U ro l o g i c E m e r g e n c i e s

a b,
Adam E. Ludvigson, MD , Lisa T. Beaule, MD *

KEYWORDS
 Urologic emergencies  Testicular torsion  Acute urinary retention  Paraphimosis
 Obstructed pyonephrosis  Fournier gangrene  Ischemic priapism

KEY POINTS
 Urologic emergencies must be identified in a timely fashion.
 Optimal management strategy should be determined when urologic services are not
available.
 An understanding of the pathophysiology of acute urologic emergencies is crucial.

ACUTE URINARY RETENTION

Overview
Urinary retention is one of the most common medical problems encountered in clinical
practice, and most health care professionals will be involved in its treatment at one
time or another. Acute and chronic urinary retention, however, are different clinical
entities that demand differing courses of treatment. Acute urinary retention (AUR) re-
quires prompt recognition and reversal by medical staff of all levels, whereas chronic
urinary retention is by definition a less immediately severe condition.

Causes/Pathophysiology
Stated broadly, AUR is the sudden inability of the bladder to empty itself of urine,
whether due to a blocked outflow tract or intrinsic abnormality of the bladder (or
both). Using this definition, AUR can be divided into obstructive and dysfunctional
categories.
In all obstructive causes of AUR, the underlying cause of retention is the physical
obstruction of the outflow tract, that is, the bladder neck or urethra. This obstruction
is most commonly due to benign prostatic hyperplasia (BPH), a common condition
among older men. As men age, the central zone of the prostate (the area lining the ure-
thra) undergoes a slow but steady enlargement, causing progressive narrowing of the
urethra. Because the onset is insidious, a patient may chronically retain increasing

There are no disclosures to report.

a
Division of Urology, Maine Medical Center, 100 Brickhill Ave., South Portland, Maine 04106,
USA; b Division of Urology, Maine Medical Center, Tufts University School of Medicine, 100
Brickhill Ave., South Portland, Maine 04106, USA
* Corresponding author.
E-mail address: beaull@mmc.org

Surg Clin N Am 96 (2016) 407–424

http://dx.doi.org/10.1016/j.suc.2016.02.001 surgical.theclinics.com
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408 Ludvigson & Beaule

amounts of urine for many years before a precipitating event suddenly leads to the
complete inability to urinate. The inciting event can be infection, medications, recent
trauma (such as urethral catheter insertion), locoregional anesthesia, or idiopathic.
Once in retention, the bladder becomes over-distended such that the sarcomeres
of the smooth muscle cells in the bladder wall cannot properly engage one another,
and the contractile force of the bladder is diminished, worsening the problem.
Any other process that causes urethral narrowing can produce difficulty emptying
the bladder, such as urethral stricture or bladder neck contracture. Urethral strictures
and bladder neck contractures are typically sequelae of urologic procedures, such as
traumatic urethral instrumentation or previous prostate surgery, straddle injuries, or
sexually transmitted infection. However, they may be congenital, and patients may
not be aware of them at the time of presentation.
Urine outflow can also be blocked by a foreign object. The most common cause is a
blood clot formed within the bladder of a patient with significant gross hematuria,
whether from bladder cancer, traumatic urethral catheter insertion, or recent surgery.
Any recent urologic surgery or procedure is a risk factor for hematuria. Other foreign
objects can block urine outflow as well, such as bladder or kidney stones, or material
left over from urologic procedures that involve resection of tissue.
In addition, intrinsic bladder dysfunction can produce urinary retention every bit as
acutely as a physical blockage and can worsen any underlying low-level physical
blockage as well. Common causes for bladder dysfunction include medications (anti-
cholinergics in particular), nerve damage due to diabetes or congenital defect, and, as
previously discussed, simple over-distention due to other causes1 (Box 1).

Diagnosis
The diagnosis of AUR is straightforward in theory, but occasionally challenging in
practice. Patients with AUR will usually complain of suprapubic pain/pressure, urinary
frequency, urgency, voiding in small amounts, bladder spasms, penile pain, and
inability to urinate, but some patients may be unable to relate their symptoms, or
may actually be asymptomatic. If patients have diminished bladder sensation, their
symptoms can be nonspecific: these patients often present with only shortness of
breath and diaphoresis.
A bladder scanner may be used to quantify the amount of urine present in the
bladder to aid diagnosis, but the results should be interpreted carefully. The bladder
scanner is frequently fooled by the presence of intra-abdominal fluid, oddly shaped

Box 1
Common drugs leading to bladder dysfunction

Benadryl (diphenhydramine)
General/locoregional anesthetics
Opioids
Alcohol intoxication
Antidepressants (tricyclics especially)
Decongestants
Muscle relaxants

