2007 AUA Update Series Lesson 12

AUA Update Series
Lesson 12
Volume 26
2007
Anatomy, Physiology and Diseases of the Epididymis
Learning Objective: At the conclusion of this continuing medical education activity, the
participant will be familiar with the anatomy and physiology of the epididymis, and
understand the evaluation and treatment of benign and malignant conditions that affect
this reproductive organ.
Chad Tracy, M.D.
Disclosures: Nothing to disclose
and
William Steers, M.D.
Disclosures: Astellis, Novartis, Sanofi and Lilly ICOS: Consultant/Advisor; Watson: Meeting Participant/Lecturer; Pfizer: Scientific Study/Trial
Hovey Dabney Professor and Chair
Department of Urology
University of Virginia School of Medicine
Charlottesville, Virginia
This self-study continuing medical education activity is
designed to provide urologists, Board candidates
and/or residents affordable and convenient access to
the most recent developments and techniques in
urology. The American Urological Association
Education and Research, Inc. is accredited by the
Accreditation Council for Continuing Medical Education
(ACCME) to provide continuing medical education for
physicians. The American Urological Association
Education and Research, Inc. takes responsibility for
the content, quality and scientific integrity of this CME
activity.
Credit Designation Statement: The American Urological
Association Education and Research, Inc. designates
this educational activity for a maximum of 1.0 AMA
PRA Category 1 Credit™. Each physician should only
claim credit commensurate with the extent of their
participation in the activity.
AUA Disclosure Policy: As a provider accredited by the
ACCME, the American Urological Association
Education and Research, Inc. must insure balance,
independence, objectivity and scientific rigor in all its
activities. All faculty participating in an educational
activity provided by the American Urological
Association Education and Research, Inc. are required
to disclose to the audience any relevant financial
relationships with any commercial interest to the
provider. The intent of this disclosure is not to
prevent faculty with relevant financial relationships
from serving as faculty, but rather to provide members
of the audience with information on which they can
make their own judgments. The program planners
must resolve any conflicts of interest prior to the
commencement of the educational activity. It remains
for the audience to determine if the faculty’s
relationships may influence the educational content
with regard to exposition or conclusion. When
unlabeled or unapproved uses of drugs or devices are
discussed, these are also indicated.
Unlabled/Unapproved Uses: It is the policy of the
American Urological Association Education and
Research, Inc. to require the disclosure of all
references to unlabeled or unapproved uses of drugs
or devices prior to the presentation of educational
content. Please consult the prescribing information for
full disclosure of approved uses.
Publication date: March 2007
Expiration date: March 2010
© 2007 American Urological Association, Education and Research Inc., Linthicum, MD
KEY WORDS: epididymis, scrotum, humans, male, neoplasms
OVERVIEW
The epididymis is a scrotal organ and its functions include sperm
transport, maturation and storage. It is a common site of infection
in the male and accounts for a substantial portion of chronic scrotal
pain. Fortunately, the vast majority of masses involving this organ
are benign. We review the relevant anatomy, physiology and disease
processes involving the epididymis. Relevant imaging of the epididymis with disease will also be reviewed. Data on clinical evaluation
and management of inflammatory disorders will be presented.
ANATOMY
The epididymis is a 3 to 4 meter tubule that is coiled on itself
and encapsulated within the tunica vaginalis.1 Connective tissue
from the tunica vaginalis extends into the interductal spaces to form
histologically and functionally distinct compartments within the
epididymis.2 Grossly, the epididymis is divided into the caput
(head), corpus (body) and cauda (tail) (fig. 1). The caput epididymis
contains 8 to 12 efferent ducts extending from the body of the
testis, which join to form a coalesced epididymal tubule (ductus
epididymis).3 This tubule then progresses through the corpus epididymis, where the ductal lumen initially widens, but remains consistent in diameter before entering the cauda epididymis, where the
ductal lumen increases substantially before forming the vas deferens.
The epididymis receives a segmental blood supply from the
testicular artery, deferential artery and cremasteric artery.4
The testicular artery supplies the majority of the epididymis with
the superior epididymal branch supplying the caput epididymis and
the inferior epididymal artery supplying the corpus epididymis.5
The deferential artery, a branch from the inferior vesical artery
derived from the internal iliac artery, provides a collateral blood
supply primarily to the cauda epididymis and, via an anastomotic
network, to the remainder of the epididymis and testicle. The cremasteric artery, a branch of the inferior epigastric artery originating
from the external iliac artery, provides minimal contribution to
epididymal blood flow.4 Lymphatic and venous return from the
epididymis follows the arterial blood supply with lymphatics of
the caput and corpus draining into preaortic and retroperitoneal
lymph nodes, and lymphatics from the cauda epididymis draining
into the external iliac and pelvic lymph nodes.6 Thus, malignant
testis tumors that invade the epididymis have the added propensity
to metastasize to external iliac lymph nodes.
