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Urinary Retention
Michael Billet, MDa, *, Thomas Andrew Windsor, MDb

KEYWORDS

Retention Urinary retention Catheter Catheterization Foley

Benign prostatic hyperplasia

KEY POINTS

Urinary retention is caused by obstructive, infectious, pharmacologic/iatrogenic, and

neurogenic processes. Obstructive retention due to benign prostatic hyperplasia (BPH) is
the most common single cause.
Bladder decompression is the mainstay of treatment of acute retention; with few excep
tions, laboratory workup and imaging should not delay decompression.
Laboratory workup for acute retention should include urinalysis to exclude infection. Renal
function and electrolytes should be obtained in severe or prolonged retention, or with
postobstructive diuresis.
Patients who are hemodynamically stable, have normal postdecompression urine output
and renal function, and are capable of maintaining their catheters can be discharged with
outpatient follow-up.

INTRODUCTION

Urinary retention is a common problem encountered in the emergency department.

Acute urinary retention (AUR) presents as a sudden inability to voluntarily void, and is
typically associated with lower abdominal pain. Although the most common cause is
prostatic enlargement, particularly benign prostatic hyperplasia (BPH), its etiology can
be varied and multifactorial.1 Treatment of all types of retention aims to decom press
the bladder and mitigate the underlying cause of retention. This can generally be
accomplished in the emergency department without immediate urologic consulta tion;
however, certain clinical features may require specialist involvement in the emer gency
department or outpatient setting. This article provides an overview of the common
causes of AUR, as well as emergency department evaluation, treatment, and disposition
of AUR in men and women.

Disclosure Statement: The authors have nothing to disclose.

a
Department of Emergency Medicine, University of Maryland School of Medicine, Baltimore, MD,
USA; Department
b
Paca of Emergency
Street Medicine,
- Suite 200, University
Baltimore, of Maryland
MD 21201, USA * School of Medicine,
Corresponding 110110
author. South
South Paca Street, Suite 200, Baltimore, MD 21201, USA.

E-mail address: mbillet@som.umaryland.edu

Emerg Med Clin N Am 37 (2019) 649–660

https://doi.org/10.1016/j.emc.2019.07.005 emed.theclinics.com
0733-8627/19/ª 2019 Elsevier Inc. All rights reserved.
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650 Billet & Windsor

DEFINITION AND PRESENTATION

The International Continence Society defines AUR as, “a painful, palpable or percuss
able bladder, when the patient is unable to pass any urine.”2 It would therefore be ex
pected that most patients with AUR will describe suprapubic or low abdominal pain
and associated difficulty spontaneously voiding. While true in most patients, this pre
sentation is not guaranteed; those with acute on chronic retention, acute spinal cord
compression, or those with underlying neuropathy may be less sensitive or insensitive
to the pain associated with bladder overdistension.3 These patients will also be more
likely to have overflow incontinence, which can rarely be mistaken for continued spon
taneous voiding, and sometimes even frequent urination. A history of prior retention or
other lower urinary tract symptoms such as straining, terminal dribbling, or nocturia
can be helpful in identifying patient at risk for painless retention.
The physical examination may reveal suprapubic distension and dullness to percus
sion. In urology literature, bladder volumes greater than 300 mL are often cited as the
minimum value necessary to identify a distended bladder on examination in the non
obese patient.4 Examiner proficiency and issues blinding have made validation of this
claim difficult, and patient habitus can completely preclude palpation or percussion of
a distended bladder.5 In the American Urologic Association’s consensus statement on
chronic urinary retention (CUR), 300 mL is the minimum postvoid residual volume
necessary to diagnose CUR.6 The statement also emphasizes the largely historical un
derpinnings of this threshold, and recommends a symptom-based approach to acute
and chronic retention. Bedside ultrasound and automated bladder volume devices
can quickly differentiate retention from other causes of urinary incontinence, dis cussed
more in the workup section.