Adapted from Vilke GM, Ufberg JW, Harrigan RA, et al. Evaluation and treatment of acute uri-
nary retention. J Emerg Med 2008;35(2):194.
 Urologic Emergencies 409

bladders, and recent surgeries causing inflammation in the area, which leads to esti-
mates of urine that are too high or too low. The bladder scanner should never be used
to follow urine output if the patient’s fluid status is in doubt. Absent any indications that
the number may be inaccurate, and assuming the patient is not chronically retentive of
large volumes of urine, a bladder scanner reading of 400 mL or higher should prompt
catheterization.
If a dedicated bladder scanner is not available, simple ultrasonography can be used
to directly visualize the bladder. Physical examination will frequently reveal a palpable
bladder above the pubic bone as well as suprapubic tenderness. A digital rectal exam-
ination can identify prostatic enlargement or tenderness. A basic metabolic panel
(BMP) should be obtained to rule out electrolyte disturbances, and a complete blood
count (CBC) should be obtained if hematuria is the presenting complaint, because pa-
tients can lose a surprising amount of blood via this mechanism.
Patient history should focus on the length of time since the last void, the color and
consistency of the urine, and baseline voiding characteristics. The clinician should
ascertain whether the patient has trouble emptying their bladder normally and inquire
specifically as to any recent or past urologic interventions. A suprapubic or midline
abdominal incision or radiation tattoos may be associated with prior prostate or
bladder surgery or radiation therapy; in this instance, a smaller catheter should be
considered, as the cause is less likely to be BPH and more likely to be urethral stricture
of bladder neck contracture. Special attention should be paid to any scrotal prosthesis
that may represent a pump for an artificial urinary sphincter (AUS). In this case, urologic
consultation should always be obtained before placement of a urethral catheter to
deactivate the AUS in order to avoid erosion and damage to the device (Box 2; Fig. 1).
Treatment
The initial management of urinary retention is always drainage of the bladder. In the
vast majority of cases, this is accomplished by the insertion of a urethral catheter.
Any clinician who is treating a patient with AUR should first attempt placement of a
urethral catheter, unless there is some obvious anatomic complication that necessi-
tates the involvement of Urology. In general, if the urethral meatus is visible, urethral
placement should be attempted through it at least once.2
Urethral catheter placement technique
The first consideration is the size of the catheter, measured in the French catheter
scale. A catheter’s size in French is exactly 3 times its outer diameter in millimeters
(therefore, its circumference is slightly larger, because the circumference is the diam-
eter times pi). For example, an 18-French catheter has an outer diameter of 6 mm.
Outer diameter is stressed here to emphasize that a regular and 3-way 20-French

Box 2
Workup of acute urinary retention

Review of surgical history (especially urologic)

Assess baseline voiding function
Bladder scan
Basic metabolic panel (BMP)
Complete blood count (CBC) if hematuria
Digital rectal examination (DRE)
410 Ludvigson & Beaule

Fig. 1. CT scan: severely distended urinary bladder secondary to urinary retention. (From
Sharma A, Naraynsingh V. Distended bladder presenting with constipation and venous
obstruction: a case report. J Med Case Rep 2012;6:34.)

catheter will have different internal diameters, because a 3-way catheter must incor-
porate 3 internal channels into the same outer tube.
When trying to pass a urethral catheter through a large prostate, a larger catheter
should be used, rather than a smaller one. Many insertion attempts fail because a
small catheter was used, which lacks the stiffness necessary to push past the lobes
of an enlarged prostate. A reasonable starting point is 18 French. If resistance is
consistently encountered, further attempts should be abandoned to avoid the possi-
bility of creating a false passage that will hinder further attempts. A Coudé (French for
“elbow”) catheter, a catheter with an upwards bend at the tip, can and should be used
if BPH is suspected. The catheter is inserted perpendicular to the patient as with a
normal catheter placement and then lowered toward the bed when resistance is
encountered at the prostate, allowing the bent tip to negotiate the enlarged prostate
(Box 3; Fig. 2).
If urethral catheter placement is not possible, a flexible cystoscope can be used to
gain access to the bladder under direct visualization in order to place a wire for guid-
ance. In some cases, the wire can be placed blindly, although this should be done with
extreme caution. The urethral stricture can then be serially dilated with sounds as
needed to facilitate urethral catheter placement. If all else fails, the bladder can be
drained directly via suprapubic decompression or formal suprapubic tube placement.
Ultrasound guidance, which is available in most emergency departments, can be help-
ful and safer than blind placement.
If the patient is in clot retention (that is, blood clots are blocking urine flow), the best
catheter to place is a large-bore single-channel catheter, such as a silastic or 6-eye

Box 3
Common catheter choices

BPH: 18-French Coudé catheter

Clot retention: 22- to 24-French silastic catheter, 22-French 6-eye if unavailable
Continuous bladder irrigation: 20- to 24-French 3-way catheter
 Urologic Emergencies 411