The epididymis is innervated by autonomic fibers from the postganglionic sympathetic neurons in the hypogastric plexus and the
preganglionic parasympathetic neurons in the pelvic plexus by way
of the intermediate and inferior spermatic nerves, respectively.7
Autonomic fibers from the superior spermatic nerve originate from
the renal and superior mesenteric ganglia, travel with the spermatic
artery and form a neurovascular plexus with neurons from the
inferior spermatic nerve that travel along the vas deferens. As the
plexus progresses away from the testis and efferent ductules, the
network becomes more substantial and complex in association with
progressively thicker smooth muscle cells. Efferent signals to these
smooth muscle cells are thought to be responsible for the peristaltic
movement of sperm through the ductuli efferents and epididymis.8
Afferent neurons travel within the same bundles as the aforementioned efferent neurons. Electrophysiological studies have demonstrated polymodal receptors (thermal, mechanical and chemical)
running from the epididymis to the spinal cord via the superior
spermatic nerve which are likely important in nociception.9 Tamura
et al demonstrated a bimodal distribution of afferent neurons, with
the superior spermatic nerve entering the thoracolumbar (T11-L4)
dorsal root ganglia and the inferior spermatic nerve entering the
sacral (S1-S3) dorsal root ganglia. 10 The primary input from the
epididymis is to the L1-L2 dorsal root ganglia, which is similar to
the input of renal afferents and helps explain why renal pathology
such as obstructing calculi may present as testicular or epididymal
pain or vice versa. This distribution of afferent projections also
helps explain the common occurrence of referred pain from the
epididymis to the inguinal, groin, thigh and perineal regions seen
with inflammatory conditions of the epididymis.
PHYSIOLOGY
The 3 roles of the epididymis are sperm maturation, transport
and storage. In regard to sperm maturation, the epididymis plays
an active role in the development of sperm functionality. It remains
speculative whether this organ serves any immunogenic role to
protect the testis from descending genital or urinary infections. The
identification of endogenous antimicrobial proteins called defensins
in this organ is consistent with this defensive role.11 Compartmentalization of the epididymis provides the environment necessary for
the 3 phases of sperm maturation, which are motility, fertility and
FIG. 1. Normal cross-sectional anatomy of testicle, epididymis and vas deferens. Reprinted with permission from Focosi D:
www.mm.interhealth.info.
ABBREVIATIONS: Hx (history), MRI (magnetic resonance imaging), TB (tuberculosis), Tx (therapy), VHL (von Hippel-Lindau)
114
metabolic maturation. As sperm progress proximally from the caput
to the cauda epididymis they acquire increased motility as well as
‘‘mature’’ motility patterns.12 Metabolic maturation, involving an
increased capacity for glycolysis13 and an increase in adenylate
cyclase activity,14 as well as biochemical changes in membrane
components, aid in fertility maturation so that testicular sperm,
which are initially incapable of unassisted egg fertilization, acquire
this ability by the time they reach the distal corpus epididymis.15
In addition to its role in sperm maturation, the epididymis acts
as a storage vessel and a conduit for passage of sperm from the
testicle to the vas deferens. Sperm travel into the caput epididymis
within the rete testis fluid. Once deposited in the epididymis, contractile cells lining the epididymal duct propel sperm antegrade
toward the distal epididymis. Transport through the epididymis is
highly variable and may take anywhere from 2 to 12 days16 depending on daily sperm production and whether there have been
any recent emissions.17 Once sperm reach the cauda epididymis,
they can be stored for various lengths of time depending on the
frequency of seminal emission, with approximately 50% of epididymal sperm stored within the cauda epididymis at any given time.18
During transport of sperm through the epididymis, water is actively
pumped out of the lumen resulting in progressive concentration of
sperm by the time it reaches the cauda epididymis.19
Function of the epididymis is under neurological, hormonal and
thermal control. Neurological control regulates peristaltic progression of sperm through the ductus epididymis. However, denervation
of the epididymis does not result in infertility, indicating the importance of thermal and androgen control in sperm maturation. Compared to serum, testosterone levels within the interstitial compartment of the epididymis are significantly elevated. High levels of
5␣-reductase are found within the epididymis and are responsible
for conversion of testosterone to dihydrotestosterone, the latter of
which is responsible for maintaining the structure of the epididymis
and performing its functions in sperm maturation and storage.20
The cooler temperature within the scrotum (2 to 3°C) is necessary
for sperm storage as well as electrolyte transport. Elevated scrotal
temperatures change the ionic and protein composition of cauda
fluid by virtue of effects on the cauda epithelium, and eliminate
the special ability of the cauda to store and prolong the life of
spermatozoa. Artificial elevation of rat epididymal temperatures
leads to decreased sperm in the first ejaculate, with a steep decline
in the number in subsequent ejaculates.21 Changes in epididymal
function occurring from increased epididymal temperatures may
contribute to the variable fertility of patients with cryptorchidism
or varicocele.