BACKGROUND AND PREVALENCE

The incidence of AUR has been estimated as 3.0 to 6.8 cases per 1000 person-years in
the general male population.7Most cases of AUR occur inmen because of the longer ure
thra and presence of the prostate. Furthermore, there is a clear increase in the prevalence
of AUR with aging, secondary to prostatic hypertrophy that occurs in essentially all men
as part of the aging process. By the eighth decade of life, the incidence of AUR in men
increases fivefold to tenfold from rates in middle age, with an estimated 1 case per 10
men in their 70s, and 1 case per 3 men in their 80s experiencing AUR at some point.8
The increased incidence with age is not limited to men with prostatic hypertrophy;
diabetes-related nerve damage and retention secondary to medication effects similarly
increase with age. Cases of AUR that occur in women or younger men are often infection
related, iatrogenic, or a consequence of medication effects.9

ETIOLOGY
Obstructive

Obstructive urinary retention is caused by any process leading to narrowing or

compression of the urinary tract at or distal to the neck of the bladder. This obstruction
can be divided into intrinsic causes, with the obstruction coming from within the uri nary
tract, and extrinsic causes, with the obstruction arising from compression by
an external structure or mass. Among intrinsic causes, BPH is overwhelmingly the
most common cause of urinary retention in men.1 Other intrinsic processes leading
to AUR include lower urinary tract malignancy, blood clots, urethral stricture, and
bladder stones. The presence of blood clots leading to obstruction should prompt
consideration of urinary tract malignancy.
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Urinary Retention: Diagnosis and Management 651

A detailed history and physical examination should be performed in any patient with
suspected or confirmed urinary retention. This should include thorough examination of
the external genitalia in men, and pelvic examination in women. Extrinsic causes of
AUR include abdominal and pelvic tumors, phimosis, and paraphimosis in men, and
pelvic organ prolapse in women. Paraphimosis is a true urologic emergency because
of the high risk of vascular compromise; immediate manual reduction should be
attempted after adequate analgesia. Compression of the glans can aid in manual
reduction. If initial attempts are unsuccessful, further attempts should be limited
because of the risk of worsening inflammation, and a urologist should be emergently
consulted to perform a dorsal slit procedure.10 Although rare, pelvic organ prolapse
can cause vascular compromise or ureteral kinking and upper urinary tract obstruc
tion.11 Pelvic organ prolapse can be manually reduced by the emergency physician
with essentially no contraindications. A more extensive list of obstructive causes of
AUR can be found in Table 1.
Infectious
Genitourinary infection can lead to urinary retention through various mechanisms.
Inflammation of the urinary tract at any level can cause narrowing and obstructive uri
nary retention. Patients with underlying urinary tract pathology, particularly BPH, are
more susceptible to have infection lead to obstruction compared with the general pop
ulation.12 Recurrent urinary tract infections are therefore a risk factor for future reten
tion and a consequence of inadequately treated retention. The most common
causative organism leading to UTI is Escherichia coli, cultured in 75% to 95% of un
complicated UTIs in adults.13 Among patients with underlying urinary tract pathology,
E coli remains the most common causative organism; other less common organisms
include Enterococcus spp., Klebsiella pneumoniae, Candida spp., Staphylococcus
aureus, Proteus mirabilis, Pseudomonas aeruginosa, and group B streptococcus.14
Because of high regional variability in antibiotic resistance, local antibiograms should
be consulted when possible to determine the optimal antibiotic regimen.15 Sexually
transmitted infections can also cause retention, through direct inflammation of the uri
nary tract, pain leading to sympathetic overactivity, or stricture development caused
by chronic or frequent infection.
Neurogenic
The innervation of the bladder and lower urinary tract is complex, with voluntary void
ing (micturition) requiring sympathetic, parasympathetic, and somatic pathways.16
Sensation of bladder fullness is mediated through pelvic sensory nerves, and

Table 1
Causes of obstructive urinary retention

Level of Obstruction Example

Bladder Calculi, malignancy, hemorrhage
Prostate BPH, prostatic calculi, abscess, malignancy
Urethra Stricture, calculi, diverticulum, urethral valve, periurethral abscess
External male genitalia Phimosis, paraphimosis, metal stenosis
Female genitalia Atrophic vaginitis, vulvovaginitis, pelvic organ prolapse
Any level Abdominal or pelvic tumor, abdominal aortic aneurysm, pelvis
fracture

Data from Klahr S. Obstructive nephropathy. Intern Med. 2000;39(5):355-61.