Fig. 2. Large-diameter catheters. A, Conical-tip urethral catheter. B, Robinson urethral cath-

eter. C, Whistle-tip urethral catheter. D, Coudé hollow olive-tip catheter. E, Malecot self-re-
taining, four-wing urethral catheter. F, Malecot self-retaining, two-wing urethral catheter.
G, Pezzer self-retaining drain, open-end head, used for cystostomy drainage. H, Foley-
type balloon catheter. I, Foley-type, three-way balloon catheter, one limb of distal end for
balloon inflation (1), one for drainage (2), and one to infuse irrigating solution to prevent
clot formation within the bladder (3). (From Thompson JR. Bladder catheterization. In: Stehr
W, editor. The Mont Reid surgical handbook. 6th edition. Philadelphia: Saunders; 2008.
p. 839–48; with permission.)

catheter, because the patient will need his or her bladder irrigated thoroughly to
remove the clots. Although a 3-way catheter will eventually need to be placed to allow
continuous bladder irrigation to stop more clots from forming, this catheter cannot be
hand-irrigated well and should only be placed once clots have been evacuated from
the bladder, not before.

FOURNIER GANGRENE
Overview
Fournier gangrene is a term given to a severe and rapidly progressive necrotizing
infection of the skin and soft tissue of the perineal region, including the genitalia. It
is one of the few true urologic emergencies and prompt recognition is critical in order
to save as much tissue as possible (as well as the patient’s life). Morbidity is signifi-
cant; however, in the modern era with rapid surgical intervention and broad-
spectrum antibiotics, the mortality has decreased somewhat. Treatment remains
invariably morbid, and a multidisciplinary approach is required to manage the myriad
clinical challenges that arise both during and after the acute treatment period.
Causes/Pathophysiology
The exact cause of Fournier gangrene is not known presently, although most patients
have comorbid factors that predispose them to infection and skin breakdown (eg,
obesity, diabetes, immune compromise, or perirectal abscess). Bacterial isolates
from patients frequently reveal a polymicrobial milieu involving both anaerobic and
aerobic bacteria. A common event to all cases appears to be bacterial access to
412 Ludvigson & Beaule

the deep fascial planes, whereby rapid necrosis of tissue causes an ideal anaerobic
environment for proliferation of still more bacteria. Once established, the infection
spreads very rapidly, due to the causative organisms’ secretion of various tissue
toxins and virulence factors. Mortality varies according to numerous factors and has
been associated most closely with hypertension, congestive heart failure, renal failure,
and coagulopathy.3 The same study reported an overall mortality of 7.5%, and centers
with experience in treating this condition have been shown to have significantly
improved outcomes (Box 4).

Diagnosis
Patients will usually present with complaints of severe perineal pain. As with necrotizing
fasciitis, this pain is out of proportion to any external signs. Erythema is often present,
progressing rapidly to dark or black necrosis and sloughing of tissue. Patients may
report tightness and discomfort in the perineal/genital region before the onset of
pain. Clinical suspicion should remain high for patients with the appropriate risk factors
who exhibit these symptoms, especially given the dramatically high rate of progression
once an infection begins. Crepitus, or a computed tomographic (CT) scan finding of
subcutaneous air, is pathognomonic, although operative management should under
no circumstances be delayed for definitive imaging. Patients may become hemody-
namically unstable very quickly as tissue death accelerates (Figs. 3–5).
The use of serum markers of infection is usually low-yield, because the disease
invariably declares itself very rapidly. Electrolytes should by all means be monitored
closely, but these tend to serve as a guide for the management of severe sepsis as
one would for any patient and do not exhibit derangements specific to Fournier.

Treatment
The first step of treatment is initiation of broad-spectrum antibiotics, chosen according
to the hospital’s antibiogram. However, antibiotics only serve to halt the spread of sys-
temic illness. The only definitive treatment option for Fournier gangrene is swift and
aggressive debridement of all affected tissue. Tissue is excised sharply until bleeding
is encountered; this is usually the indication that healthy, viable tissue has been reached.
Tissue Gram stain and culture can be helpful in directing ongoing antimicrobial treat-
ment. Hemostasis can be achieved via liberal use of cautery, tying off larger vessels
as necessary. In men, the scrotal skin is frequently involved, and at times almost
none of it can be saved—however, the testicles are rarely involved and are often left
exposed at the conclusion of debridement. Testicular thigh pouches can be created
in subsequent procedures to maintain the testicles and to facilitate dressing changes,
but wet-to-dry packing is all that is required to protect them in the short term.

Box 4
Risk factors for Fournier gangrene

Diabetes
Immunosuppression
Obesity
Pre-existing perineal soft tissue infection
Liver disease
 413

Fig. 3. Fournier gangrene demonstrating dark, necrotic skin and soft tissue involving the
right hemiscrotum and extending into the left hemiscrotum and perineum. (From Kessler
CS, Bauml J. Non-traumatic urologic emergencies in men: a clinical review. West J Emerg
Med 2009;10(4):286.)