IMAGING
Ultrasonography is the primary imaging modality for evaluation
of the scrotum and scrotal contents. Technological advancements
in probe resolution (5 to 10 MHz) and color Doppler allow investigators to differentiate between a wide variety of disorders with a
high degree of sensitivity and specificity.22 Sonographically the
normal epididymis varies from isoechoic to slightly more hyperechoic compared to the testicle. To evaluate the long axis of the
epididymis, the scrotum should be elevated on a soft towel and the
probe directed in a longitudinal manner, with the superior aspect
of the probe placed over the caput epididymis. Typically, the caput
epididymis measures 10 to 12 mm, tapering to 4 mm in the mid
portion of the corpus before narrowing substantially as the cauda
epididymis joins the vas deferens.23
Within the last 20 years color Doppler ultrasound has become
increasingly important in evaluating patients with an acute scrotum
to rule out testicular torsion. A decrease in flow relative to the
contralateral testis using color Doppler ultrasound predicts testicular
torsion with 80% to 90% sensitivity and 93% to 100% specificity.24,25 While a small amount of vascularity is normally detectable
by ultrasound within the epididymis,26 increased vascular flow can
be used to detect epididymal inflammation (fig. 2). While color
Doppler ultrasound is highly sensitive in detecting inflammation
and vascular flow, its current use is primarily for evaluating testicular torsion, and its use for detection of epididymitis has not been
extensively evaluated.
Magnetic resonance imaging allows for detailed evaluation of
extratesticular lesions and may be used when ultrasound alone is
unable to diagnose an epididymal lesion.27,28 On T1-weighted images the testis and epididymis have intermediate signal intensity,
while the high water content of the testicle makes it hyperintense
compared to the epididymis on T2-weighted images. The tunica
albuginea surrounding the testis has a low signal intensity, forming
a natural delineation between testis and epididymis.
Scrotal radionuclide scintigraphy may be used with a relatively
high degree of sensitivity and specificity in differentiating testicular
torsion from epididymitis in patients with acute scrotum.29 A single
bolus of Na99TcO4− is injected intravenously and perfusion imaging
is obtained at 2-second intervals for 2 minutes. A static image is
performed after 10 minutes and compared to perfusion images. In
the non-pathological scrotum scrotal and testicular vessels are
poorly visualized in the perfusion state, and the scrotum appears
symmetric and homogeneous on static images. Patients with testicular torsion have an asymmetric decreased uptake in the affected
testicle on perfusion imaging and decreased or absent uptake on
static images. Conversely, patients with epididymitis have increased
uptake of the radionuclide on perfusion and static images. Late
torsion may elicit inflammatory changes that are confused with
epididymitis.
PATHOLOGY
A variety of inflammatory conditions target the epididymis including bacterial, viral and fungal infections. Acute epididymitis is
characterized by inflammation of the epididymis presenting as pain
and swelling, generally occurring on 1 side and developing over a
several day period. Epididymitis affects a large segment of the
population and is seen across a wide age range. It is the fifth most
common urological diagnosis in men between the ages of 18
and 50 years,30 and accounts for a greater loss of man hours
in the United States military than any other urological diagnosis.31 In the recently released Canadian PIE study Nickel et al found
that slightly less than 1% of men presenting to Canadian outpatient
urologists were diagnosed with epididymitis.32 Of those patients
more than 80% were diagnosed with chronic epididymitis (defined
as duration >3 months). Multiple objective findings of epididymitis
have been identified and in variable degrees may include positive
urine cultures defined as >10,000 cfu/ml, fever >38.5°C, erythema
of the scrotal skin, leukocytosis defined as white blood count
>11,000/mm3, urethritis defined as >4 white blood cells per high
power field and involvement of the adjacent testis. 33,34 Ultrasound,
which is primarily used for ruling out torsion of the spermatic
cord in cases of acute scrotum, will often demonstrate epididymal
hyperemia and swelling in patients with epididymitis. However,
differentiation between testicular torsion and epididymitis is based
115
FIG. 2. Color Doppler ultrasound demonstrates normal vascular flow in epididymis (A). Increased epididymal vascular flow in patient with clinical epididymitis (B).
on clinical evaluation, as partial spermatic cord torsion may mimic
epididymitis on scrotal ultrasound (fig. 3).
The pathophysiology of acute epididymitis remains unclear, although it is postulated to occur secondary to retrograde flow of
urine into the ejaculatory duct. This hypothesis is strengthened by
the finding that 56% of men older than 60 years with epididymitis
exhibit lower urinary tract obstruction, including benign prostatic
hyperplasia, prostate cancer and urethral stricture at the time of
diagnosis.35 In addition, multiple animal models have shown that
injection of Escherichia coli or Chlamydia trachomatis into the vas
deferens results in epididymitis that mimics clinical and microbiological findings of human epididymitis.36-38
Evidence of retrograde inoculation of the epididymis is supported
by the increased risk of epididymitis following instrumentation of
the urethra or bladder. In particular, patients who have infected
urine during instrumentation are at highest risk for infectious epididymitis. Patients with complicated urinary tract infections, such
as those requiring clean intermittent catheterization, account for
approximately 50% of all patients with infectious epididymitis.3941
In fact, the risk of epididymitis following transurethral resection
of the prostate led many physicians to perform prophylactic vasectomy in the 1970s and 1980s. By disrupting the pathway from the
urinary tract to the epididymis, Schmidt and Hinman were able to
reduce the incidence of post-prostatectomy epididymitis from 9.1%
to 2.7%.42
Small case studies suggest that 15% to 80% of all cases of epididymitis are bacterial in origin.43-45 The true incidence of bacterial
epididymitis is likely at the lower end of this range based on 2
large epidemiological studies involving more than 1000 patients in
whom bacteria were identified in fewer than 25% of subjects with
FIG. 3. Gray scale ultrasound of 15-year-old boy with sudden onset of scrotal pain demonstrates swelling in spermatic cord (A) and
epididymis (B). Color Doppler ultrasound revealed hypervascularity of epididymis with normal testicular flow. Patient was treated
for epididymitis but returned 2 days later with increased pain and was found to have testicular torsion on scrotal exploration.