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processed centrally through the pontine storage and micturition centers. Once the
sensation to void is processed, the action of micturition requires a closely coordinated
interaction between bladder contraction (detrusor muscle stimulation) and relaxation
of the bladder outlet (Fig. 1). As such, these pathways are highly susceptible to neuro
logic insult, which can be acute or chronic. Alteration of activity at the neuromuscular
junction in any of these sites can also lead to AUR; further discussion of pharmaco
logic causes of AUR is provided.
Acute causes of neurogenic bladder include compression of the spinal cord or
nerve roots in the cauda equina. In fact, AUR is considered to be the earliest and
most sensitive examination finding in patients with acute cauda equina syndrome
(CES), with AUR identified on presentation in 50% to 70% of patients with
CES.17 Other studies have shown a postvoid residual volume greater than
200 mL to have a sensitivity of 90% and specificity of 95% when combined with
a history consistent for acute CES.18 Patients with acute central nervous system
emergencies, particularly stroke, are also susceptible to developing urinary reten tion;
the incidence of AUR after ischemic stroke has been reported to be 21% to
29% at 3 weeks after infarction.19 Chronic insult can also lead to dysfunction of
the pathways regulating voiding, particularly diabetic neuropathy. Nearly half of di
abetics will experience some form of lower urinary tract symptoms.20 Although
detrusor overactivity is the most common form of urinary dysfunction among dia betics,
23% will experience detrusor areflexia and are subsequently prone to reten tion, which
can present acutely or chronically.21

Iatrogenic/Pharmacologic
Iatrogenic causes of AUR can be grouped into pharmacologically and nonpharmaco
logically mediated processes. All patients presenting with AUR should undergo a
thorough medication history, as the complex innervation of the urinary tract makes

Fig. 1. Innervation of the lower urinary tract. Sympathetic innervation arises from the lower
thoracic and upper lumbar spinal nerve roots, passing through the sympathetic chain, and
innervates the bladder and internal sphincter via the hypogastric nerves. Parasympathetic
fibers arise from the sacral nerve roots and provide innervation to the bladder via the pelvic
nerve. Somatic innervation is provided to the external sphincter via the pudendal nerve.
Adapted from Wikimedia Commons. Available at: https://commons.wikimedia.org/wiki/
File:Diagram_showing_the_layers_of_the_bladder_CRUK_304.svg.
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Urinary Retention: Diagnosis and Management 653

retention a common adverse effect of many frequently prescribed medications. Partic ular attention
should be given to medications with anticholinergic properties, both
those that are used specifically for those properties and the wide variety of medica tions with
anticholinergic effects. A list of common medications that have been impli cated in AUR can be seen
in Table 2; those with anticholinergic properties are
specifically noted.
Recent surgeries should also be noted, particularly those involving general
anesthesia, large volumes of fluid administration, or intraoperative urinary catheter ization, as these
are all independent risk factors for developing postoperative uri nary retention.22 Postoperative AUR
is not limited to surgeries involving the
urinary tract or even the abdomen; AUR is a frequently encountered complication
of nearly all types of surgery. This specific subtype of iatrogenic retention
may be less frequently encountered in the emergency department, as postopera tive retention
typically presents in the immediate postoperative period. One study
demonstrated that nearly half of all patients who will go on to develop postopera tive retention are
able to be identified by ultrasound in the postanesthesia care
unit.23
A history of lower urinary tract surgery or prior urinary catheterization should also be
noted, as this history increases the likelihood of urethral stricture development. Iatro genic causes
are the leading etiology of urethral strictures, accounting for 32% to 45%
of all cases.24 The most common surgeries and procedures leading to stricture devel opment are
hypospadias correction, transurethral surgery, and repeated passage of
large catheters. Open or laparoscopic prostatectomy and simple cystoscopy have a
relatively lower rate of this complication.25