Fig. 4. Fournier gangrene demonstrating expanding necrotic tissue involving the genitalia,
right inguinal region, and left inner thigh. (From Kim DJ, Kendall JL. Fournier’s gangrene
and its characteristic ultrasound findings. J Emerg Med 2013;44(1):e100; with permission.)

Fig. 5. Subcutaneous gas in Fournier gangrene on scrotal ultrasound (A) and CT scan of
scrotum (B). (From Mirochnik B, Bhargava P, Dighe MK, et al. Ultrasound evaluation of
scrotal pathology. Radiol Clin North Am 2012;50(2):319, vi; with permission.)
414 Ludvigson & Beaule

If enough penile tissue remains, a urethral catheter is left in place to prevent urine
drainage onto open wounds. In some cases, it may be necessary to place a suprapu-
bic tube to allow perineal and penile tissues to heal appropriately.
Under no circumstances should attempts be made to reconstruct a scrotum at the
time of initial debridement, because the wound is still actively infected, and the patient
is unlikely to tolerate lengthy surgery. Once the infection has been adequately treated
and all necrotic tissue has been debrided, attention can be turned to reconstruction.
Plastic surgery consultation is often useful, because muscle flap rotations are some-
times needed to fill in the large defects left after aggressive debridement.
Patients will almost invariably require treatment in an intensive care unit following
surgery, because they are very often systemically ill—most deaths occur late in this
postoperative period, not during the initial acute surgically managed phase.3

ISCHEMIC PRIAPISM
Overview
Priapism is an uncommon urologic emergency that presents as an unwanted erection
that persists longer than 4 hours. This condition is subdivided into ischemic, or low-
flow, priapism; and non-ischemic, or high-flow, priapism. Ischemic priapism is the
focus of this section, because its treatment should be as urgent as possible to prevent
possible long-term sequelae, whereas nonischemic priapism can be treated far less
urgently and portends no loss of tissue or function. Although only male priapism will
be discussed here, it is important to note that clitoral priapism can occur in very
rare cases as well, due to the presence of erectile tissue.4

Causes/pathophysiology
An erection is produced by the corpora cavernosa, two tubelike structures that run the
length of the shaft of the penis and project into the pelvis for anchoring purposes. Each
corporal body consists of a spongy mass of highly vascularized tissue surrounded by a
tough fibrous coating. During sexual arousal, the vessels feeding the corpora dilate under
autonomic control, allowing more blood into the corpora; this in turn tamponades the
outflow vessels. The result is that the spongy tissue within each corporal body expands
against the inflexible fibrous sheath, producing rigidity. During detumescence, the inflow
vessels constrict again, allowing a net amount of blood to leave the corpora, which re-
duces the tamponade of the outflow vessels, which allows more blood to leave, and so on.
However, if this process is interrupted, the corpora can enter a state of sustained
engorgement that quickly becomes painful and begins to threaten tissue—it is essen-
tially a compartment syndrome of the penis.5 The physiologic internal pressure of the
corpora, in addition to preventing venous outflow, begins to impede inflow as well,
leading to tissue ischemia and eventually necrosis. For this reason, any erection
that has persisted longer than 4 hours should be dealt with promptly to prevent serious
immediate or future complications.
This disruption is often related to medications, especially those with a-adrenergic
effects. Oral erectile dysfunction agents are rarely implicated, and in fact, extremely
high doses of these medications can be ingested without producing priapism.6 Blood
disorders such as sickle cell anemia, which causes clogging of the outflow vessels and
persistence of the erection, is a significant risk factor; this is in contrast to high-flow or
nonischemic priapism, in which fistulization between arterial and venous systems
within the penis produces erection through too-rapid inflow of arterial blood into the
corpora. Although the erection is persistent, it is the result of an overabundance of
well-oxygenated blood, and therefore, is neither painful nor an emergency (Box 5).
 Urologic Emergencies 415

Box 5
Pharmacologic agents leading to ischemic priapism

Vasoactive agents used for erectile dysfunction (eg, phentolamine, prostaglandin E1)
a-Blocking agents (eg, prazosin, terazosin, tamsulosin)
Hydroxyzine
Antidepressants and antipsychotics
Certain antihypertensives (eg, hydralazine, propranolol, labetolol)
Cocaine
Ethanol

Adapted from Anele UA, Le BV, Resar LM, et al. How I treat priapism. Blood 2015;125(23):3553.