116
clinical signs of epididymitis.39,40 Bacterial etiology depends on
patient age, as men younger than 35 years are much more likely
to have C. trachomatis than those older than 35 years in whom
coliforms and pseudomonas are more common.41,46,47
Treatment of epididymitis includes bed rest, scrotal elevation,
analgesics, nonsteroidal anti-inflammatory drugs and empiric antibiotics when infection is suspected. Antibiotics continue to be
the primary treatment modality for epididymitis, despite evidence
demonstrating that up to three-quarters of patients do not have
an identifiable bacterial infection.39,40 The choice of antibiotics
depends on patient age as well as their recent history including
urinary tract instrumentation and sexual history. Current recommendations rely on the presumed bacterial etiology (see Appendix). Patients who are younger than 35 years or have a
recent sexual risk factor are typically treated with a 10 to 14day course of doxycycline, while those with risk factors for
enteric pathogens (age >35 years, outlet obstruction, recent
instrumentation) are treated with quinolone antibiotics.48 Antibiotic sensitivities should be obtained in patients with recent urinary
tract instrumentation as this population may have higher rates of
antibiotic resistance.
Epididymitis in children based on ultrasonography or surgical
exploration has often been attributed to viral infections. A prospective study by Somekh et al, using viral cultures of throat, urine and
stool specimens, and serological tests for common viruses, revealed
significantly elevated titers to certain pathogens in patients with
epididymitis compared with controls, including M. pneumoniae
(53% vs 20%), enteroviruses (62.5% vs 10%) and adenoviruses
(20% vs 0%).49 Mumps infection, which was a frequent cause of
viral epididymo-orchitis in the past, has been virtually eliminated
since the introduction of mumps vaccine in the United States in
1985. Because the majority of pediatric epididymitis is thought to
be due to a viral etiology, management of non-bacterial epididymitis
in children, defined by absence of pyuria, is often treated conservatively with ice and analgesics,50 which is in stark contrast to treatment of the adult population.39
Chronic infectious epididymitis is most frequently seen in conditions associated with granulomatous reaction.51 Tuberculosis is the
most common granulomatous disease affecting the epididymis. Although renal involvement is often seen with epididymal TB, seeding
of the epididymis is thought to occur from hematogenous spread
of M. tuberculosis rather than seeding of the urinary system via
the kidneys.52 Up to 25% of patients may have bilateral disease
with ultrasound demonstrating an enlarged hyperemic epididymis
with multiple cysts and calcifications.
Tuberculous epididymitis should be suspected in all patients with
a known history of or recent exposure to TB, including visitation
to an endemic area, or in patients whose clinical status worsens
despite appropriate antibiotic treatment. Tuberculin skin testing is
positive in 90% of cases, although it is not specific for epididymal
involvement. Diagnosis of genitourinary TB specifically is often
difficult since organisms are identified in the urine in less than half
of the cases.53 When present, cultures of a draining scrotal sinus
may be used to identify epididymal TB. If a patient without a
history of TB is confirmed to have tuberculous epididymitis, he
should undergo the appropriate evaluation for systemic TB including chest x-ray, renal function tests and computerized tomography
or excretory urography if indicated. Treatment involves a 6-month
triple drug course with isoniazid, rifampin and pyrazinamide. Ethambutol should be added to the antimicrobial regimen while bacterial sensitivities are pending if the patient comes from an area
with high drug resistance.54 Extensive or protracted tuberculous
epididymitis may have a significant effect on fertility due to damage
of epididymal tissues.55
Other causes of granulomatous epididymitis, including sarcoidosis, brucellosis, syphilis, parasitic infection (filariasis) and fungal
infection (actinomycoses), occur at a lower frequency than tuberculous epididymitis. Sarcoidosis, a non-infectious, non-caseating,
chronic granulomatous disease that is more common in black patients, affects the genitourinary system in approximately 1% to 5%
of cases.51,56 Genitourinary manifestations include nephrocalcinosis, uremia, granulomas of the epididymis, testis and vas deferens as well as cutaneous genital lesions. The typical presentation
involves progressive enlargement of the epididymis in patients with
a known history of sarcoidosis, occurring bilaterally in up to 30%
of patients.51 Ultrasound findings are variable but often reveal
an enlarged heterogeneous epididymis that may contain distinct
nodules.57-59 Treatment with corticosteroids relieves pain and swelling in the majority of cases and should be used before consideration
of scrotal exploration. In the rare patient requiring exploration
frozen sectioning should be performed to prevent needless epididymectomy or orchiectomy.56 In addition, patients should be counseled preoperatively on the risks of testicular damage with epididymal exploration.
