM, Chacko S. Expression of smooth muscle myosin isoforms in urinary bladder smooth muscle during hypertrophy and regression. Lab Invest 1995;73:244-51.  Back to cited text no. 20
21.Arner A, Malmquist U, Uvelius B. Metabolism and force in hypertrophic smooth muscle from rat urinary bladder. Am J Physiol 1990;258:C923-32.  Back to cited text no. 21
22.Kato K, Lin AT, Haugaard N, Longhurst PA, Wein AJ, Levin RM. Effects of outlet obstruction on glucose metabolism of the rabbit urinary bladder. J Urol 1990;143:844-7.  Back to cited text no. 22
23.Kaplan SA, Bowers DL, Te AE, Olsson CA. Differential diagnosis of prostatism: A 12-year retrospective analysis of symptoms, urodynamics and satisfaction with therapy. J Urol 1996;155:1305-8.  Back to cited text no. 23
24.Sirls LT, Kirkemo AK, Jay J. Lack of correlation of the American Urological Association symptom 7 index with urodynamic bladder outlet obstruction. Neurourol Urodyn 1996;15:447-57.  Back to cited text no. 24
25.George NJ, O'Reilly PH, Barnard RJ, Blacklock NJ. The practical management of patients with dilated upper tracts and chronic retention of urine. Br J Urol 1984;56:9-12.  Back to cited text no. 25
26.Gulmi FA, Mooppan UM, Chou S, Kim H. Atrial natriuretic peptide in patients with obstructive uropathy. J Urol 1989;142:268-72.  Back to cited text no. 26
27.Abrams PH, Dunn M, George N. Urodynamic findings in chronic retention of urine and their relevance to results of surgery. Br Med J 1978;2:1258-60.  Back to cited text no. 27
28.Bishop MC. Diuresis and renal functional recovery in chronic retention. Br J Urol 1985;57:1-5.  Back to cited text no. 28
29.Selius BA, Subedi R. Urinary retention in adults: Diagnosis and initial management. Am Fam Physician 2008;77:643-50.  Back to cited text no. 29
30.Lane IF. Diagnosis and management of urinary retention. Vet Clin North Am Small Anim Pract 2000;30:25-57.  Back to cited text no. 30
31.Gould F, Cheng CY, Lapides J. Comparison of rapid versus slow decompression of the distended urinary bladder. Invest Urol 1976;14:156-8.  Back to cited text no. 31
32.Glahn BE, Plucnar BJ. Quick complete emptying of the bladder in 300 cases of urinary retention. The occurrence of haematuria. Dan Med Bull 1984;31:68-70.  Back to cited text no. 32
33.Nyman MA, Schwenk NM, Silverstein MD. Management of urinary retention: Rapid versus gradual decompression and risk of complications. Mayo Clin Proc 1997;72:951-6.  Back to cited text no. 33
34.Perry A, Maharaj D, Ramdass MJ, Naraynsingh V. Slow decompression of the bladder using an intravenous giving set. Int J Clin Pract 2002;56:619.  Back to cited text no. 34
35.Kalejaiye O, Speakman MJ. Management of acute and chronic retention in men. Int J Clin Pract 2009;8:523-9.  Back to cited text no. 35
36.Flanigan RC, Reda DJ, Wasson JH, Anderson RJ, Abdellatif M, Bruskewitz RC. 5-year outcome of surgical resection and watchful waiting for men with moderately symptomatic benign prostatic hyperplasia: Department of veteran affairs cooperative study. J Urol 1998;160:12-7.  Back to cited text no. 36


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