The incidence of priapism has been shown to be bimodal, with most patients pre-
senting between 5 to 10 and 20 to 50 years of age. The incidence is much higher in
those affected by sickle cell anemia, for previously discussed reasons. For this patient
population, lifetime incidence can reach as high as 42%, with significant clinical
sequelae.7

Diagnosis
The patient should be asked if he has a history of priapism, sickle cell disease, or
trauma to the penis. An adequate history of present illness (HPI) is important as the
length of time the erection has persisted is a critical piece of information. High-flow pri-
apism will present as a persistent erection that is not rigid and is not painful. Patients
will frequently present very late in the time course of this process because of this char-
acteristic lack of pain.
The diagnosis of ischemic priapism can usually be made clinically. Patients almost
always present with a very rigid, painful erection that has persisted much longer than
4 hours (acute embarrassment often prevents a more timely visit to the hospital). The
glans penis is usually not engorged. Skin changes, if present, are an ominous sign.
Even if clinical suspicion is high, a penile blood gas should be drawn to ensure ac-
curate diagnosis, because performing a procedure to reverse ischemic priapism
carries certain risks and should never be undertaken for high-flow priapism. This pro-
cedure is performed by using a large-bore intravenous needle with an angiocatheter to
access the corporal body (after the injection of local anesthesia) and gently draw off 5
to 10 mL of blood for analysis. Withdrawing too hard will collapse the surrounding
veins and prevent aspiration. The angiocatheter should be left in place to assist with
future irrigation. Blood gas analysis in ischemic priapism usually reveals acidosis, hyp-
oxia, and hypercapnia; values consistent with arterial blood indicate high-flow pria-
pism instead. Color Doppler ultrasonography can be used as well, although penile
blood gas analysis is more common and is generally sufficient to make the diagnosis
(Fig. 6).

Treatment
Treatment of ischemic priapism hinges on the removal of accumulated blood and clot
from within the corpora, and reversal of the underlying cause. The mainstay of treat-
ment in the emergency room is injection of an a-agonist agent, usually phenylephrine,
to produce vasoconstriction of the inflow channels and allow blood to drain passively
from the corpora. Sometimes, a single injection is sufficient to achieve detumescence;
however, penile irrigation is often required in conjunction. This is accomplished by the
416 Ludvigson & Beaule

Fig. 6. Ischemic priapism. Ecchymosis (from attempted corporal injection of a-adrenergic

agonist and aspiration) spares the glans penis. (From Ralph DJ, Garaffa G, Muneer A,
et al. The immediate insertion of a penile prosthesis for acute ischaemic priapism. Eur
Urol 2009;56(6):1035; with permission.)

placement of a single large-bore angiocatheter into the corpora to allow instillation and
aspiration of saline solution. Placement of the angiocatheter is sufficient to correct the
problem in most cases and rarely results in significant complications (aside from the
complications inherent to the condition itself).
If priapistic episodes recur, the surgeon may elect to perform a shunting procedure
to reduce the likelihood of future events. Shunt placement consists simply of creating
a defect in the corpora, to improve the ability of blood to drain out. Shunts can be
created between the corpora and either the glans, corpus spongiosum, or dorsal
vein of the penis; they are preferably created as distally as possible to minimize the
chances of erectile dysfunction. The preferred approach (for which multiple technical
methods exist) is to insert a large-bore needle or scalpel through the glans into the tip
of each of the corpora, creating a passage for blood into the tissue of the glans. Prox-
imal shunts, if necessary, can be a morbid procedure8 (Fig. 7).
Long-term sequelae of recurrent or long-lasting priapistic episodes can include
erectile dysfunction and scarring of the corpora, leading to penile curvature and

Fig. 7. T-shunt technique, a type of distal glandulocavernosal shunt, used to treat ischemic
priapism that is unresponsive to corporal irrigation and injection. (A) Initial incision and
markings, (B) completed procedure with brisk outflow of blood. (From Zacharakis E,
Raheem AA, Freeman A, et al. The efficacy of the T-shunt procedure and intracavernous
tunneling (snake maneuver) for refractory ischemic priapism. J Urol 2014;191(1):165; with
permission.)
 Urologic Emergencies 417

painful erections. These conditions can sometimes be corrected with future proce-
dures, but return to normal function is far from assured.

OBSTRUCTIVE PYONEPHROSIS
Introduction
Although nephrolithiasis may be a painful condition, it rarely has the potential to cause
serious medical harm. An obstructing, infected stone is another matter entirely, how-
ever. When infection develops behind an obstructing ureteral stone, the resulting
illness can progress very rapidly, and for this reason, any patient with findings indica-
tive of infection along with a kidney stone is treated promptly. The term obstructive
pyonephrosis refers to a severe infection in a hydronephrotic or obstructed kidney
that can lead to parenchymal destruction and loss of function; it is a more severe
form of urosepsis and can be clinically indistinguishable.