Sarcoid involvement of the epididymis usually demonstrates a
periductal distribution and can lead to azoospermia due to extrinsic
compression of epididymal ducts and/or Leydig cell disruption.60
Because of the possibility of male genital tract involvement, it is
recommended that a semen analysis be obtained at disease diagnosis
in all patients interested in paternity and those undergoing scrotal
exploration. If oligospermia is noted, the patient should be offered
the use of sperm banking for possible future assisted reproductive
techniques. If azoospermia is identified, serial semen analyses
should be performed to evaluate for temporary resolution of the
epididymal obstruction and allow for the use of sperm banking
during those intervals. In addition, empiric evidence indicates that
steroid therapy may assist with transient restoration of genital tract
patency.61
Brucella is a gram negative facultative coccobacillus that causes
epididymitis in 2% to 10% of patients with brucellosis.62 Infection
with Brucella typically occurs from direct contact with infected
animals or ingestion of their non-pasteurized milk, and primarily
in endemic areas, including the Mediterranean basin, Arabian Gulf,
southern India, and parts of Mexico, and Central and South
America.63 In the United States brucellosis occurs primarily in
California and Texas due to their proximity to the Mexican border.64
Patients with Brucella epididymitis are clinically similar to those
with other causes of infectious epididymitis, although they are
more likely to have complex septated hydroceles on ultrasound
examination.65 The diagnosis of brucellosis can be confirmed based
on patient history and serological testing demonstrating a single
titer of >1:160 or a greater than 4-fold increase in agglutinating
antibodies during a 4 to 12-week period. Patients with Brucella
epididymitis should be treated with 100 mg doxycylcine orally
twice daily for 6 weeks and either 1 gm streptomycin intramuscularly daily for 14 days or 600 to 900 mg rifampin orally daily for
6 weeks.66,67
Although rare in the United States, funiculoepididymitis may
occur from filarial invasion of the lymphatic system leading to
scarring and formation of cord masses, large hydroceles and lymphedema.68 More than 90% of human lymphatic filariasis is caused
117
by Wucheria bancrofti, with Brubia timori and Brugia malayi accounting for the remainder of cases. Infection typically centers in
the epididymis and lower spermatic cord, and then spreads centrifugally. Death of the microfilaria leads to development of fever,
localized lymphangitis, edema and hydrocele. In addition patients
may present with chyluria due to lymphatic obstruction. Ultrasound
typically reveals enlarged lymphatic channels and real-time imaging
may demonstrate random movements of viable microfilaria (‘‘dance
sign’’). Definitive diagnosis relies on identification of filaria on
blood smear, and treatment consists of testis/cord preserving surgical excision and use of diethylcarbamazine or ivermectin to control
microfilaremia.
Several cases of non-infectious epididymitis have been linked
to Behcet’s disease, an idiopathic multi-organ vasculitic disease.
Clinically, patients with Behcet’s disease can be affected by a large
number of signs and symptoms including recurrent aphthous ulcers,
genital ulcers, uveitis and epididymitis. In addition, patients may
have renal, gastrointestinal, cardiovascular or central nervous system involvement. Genital ulcers, which are tender to touch, are
most common on the scrotum, although they may occur on the
prepuce, glans or penile shaft. In a review of a large number of
patients with Behcet’s disease 4.6% had evidence of epididymitis.69
All patients had onset of epididymal pain and swelling with no
objective evidence of urethritis or infection on urinalysis, urethral
swab or urine culture. Patients with epididymal involvement were
more likely to have genital ulcers, cutaneous involvement and
arthritis than those without epididymal involvement. Medical therapy for Behcet’s disease is limited, with treatment primarily revolving around symptomatic relief and empiric treatment with topical
or systemic corticosteroids.
Epididymitis in adults and children can also be caused by drugs,
most notably the anti-arrhythmic amiodarone.70 High levels of this
drug are achieved in the epididymis relative to serum (300 ×),
leading to development of anti-amiodarone antibodies that then
attack the epididymis lining resulting in pain and swelling. The
incidence of epididymitis appears to be dose related, with clinical
epididymitis developing in up to 11% of patients on high dose
amiodarone.71 Temporary discontinuation of the drug or a decrease
in dosage is recommended for treatment of non-infectious epididymitis in patients on amiodarone therapy.