Table 2
Medications with urinary retention as a known adverse effect

Class Implicated Medications

Anticholinergic
Antihistamines (anticholinergic
mediated, class-wide effect)
Atropine, cyclopentolate, homatropine,
tropicamide, scopolamine, ipratropium,
tiotropium
Diphenhydramine, hydroxyzine, doxepin,
promethazine, cetirizine, fexofenadine,
loratadine

Analgesics Opioids (class-wide effect), nonsteroidal anti inflammatory

drugs (class-wide effect)
Benzodiazepines Class-wide effect

Calcium channel antagonists Class-wide effect

Antidepressants Tricyclic antidepressants (A), fluoxetine, reboxetine

Antipsychotics, antiparkinsonians
Antiarrhythmics
Sympathomimetic (alpha-adrenergic)
Sympathomimetic (beta-adrenergic)
Muscle relaxants
Chlorpromazine (A), thioridazine (A), clozapine (A),
risperidone (A), ziprasidone (A), amantadine (A),
haloperidol (A)
Disopyramide (A), flecainide
Phenylephrine, pseudoephedrine
Isoproterenol, terbutaline, epinephrine,
norepinephrine
Baclofen, cyclobenzaprine

Medications with anticholinergic properties are noted with (A).

Data from Verhamme KM, Sturkenboom MC, Stricker BH, Bosch R. Drug-induced urinary reten tion: incidence,
management and prevention. Drug Saf. 2008;31(5):373-88.
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EVALUATION
Laboratory Workup
Laboratory studies are not required to diagnose AUR, but may be useful in identifying
associated complications. Concern for significant or prolonged obstruction that may
cause hydroureteronephrosis warrants a chemistry panel to evaluate for a postrenal
acute kidney injury (AKI). Urinalysis and urine culture should be obtained in patients
with AUR, for the main purpose of evaluating for urinary tract infection. Microscopic
and gross hematuria following decompression are typically benign and self-limited.26

Imaging
Imaging studies can be helpful to identify the presence, cause, or degree of AUR.
Several commercial products exist to quickly estimate bladder volume (eg, Bladder
Scan, Verathon Incorporated [Bothell, Washington]). These automated point-of-care
devices utilize 3-dimensional ultrasound to estimate bladder volume, and can be use
ful both on presentation and after attempted decompression. These devices may be
limited by patient habitus or the presence of hemoperitoneum, ascites, or other extra
vesicular fluid that can artificially increase the calculated bladder volume.27 Bedside
point-of-care ultrasound (POCUS) is commonly available in the emergency depart ment
and can rapidly identify and quantify bladder volume. Furthermore, POCUS
can identify bladder clots, prostatic hypertrophy, bladder or urethral stones, and
hydronephrosis in a way that automated devices cannot.28
Computed tomography (CT) may be particularly helpful to evaluate for abdominal or
pelvic masses, yet it is less sensitive than MRI if there is suspicion for a spinal cord
compression or cauda equina syndrome.29 Although recent literature suggests that
venous-phase iodinated contrast may not pose a significant risk for contrast induced
nephropathy, institutional policy may limit the use of intravenous contrast
to patients with normal renal function, precluding use of contrast-enhanced CT in pa
tients with acute or chronic kidney disease.30 Conversely, noncontrast-enhanced ul
trasound can be performed in patients with acutely or chronically impaired renal
function, with essentially no contraindications. For nontraumatic cases of AUR, labo
ratory testing and imaging need not delay prompt relief of the obstruction.31

TREATMENT

Prompt bladder decompression is the mainstay of treatment for nearly all etiologies of
AUR. This can be accomplished by urethral or suprapubic catheterization. Both routes
have advantages, disadvantages, and contraindications. If imaging studies are un
available or inconclusive regarding the degree of retention, catheterization can be
diagnostic and therapeutic.