Causes/Pathophysiology
Renal stones are present in many asymptomatic individuals, who may go their entire
lives without having an attack of renal colic. Men tend to be affected more than
women, and Caucasians more often than Hispanics, Asians, and African Americans,
in descending order.9 Stone disease before age 20 is rare, with rates increasing until
about the fourth to sixth decade of life.10
When a renal stone migrates into the ureter and causes obstruction, distention of the
urothelial tract produces intense pain. Imaging will usually demonstrate hydronephrosis
(dilation of the renal pelvis) in this case. If symptoms of flank pain are well-controlled on
oral pain medications, and there is no associated infection, intractable emesis, or acute
renal injury, then a trial of medical expulsive therapy is reasonable. This usually consists
of hydration, an a-adrenergic blocker such as tamsulosin (Flomax), and narcotic pain
control. Notably, there is increasing evidence that tamsulosin does not affect the suc-
cess rate; however, it can improve ureteral pain.11 If hydronephrosis is prolonged or se-
vere, forniceal rupture can occur, which refers to extravasation of urine through the
junction of the distal convoluted tubule and collecting duct of the kidney. This rupture
is a normal physiologic pressure-release mechanism of the kidney. CT and ultrasound
will show a perinephric fluid collection in this case, but no specific surgical intervention
or antibiotics are required—treatment of the obstruction is sufficient, as discussed
later12 (Fig. 8).
When a stone obstructs the ureter, the buildup of urine behind it is susceptible to
infection. If this occurs, the condition is known as obstructive pyonephrosis. Because
infected urine can reflux directly into the bloodstream, patients can become septic
very rapidly and require aggressive medical treatment. Drainage of the infected urine
is imperative and is the mainstay of therapy, aside from appropriate antibiotic treatment.
Obstructive pyonephrosis can develop immediately in response to a stone, or it can
develop as a chronic stone progresses to complete obstruction. The stone itself can
serve as a nidus of infection. Infection with certain types of bacteria, particularly the
Proteus genus, can lead to large and rapid accumulations of struvite stone, which
can fill the entire collecting system and result in a “staghorn calculus.”

Diagnosis
A high degree of clinical suspicion is necessary to successfully treat this condition,
because the patient’s condition can worsen rapidly. Urinalysis (UA) should be ob-
tained, and urine sent empirically for culture. The clinician should keep in mind that
if the stone is completely obstructing, infected urine may not reach the bladder, and
418 Ludvigson & Beaule

Fig. 8. Forniceal rupture with resulting fluid around right kidney associated with moderate
hydronephrosis (personal patient).

a UA may therefore be normal. Negative test results should not delay treatment if the
overall clinical picture suggests infection.
Imaging, whether CT or ultrasound, can help confirm the presence and severity of
obstruction. Findings of hydronephrosis along with any findings suggestive of infection
indicate urgent treatment. If obstruction due to kidney stone is suspected, no contrast
is necessary for CT imaging; in fact, the lack of contrast enhances the ability to locate
small stones.

Urinalysis interpretation
Interpreting UA results can be difficult at times. The most important test results when
assessing a patient for infection in the setting of ureteral obstruction are leukocyte
esterase, leukocytes, erythrocytes, nitrites, and bacteria. The presence of an
indwelling ureteral stent can cloud the picture, because the stent itself will lead to he-
maturia and leukocytes in the urine. However, very high leukocyte esterase values
(greater than 400), or the presence of nitrites, are rarely due to ureteral stents and
should be treated as infection. As previously discussed, a negative UA should not
delay treatment if infection is suspected on a clinical basis, because infected urine
cannot drain to the bladder in the setting of complete obstruction.

Treatment
Prompt drainage is the only treatment option for obstructive pyonephrosis. Ideally, this
can be accomplished by placing a ureteral stent, allowing infected urine to bypass the
obstruction and temporizing the patient so that definitive treatment can be performed
when infection has cleared. Kidney stones themselves are never treated or removed in
the setting of infection, because the trauma to the urothelium can introduce bacteria
into the bloodstream and worsen the patient’s illness. During placement of the stent,
urine can be obtained directly from the renal pelvis using a ureteral catheter, allowing
an accurate urine culture to be sent. This ureteral catheter is especially helpful if the
blockage is complete enough to prevent any infected urine from draining into the bladder.
If ureteral stenting is not possible or if the patient is showing signs of hemodynamic
instability, a percutaneous nephrostomy tube should be placed by an Interventional
 Urologic Emergencies 419

Radiologist or qualified Urologist without delay. Definitive treatment of the stone or

other obstruction is then scheduled once the patient has recovered sufficiently.

