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149]

Review Article

Pathophysiology and management of urinary

retention in men
Ahmed Muhammed, Abdulkadir Abubakar1
Department of Surgery, Division of Urology, Ahmadu Bello University Teaching Hospital, Zaria, 1Department of Surgery,
Division of Urology, Bayero University/Aminu Kano Teaching Hospital, Kano, Nigeria

ABSTRACT
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.

Key words: Management, pathophysiology, urinary retention and men

Introduction void or the residual urine after voiding is about or greater

than the bladder capacity. The International Continence
Urinary retention represents a clinical state in which the Society defines chronic retention as non-painful bladder,
amount of urine drained or measured using ultrasound which remains palpable or percussible after the patient
in the urinary bladder of patient who is either unable to has passed urine. Such patients may be incontinent.[1]
Urinary retention may be acute or chronic; the acute may
Address for correspondence: Dr. Ahmed Muhammed,
be spontaneous or precipitated. Precipitated acute urinary
Department of Surgery, Ahmadu Bello University/Ahmadu Bello
University Teaching Hospital, Zaria, Nigeria. retention (AUR) has a better prognosis.[2-4] Chronic retention
E-mail: darm313@yahoo.com may be low pressure or high pressure, and the reason why
a patient develops either the high-or low-pressure retention
Access this article online has not been elucidated.[5] AUR is painful inability to void
Quick Response Code: which is usually relieved by drainage of the bladder. The
Website:
mere inability to void or voiding of scanty urine associated
www.archintsurg.org
with suprapubic pain is insufficient to make a diagnosis
DOI:
as other disease conditions can be associated with lower
10.4103/2278-9596.110018 abdominal pain and reduced urine volume. Thus, a major
criterion in the diagnosis of urinary retention is the

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Muhammed and Abubakar: Urinary retention in men
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
11th (with the rate of 15 per million population) in terms of
cause of death due to kidney and urologic diseases. It is
also ranked 9th 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
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
Urinary retention may be acute, acute-on-chronic,
64
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 H2O) 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
Urodynamic
Initially the hypertrophic response of the bladder meets
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Muhammed and Abubakar: Urinary retention in men
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
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
Archives of International Surgery / July-December 2012 / Vol 2 / Issue 2
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
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 H3-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
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]
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Muhammed and Abubakar: Urinary retention in men
Etiology of Contractile Dysfunction
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 Ca2+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.[17,19-22] 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
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
66
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
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
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
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Muhammed and Abubakar: Urinary retention in men
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
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
Archives of International Surgery / July-December 2012 / Vol 2 / Issue 2
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
mol/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.[29-33]
Postobstructive Hematuria
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.
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Muhammed and Abubakar: Urinary retention in men
Persistent Elevation of Urea and
Creatinine
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
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.
68
Conclusion
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.
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How to cite this article: Muhammed A, Abubakar A. Pathophysiology
and management of urinary retention in men. Arch Int Surg 2012;2:63-9.
Source of Support: Nil. Conflict of Interest: No.
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