Urethral Catheterization

Urethral catheterization is the most common type of catheterization in the emergency

department. For adult patients, initial attempts should be made with a standard tip 16-
French Foley catheter, but the clinical scenario may necessitate other sizes or types of
catheter (Fig. 2). Sterile procedure should be observed to limit the exposure to
catheter-related urinary tract infections (CAUTIs).32 Although catheter advancement
should occur with minimal force, conditions that decrease urethral diameter, such
as prior stricture or BPH, can make placement more difficult. If the initial attempt is un
successful in a patient who is unlikely to have BPH, or in a patient with history of ure
thral stricture, it is reasonable to attempt to pass a smaller catheter. In the setting of
prostate enlargement, the increased rigidity of a larger catheter (18- or 20-French)
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Urinary Retention: Diagnosis and Management 655

Fig. 2. Indwelling urethral catheters. Top: 16-French, standard tip; middle: 18-French 3-way,
short tip; bottom: 14-French, Coude´ tip (Tiemann type). (ª 2019 C. R. Bard, Inc. Used with
permission.)

may aid successful placement.33 A semirigid angulated Coude´ catheter may aid in
advancing past the prostatic lobes, because it is designed to match the curvature
of the bulbar urethra.34 For the patient with gross hematuria or passage of clots
contributing to AUR, a 3-way catheter allows for continuous bladder irrigation if output
remains bloody after the initial flushing.35
Blind urethral catheterization is contraindicated in patients with recent urologic sur
gery, or confirmed or suspected urethral trauma.31 Urologic consultation may be
necessary if passage of a catheter consistently fails despite a reasonable number of
attempts. Excessive attempts in the face of resistance or patient-reported discomfort
are inappropriate as this can worsen underlying urinary tract pathology or inflamma
tion. For this reason, clean intermittent self-catheterization (CISC) is not recommen
ded for AUR, particularly obstructive AUR. This is in contrast to chronic retention,
where CISC is the preferred method of bladder decompression.36,37

Suprapubic Catheterization
Suprapubic catheterization, although less common than urethral catheterization, can
be performed by adequately trained emergency physicians.35 The suprapubic
approach is typically reserved for situations in which placement of a urethral catheter
is either contraindicated or unsuccessful despite appropriate attempts. The decision
to perform this procedure should be made in conjunction with a consulting urologist.
To place a suprapubic catheter, the bladder must be identified through palpation, and
ideally visualized in real-time with ultrasound. Several techniques exist to place the
catheter; the 2 main approaches are a percutaneous Seldinger technique with pas
sage of a guidewire into the bladder, dilation of the tract, and over-wire catheter inser
tion; and insertion of a trocar, through which a catheter is subsequently placed.38 A
risk unique to the suprapubic approach is bowel injury, occurring with a reported inci
dence of 2.4% to 2.7%.39

Pharmacotherapy
Medications do not typically resolve AUR by themselves, but they are commonly initi
ated in the immediate treatment phase and continued for ongoing prevention, partic
ularly when prostatic obstruction is the suspected etiology. The two main classes of
medications used for AUR due to an enlarged prostate are alpha blockers and 5-alpha
reductase inhibitors.40 Contraction of the bladder neck, urethra, and prostate are
mediated through alpha-1 adrenergic activity.41 As such, blockade of alpha-1 recep
tors is a mainstay of pharmacotherapy in both acute and chronic urinary retention.
Alpha blockers have been demonstrated to reduce rates of catheter reinsertion after
a trial without catheter.42,43 Caution should be taken when using alpha blockers in
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patients at risk for orthostatic hypotension, as alpha-1 blockade reduces vascular

responsiveness to postural changes.41 5-alpha reductase inhibitors act by
decreasing the conversion of testosterone to dihydrotestosterone, which has a
higher affinity for the androgen receptor present in the prostatic urethral epithelium;
this blockade has the long term effect of slowing prostate growth.44 Due to their
hormone mediated mechanism of action, 5-alpha reductase inhibitors are unlikely
to improve AUR in the short-term, but are beneficial in preventing ongoing prostate
hypertrophy and future episodes of retention.45

Surgical Treatment
Several surgical options exist for the management of patients with recurrent
symptoms, failed trial without catheter, or underlying urinary tract pathology that is
unlikely to improve with conservative management. Surgical or procedural
intervention is most commonly used for obstructive AUR. Transurethral prostate
ablation is a commonly performed procedure for mild or intermittent retention or
other lower urinary tract symptoms related to BPH. For more severe cases of AUR
caused by underlying prostatic enlargement, transurethral radical prostatec tomy
(TURP) is a traditionally successful surgery.46 In recent decades, several mini mally
invasive and robotic assisted procedures have been developed.47 Urethral dilation
or stenting can be of benefit if urethral stricture or external compression is the
suspected etiology. Women with retention secondary to atrophic vaginitis or pelvic
organ prolapse should be referred to a urogynecologist after treatment of the acute
retention.