PARAPHIMOSIS
Introduction
Paraphimosis is a painful and potentially serious condition characterized by the
inability to return the foreskin to its normal position after it is retracted. It is usually
seen in the hospital or chronic care setting following insertion of a urethral catheter
into an uncircumcised male patient, during which the foreskin is retracted, allowing
it to become entrapped in that position. If left untreated, paraphimosis has the poten-
tial to lead to tissue ischemia and necrosis—it should therefore be reduced as soon as
possible.
Pathophysiology
A normal foreskin can be easily retracted back over the glans and returns to its normal
position without difficulty. However, men may have a narrow band of tissue in the fore-
skin, called a phimotic ring, that can make retraction of the foreskin difficult. Men may
not be aware of this condition, because they may seldom or never retract their foreskin
completely, or it may not interfere sufficiently with their normal life to warrant correc-
tion. When the foreskin and its phimotic ring are retracted, a biological tourniquet is
applied to the penis, causing edema to develop distally and making reduction of the
foreskin increasingly difficult.13
Even an otherwise normal penis can develop enough edema in this state to cause
paraphimosis. If a urinary catheter is in place providing an additional source of tension,
or if injury, illness, fluid overload, or other medical conditions contribute to tissue
edema, the problem is compounded.
Diagnosis
The diagnosis is usually made clinically, by physical examination, and by patient inter-
view. Patients experience increasing pain as the tissue edema progresses and will be
unable to reduce their foreskin. Patients with dementia may exhibit increasing agita-
tion, prompting a physical examination and discovery of the problem. Sedated or
noncommunicative patients, and those with neurologic conditions affecting their
penile sensation, are particularly dangerous, because their condition may not be noted
for some time. Over a period of hours, the affected tissue may become so edematous
as to impede blood flow, leading to tissue loss and necrosis. If a urinary catheter is not
present, patients may develop urinary retention as well (see Fig. 8).
Treatment
Several techniques exist for reducing paraphimosis; treatment is largely dictated by
provider preference.5,14 The singular goal is to return the foreskin to its normal position
and allow the patient’s edema to recede, but frequently the anatomy is so distorted
that even identification of foreskin, penis, and glans may be very difficult.
The authors’ preferred method is to use gentle, constantly increasing pressure to
gradually reduce edema enough to allow reduction of the foreskin. This method can
be accomplished by simply squeezing the penis firmly until the foreskin can be
retracted; alternatively, a simple compressive dressing can be applied for 10 to 15 mi-
nutes before reduction is attempted.15 Although one hand is applying steady pressure,
the other should be used to gently squeeze and push the glans until it can be slid
through the phimotic ring. In some cases, it may be easier to grasp the foreskin
with both hands and use the thumbs to gently push the glans back through the
420 Ludvigson & Beaule

phimotic ring. If using a compressive dressing, the dressing can be removed and reap-
plied/tightened as necessary (Figs. 9–11).
The amount of pressure that can be brought to bear is often limited by the patient’s
discomfort, which can obviously be significant. Liberal use of narcotic pain medication
and/or sedation may be necessary in severe cases. Topical anesthetics are often not
effective, especially in adult patients, but ice can both provide analgesia and reduce
edema. Patience is essential; an extended period of firm pressure is frequently
required to reverse enough of the tissue edema to allow a successful reduction.
If all attempts to reduce the foreskin at the bedside fail, surgical intervention is indi-
cated to prevent tissue loss. Circumcision is usually required in this instance, because
the phimotic ring must be incised sharply to relieve the pressure.

TESTICULAR TORSION
Introduction
Testicular torsion is another of the true urologic emergencies, and prognosis is strongly
determined by time to surgical intervention. The signs and symptoms of torsion are
often unambiguous enough to establish the diagnosis without imaging or further tests,
although these are certainly useful. However, no test should ever delay progression to
the operating room if torsion is suspected. If recognized and treated in a prompt
manner, torsion has a good prognosis, but the risk of sequelae is present regardless.

Pathophysiology
Testicular torsion cases peak between 12 and 16 years of age and are usually not
associated with any significant past medical history; however, the presence of mass
or malignancy on the cord, such as lymphoma, can predispose to torsion and compro-
mise of vascular supply. Cold weather has been shown to increase incidence

Fig. 9. Paraphimosis with severe edema of distal penile shaft and proximal tight phimotic
ring (not seen in photo). (From Kessler CS, Bauml J. Non-traumatic urologic emergencies
in men: a clinical review. West J Emerg Med 2009;10(4):283.)
 Urologic Emergencies 421

Fig. 10. Reduction of paraphimosis. Reduce edema of distal penile skin with manual
compression to allow for replacement of distal penile preputial tissue over the glans penis.
(A) Typical appearance of edematous penis with paraphimosis, (B) Firm manual pressure is
applied to reduce edema, (C) Gentle counter-traction is applied to reduce foreskin, (D) Fully
reduced paraphimosis with normal appearance of the penis. (From Vilke GM, Ufberg JW,
Harrigan RA, et al. Evaluation and treatment of acute urinary retention. J Emerg Med
2008;35(2):196; with permission.)