Chronic epididymitis, or epididymalgia, is a syndrome characterized by pain of at least 3 months in duration in the scrotum,
testicle or epididymis localized to 1 or each epididymis on clinical
examination. Although the true prevalence of this disorder is unknown, it may account for up to 80% of patients presenting to the
urology clinic with scrotal pain.32 Nickel et al have attempted to
classify chronic epididymitis based on clinical questionnaires.72
According to these authors, chronic epididymitis affects a wide age
range, with the average age at diagnosis being 49 years and the
average patient having symptoms present for 5 years at the time
of diagnosis. The pain tends to be mild to moderate and typically
does not affect daily activity. However, chronic epididymal pain
has a significant effect on quality of life, with 84% of patients
describing quality of life as dissatisfied, unhappy or terrible. There
do not appear to be any significant differences between men with
chronic epididymitis and normal controls, although affected patients
tend to have an increased number of sexual partners and a higher
incidence of erectile dysfunction, musculoskeletal complaints and
neurological disease. In patients with chronic epididymal pain evaluation should include assessment for chronic prostatitis and male
pelvic pain syndrome as epididymalgia may be a consequence of
118
one of these disorders. Patients who may have chronic prostatitis
or chronic prostatitis and male pelvic pain syndrome should undergo
prostatic fluid examination and careful evaluation for occult voiding
dysfunction.
The pain in chronic epididymitis is often of indeterminate etiology
as patients frequently have no history of a documented infection
or inciting event. Although there are no specific studies regarding
medical management of epididymalgia, reports of patients with
orchalgia reveal that the use of local therapy (heat), nerve blocks,
analgesics, anti-inflammatories or drugs such as tricyclics and anticonvulsants (gabapentin) are rarely effective, largely empirical and
not supported by randomized placebo controlled trials.73 Therefore,
medical management must rely on a combination of therapies with
effectiveness often being patient specific.
Attempts at treatment of idiopathic epididymal pain should begin
with use of a long-acting anti-inflammatory agent, such as naproxen
sodium, given on a daily basis for at least 2 weeks. Anti-inflammatories should be given in conjunction with limiting patient activity
as well as scrotal ice and elevation. If the patient fails to have relief
from these measures, consideration should be given to the use of
a tricylic antidepressant or an anticonvulsant such as gabapentin,
with selection based on any other comorbidities. Patients who do
not respond to a several month course of one of these centrally
acting medications may be considered for spermatic cord block
using a mixture of 6 ml 1% plain lidocaine along with 1 ml of
methylprednisolone (40 mg/ml). Despite these multiple therapies,
the vast majority of patients may continue to have substantial discomfort and may be considered for chronic pain management with
narcotics and referral to a chronic pain specialist. Only with further
placebo controlled randomized studies will we be better equipped
to medically treat this group of patients with a difficult disease.
Recent advances in the understanding of chronic visceral pain
states suggest that previous approaches such as epididymectomy74
have high failure rates (>75%) due to plasticity in circuits involved
in central pain processing. Transient relief is often followed by
either recurrence of pain or transfer of symptoms to the contralateral
epididymis. In addition, epididymectomy may be associated with
infertility or testicular loss intraoperatively or from subsequent
atrophy. Orchiectomy may be considered in patients with unrelenting epididymal pain that significantly affects their quality of life.
In a study by Davis and Noble 27% of patients undergoing inguinal
orchiectomy had only partial relief of symptoms, while 45% with
scrotal orchiectomy continued to have scrotal pain.73 Based on
these results, patients should undergo extensive conservative management as well as psychological evaluation before consideration
of orchiectomy for chronic orchalgia. In addition, the surgeon
should be aware of the medical legal aspects of this radical procedure which may fail to achieve its goal in a significant number of
patients.
BENIGN EPIDIDYMAL MASSES
Masses of the epididymis are typically benign, with epididymal
cysts representing the most common mass, occurring in 20% to
40% of asymptomatic individuals.75 True cysts, accounting for
approximately three-quarters of epididymal cysts, are lined by epithelium and contain lymphatic fluid, while spermatoceles form
secondary to obstruction of efferent ducts and contain a thick mixture of spermatozoa, lymphocytes and cellular debris. The 2 types
of epididymal cysts are indistinguishable on ultrasound but can be
differentiated from hydroceles in that they displace the testis, while
hydroceles envelop the testis.76
Other benign masses of the epididymis include sperm granulomas,
the appendix epididymis and abscesses. Sperm granulomas represent a foreign body inflammatory response to extravasated sperm
and occur at the cut ends of the vas deferens in approximately half
of men who have undergone vasectomy.77 The appendix epididymis is a remnant of the mesonephric (wolffian) duct that is
present in up to 10% of the population and is typically not
palpable (fig. 4).78 Because of its thin stalk, it may twist on its
blood supply leading to appendiceal torsion. Patients with torsion
of the appendix epididymis present with acute scrotal pain localized
to the caput epididymis, although the inflammatory response often
causes hyperemia and tenderness of the entire epididymis, which
may be confused with acute epididymitis. Rarely, the torsed appendix epididymis can be seen through the scrotal skin (‘‘blue dot
sign’’).