POSTDECOMPRESSION MANAGEMENT
Complications
The most common acute complications of bladder decompression include hematuria,
infection, and postobstructive diuresis. Urinalysis obtained after catheterization will
commonly demonstrate at least some degree of microscopic hematuria, with the
inci dence depending on factors such as time since catheterization, underlying
pathology, technical difficulty, or number of attempts.48 Gross hematuria is a less
common finding, but may also be suggestive of underlying urinary tract pathology.
If caused by the catheterization procedure, hematuria is usually self-limited.
Hemodynamically significant hematuria is a rare occurrence.49,50 Although
conventional wisdom has taught that urethral catheterization is associated with an
increased rate of CAUTIs compared with the suprapubic route, no statistical
difference in rates of CAUTI has been found in short-term catheterization.51 Further
more, likelihood of CAUTI may be of less importance for AUR, which is expected to
be brief or self-limited. However, compared with subrapubic catheterization, urethral
catheterization catheterization is associated with increased noninfectious complica
tions, particularly patient-reported discomfort.52 Postobstructive diuresis is a
condition in which elevated renal tract pressure impairs the kidneys’ ability to
concentrate urine, leading to diuresis when pressure is normal ized. It is defined as
a urinary output greater than 200 mL for at least 2 hours after decompression, or
greater than 3 L in 24 hours.53 Hemodynamic instability has been reported
secondary to volume losses, particularly in patients with decreased intravascular
reserve. Patients should be rehydrated orally or intravenously, with some sources
advocating replacement of 75% of urinary losses, although high quality evidence on
this topic is lacking.54 Despite advocacy by some practitioners, there is no evidence
that gradual or intermittent decompression decreases the risk
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Urinary Retention: Diagnosis and Management 657

of hematuria, hemodynamic instability, hydronephrosis, or postobstructive diuresis

compared with immediate decompression.55

Indications for Hospitalization

Most patients who experience successful decompression with a catheter can be dis
charged home with plans for appropriate urology follow up. Patients that present with
urosepsis, retention secondary to trauma, AKI, or have other associated inpatient
needs should be hospitalized. Hematuria that is, self-limited or resolves after contin
uous bladder irrigation does not necessitate admission.26

Discharge and Follow-up

Patients with normal postobstructive urine output, reassuring vital signs, and no indi
cations for further emergent workup after placement of a catheter can typically be dis
charged. Patients should be counseled on catheter care, how to change the drainage
bag, and when to follow-up. Most patients who are discharged should follow-up with a
urologist for a spontaneous voiding trial without a catheter. As previously mentioned,
alpha-1 blockers decrease rates of catheter reinsertion, and should be started if no
contraindications exist.42 The optimal time for catheter removal remains a subject of
debate. An observational study of over 2600 men with BPH showed that patients
whose catheters were removed in fewer than 3 days were more likely to spontane
ously void than those with longer periods of catheterization.56 Previous randomized
trials indicated that patients were more likely to void during a trial without a catheter
if left in place for 1 week.57

SUMMARY

Acute urinary retention is a common condition encountered in the emergency depart

ment. Prompt bladder catheterization is indicated for the vast majority of cases, and
most patients can be safely discharged after bladder decompression. A focused lab
oratory evaluation should be performed to identify the underlying cause of obstruction.
At the very least, this should include urinalysis to exclude urinary tract infection. Lab
oratory studies to evaluate renal function and electrolyte status may be indicated
based on clinical features and patient risk factors. Those with serious infections,
ongoing postobstructive diuresis, hemodynamic instability, significant electrolyte ab
normalities, or AKI should be hospitalized for fluid and electrolyte replacement and
specialist evaluation, if indicated.

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