somewhat, possibly due to the increased tone of dartos and cremasteric fibers, but
this hypothesis is controversial.16
The most common type of testicular torsion encountered by surgeons is intravaginal
torsion, wherein the testicle rotates within the tunica vaginalis. Intravaginal torsion is
usually due to a congenital deformity known as bell clapper deformity.17 A normal tes-
ticle is prevented from rotating within the tunica vaginalis by a broad fusion of the pa-
rietal and visceral layers along the epididymis; however, in a significant portion of men,
the area of fusion is smaller than usual, predisposing the testicle to rotation around this
narrowed axis. The compression of arterial inflow to the testicle produces ischemia
and intense pain.
422 Ludvigson & Beaule

Fig. 11. Reduction of paraphimosis. (From Buttaravoli P. Chapter 81: Phimosis and paraphi-
mosis. In: Buttaravoli P, editor. Minor emergencies. 2nd edition. Philadelphia: Mosby; 2007.
p. 330; with permission.)

In comparison, extravaginal torsion, the twisting of the entire tunica vaginalis and
spermatic cord, is primarily a perinatal event that presents as a painless, “vanishing”
testicle in a newborn baby, or as a painless swollen and discolored hemiscrotum
at birth. It is not a surgical emergency, because the window for salvage has almost
always already passed by the time torsion is recognized.18

Diagnosis
The primary symptom of torsion is intense, sudden pain in the affected testicle. The
severity of the pain means patients rarely delay seeking treatment, and therefore, often
present well within the window of treatment. On physical examination, edema may be
present, and the testicle may be observed or palpated (if allowed by the patient) higher
than usual in the scrotum. The cremasteric reflex, upward movement of the affected
testis elicited by lightly stroking the ipsilateral medial thigh, can be a helpful diagnostic
test, because the presence of a functioning reflex is strongly correlated with intact
blood flow. A UA may be obtained if the clinical picture is not completely indicative
of torsion and there is suspicion for an infectious process —for example, if pain is rela-
tively mild and urinary frequency, urinary urgency, or dysuria is present.
The mainstay of diagnostic tests for testicular torsion in recent years is the scrotal
Doppler ultrasound, which can unequivocally demonstrate lack of blood flow to the
testicle and confirm the diagnosis.19 The presence of blood flow should be compared
with the contralateral testicle, because blood flow can be reduced rather than
completely eliminated in some cases (Fig. 12).
It must be stressed: no diagnostic test should delay surgical exploration of the
scrotum if torsion is strongly suspected. Urologic consultation should be obtained
immediately at the same time confirmatory tests are being ordered. In an adolescent
patient with severe, sudden-onset testicular pain, very little clinical information would
be sufficient to warrant delaying surgery. If testicular torsion is recognized less than
6 hours after the onset of pain, the rate of testicular salvage is 95%. This rate drops
to 80% after 7 hours, and 60% after 12 hours. After 12 hours, loss of the testicle is
more likely than not.20
 Urologic Emergencies 423

Fig. 12. Left-sided testicular torsion as demonstrated by absence of intratesticular Doppler

flow on scrotal ultrasound. The right testis demonstrates normal blood flow. (A) Left testi-
cle, which demonstrates no flow on Doppler ultrasound, (B) The normal contralateral testi-
cle with intact bloodflow. (From Wang J-H. Testicular torsion. Urological Science (Urol Sci)
2012;23(3):85; with permission.)

Treatment
Manual detorsion can sometimes be accomplished, which may improve salvage rates
until surgical exploration is available; again, this should never delay the operating
room, as even a successfully detorsed testicle must be surgically explored.20 The
affected testicle should be rotated “away” from midline, as if one is opening a book,
because approximately two-thirds of torsion cases prove to be rotated in a medial di-
rection.19,20 Patients who are premedicated with narcotics will better tolerate bedside
detorsion.
Surgical detorsion and orchiopexy are accomplished through a midline incision at
the median raphe. After delivering the testicle, it is untwisted and observed closely
to determine its viability. It is common to find an inflammatory hydrocele. If the testicle
shows signs of adequate reperfusion (tissue viability, robust Doppler flow within the
spermatic cord), it is sutured in a 3-point fixation to the scrotum with nonabsorbable
suture to prevent future torsion events. If it appears necrotic or does not reperfuse af-
ter detorsion, orchiectomy is indicated. A concomitant contralateral orchiopexy
should be performed to ensure no future events, especially if an orchiectomy was
necessary.
Assuming all goes well in surgery, the long-term sequelae of testicular torsion is
somewhat unclear. Oxidative stress has been shown to impair testicular functioning
in animal models,21 but it is difficult to generalize these results to humans, and no
study has conclusively linked fertility problems to past episodes of torsion (assuming
both testicles remain intact).

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