Tumors of the epididymis are rare and typically benign. Adenomatoid tumors are mesothelial in origin and account for the
majority of epididymal tumors. They generally present as a round,
well-circumscribed, painless epididymal mass that has been present
for years without changing in size.23 They are typically found in
patients between 20 and 40 years old but may be identified in any
age group. Grossly, the tumors are white, yellow or tan and typically
range between 0.5 and 5 cm in diameter. In some cases adenomatoid
tumors may be affixed to the tunica albuginea of the testis and
are indistinguishable from primary testicular tumors. Adenomatoid
tumors are universally benign and do not require excision if they
are asymptomatic and do not exhibit signs of malignancy.51, 77
Papillary cystadenomas and leiomyomas account for the majority
of non-adenomatoid benign epididymal tumors. Papillary cystadenomas account for a third of epididymal neoplasms, with twothirds occurring in patients with von Hippel-Lindau syndrome.
A third of papillary cystadenomas are bilateral, with bilaterality
being a strong indicator of VHL disease.79 Cystadenomas, which
arise in the efferent ducts, are well-circumscribed and often contain
green, yellow or blood-tinged fluid. Microscopic staining of papillary cystadenomas reveals abundant glycogen and lipids within
clear cells, mimicking the appearance of clear cell renal cell carcinoma, which may also be found in patients with VHL disease.
Despite the microscopic similarities with clear cell renal cell carcinoma, papillary cystadenomas are benign and surgery should be
reserved for intractable pain or unusually large tumors.
Leiomyomas are benign smooth muscle tumors typically found
bilaterally and often accompanied by a hydrocele or hernia. Grossly,
leiomyomas appear as round, firm, gray-white nodules that may
grow up to 8 cm in diameter.80 Sonographic imaging reports of
epididymal leiomyomas have described a variety of appearances
but none is specific or diagnostic of leiomyoma. As with other
benign tumors of the epididymis, management of leiomyomas is
primarily conservative. When malignancy cannot be ruled out, patients should undergo epididymectomy.
MALIGNANT EPIDIDYMAL MASSES
Primary malignancies of the epididymis are exceedingly rare, with
the majority classified as adenocarcinomas or sarcomas. Adenocarcinomas are the most common malignant neoplasms of the epididymis, although there are fewer than 50 reports in the literature.81
Adenocarcinomas have occurred in patients from 22 to 82 years
old, presenting as a scrotal mass with or without associated pain
and often associated with a hydrocele. They are differentiated
from benign tumors based on the degree of epididymal destruction and peri-epididymal soft tissue invasion, necrosis and cytological features. Unlike benign tumors of the epididymis, adenocarcinomas have been reported to metastasize to retroperitoneal lymph
nodes and are associated with a relatively high mortality.81 Treatment has primarily been excision of the primary tumor followed
by retroperitoneal lymph node dissection, and in some cases chemotherapy or external beam radiotherapy.
Malignant tumors extending into the epididymis from local or
distant sites are more common than primary epididymal malignancies. Epididymal involvement has been reported from direct extension of spermatic cord, testicular, scrotal and tunica vaginalis primary malignancies. Genital tract lymphoma is generally associated
with lymphoma recurrence rather than primary disease and is predominantly found in the testis, although it may involve the epididymis microscopically or macroscopically.51 Diseases such as sarcoidosis or tuberculosis, which may also involve the testis and
epididymis, tend to disproportionately involve the epididymis,
while lymphoma tends to disproportionately affect the testicle.23
Metastatic malignancies to the epididymis may occur due to its
highly vascular blood supply. Metastases from the prostate are the
most common, with sporadic reports identifying the stomach, colon
and kidney as primary sites of malignancy.81 Primary malignancies
FIG. 4. Surgical specimen demonstrates normal appendix epididymis (A). ‘‘Blue dot’’ sign in boy with right appendix epididymis torsion (B). Reprinted with permission from Hatch DA: http://www.meddean.luc.edu/lumen/MedEd/urology/nltstscn.htm.
119
of the epididymis are generally characterized by clear cell components with malignant features. Because primary epididymal malignancies are more rare than their metastatic counterparts,
patients without clear cell features should be examined for a
primary malignancy that may have metastasized to the epididymis.81
SURGERY OF THE EPIDIDYMIS
Surgery of the epididymis is rarely indicated but may be considered in various disease states. The approach to the epididymis and
scrotal contents is dependent on careful preoperative evaluation to
differentiate between benign and malignant conditions (fig. 5). It
is important to council patients preoperatively on risks of the procedure including infertility and possible loss of the testicle intraoperatively or from subsequent atrophy. The use of loupes or the operative
microscope for dissection is essential as the epididymal tubule has
a small diameter and any injury to the tubule may result in complete
occlusion at that level.82 The multiple interconnections between
the testicular and deferential arteries at the level of the epididymis
provide its rich blood supply and, while one of these supplies may
be ligated without vascular compromise, great care should be taken
to avoid ligation of both sets of branches. Epididymal branches of
the testicular artery are medial to and separate from the main
testicular artery so that careful technique during epididymal surgery
should allow for preservation of testicular blood supply. Patients
who may have had prior injury to the testicular artery (eg prior
inguinal hernia repair) or deferential artery (eg prior vasectomy)
are more reliant on the collateral circulation and are at an increased
risk of epididymal or testicular atrophy following epididymal
surgery.
Spermatoceles and epididymal cysts are common and rarely require surgical excision, although spermatocelectomy or cyst excision may be considered in patients with abnormally large or painful
lesions not amenable to medical therapy. The testis is delivered
through a median raphe or transverse scrotal incision, and the tunica
vaginalis is opened directly over the surface of the cystic structure,
being careful not to puncture the cyst wall. The cyst is then dissected
free of the epididymis by a combination of blunt and sharp dissections in the semi-avascular plane between the cyst wall and tunica
vaginalis. Whereas epididymal cysts are not connected to the epididymal tubule, spermatoceles have a small attachment that should be
ligated with an absorbable suture to prevent sperm extravasation
and granuloma formation. The tunica vaginalis is then reapproximated with a running absorbable suture, and the dartos and skin
are closed in separate layers.
Epididymectomy for non-malignant disease is performed by delivery of the testis through a median raphe or transverse scrotal incision. If epididymectomy is performed for tuberculosis, the incision
should be extended to the level of the external ring to allow for
removal of all sinuses and the distal vas deferens.83 Once the testis
is delivered into the operative field, dissection may proceed from
a superior or inferior approach. With the superior approach a traction
suture is placed in the caput epididymis, and the epididymis is
FIG. 5. Evaluation of palpable epididymal mass
120
carefully dissected from the testis by dividing and ligating the
efferent tubules.83 The testicular vessels are identified medially and
the epididymal branch of the testicular artery is clamped and divided. Dissection is carried inferiorly, staying close to the epididymis to avoid damage to the testicular vessels. The superior approach
is completed by dividing and ligating the vas deferens at its distal
extent. With an inferior approach dissection is started by double
ligating the vas deferens and its vessels at the junction of its straight
and convoluted regions.82 The vas deferens is then traced superiorly
to its junction with the epididymis at which point the tunica vaginalis
is opened and dissection is continued in the plane between the
epididymis and the testis. The efferent ducts, located superior to
the testicular vascular pedicle, are ligated with an absorbable suture
and the epididymis is removed. After completion of the epididymectomy from either the superior or inferior approach, the opened
edges of the tunica vaginalis are oversewn with a continuous absorbable suture for hemostasis. The dartos and skin are then closed
with absorbable suture in separate layers.
Malignant epididymal tumors are exceedingly rare and require
careful preoperative planning. As with any potentially malignant
testicular mass, they should be approached through an inguinal
incision with early clamping of the cord and delivery of the testis.
Unless the mass is clearly malignant based on preoperative evaluation, the modified Chevassu maneuver may be used for intraoperative diagnosis of malignancy to prevent needless orchiectomy.84
With this maneuver the testicular vessels are occluded at the level
of the internal inguinal ring and the delivered testis is isolated in
the surgical field with a plastic dam. Scrotal hypothermia is achieved
with slush ice (up to 30 minutes), and the gubernaculum is double
ligated and divided. The tunica vaginalis is opened over the mass
to allow for direct inspection and frozen biopsy. If diagnosis of
malignancy is excluded, the epididymal tumor or cyst is excised
in a manner identical to that for a spermatocele. If the mass is
found to be malignant, a formal orchiectomy should be performed
in a manner identical to that for a testicular malignancy. Use of
this maneuver has been shown to decrease the number of orchiectomies for benign disease.
APPENDIX: CENTERS FOR DISEASE CONTROL
GUIDELINES FOR THE DIAGNOSIS AND MANAGEMENT
OF EPIDIDYMITIS
Age <35 years:
Gram stain of urethral exudate for urethritis (>5 white blood
cells per high power field)
Culture or polymerase chain reaction of urethral swab (or
urine)
Empiric antibiotics to cover N. gonorrheae and C. trachomatis
250 mg ceftrianone intramuscularly once daily *
and
100 mg doxycycline orally for 10 days *
Age >35 years:
Culture and gram stain of voided urine
Empiric antibiotics to cover coliform bacteria:
500 mg ciprofloxacin twice daily for 10 days
or
500 mg levofloxacin daily for 10 days
or
400 mg ofloxacin daily for 10 days
*Patients with allergies to penicillins or tetracyclines may be
treated with the same antibiotics as those older than 35 years.
REFERENCES
1. Lanz T and Neuhauser G: Morphometrische analyse des
menschlichen nebenhodens. Z Anat Entwicklungsgesch 1964;
124: 126.
2. Kormano M and Reijonen K: Microvascular structure of the
human epididymis. Am J Anat 1976; 145: 23.
3. Schlegel PN and Su LM: Physiological consequences of testicular sperm extraction. Hum Reprod 1997; 12: 1688.
4. Artyukhin AA: Intersystemic arterial anastomoses in testicles.
Bull Exp Biol Med 2002; 133: 623.
5. MacMillan EW: The blood supply of the epididymis in man.
Br J Urol 1954; 26: 60.
6. Wenzel J and Kellerman P: Vergleichende untersuchungen
über das lymphgefasssytem des nebenhodens und hodens von
mensch, hund und kaninchen. Z Mikrosk Anat Forsch 1966;
75: 368.
7. Mitchell GAG: The innervation of the kidney, ureter, testicle
and epididymis. J Anat 1935; 70: 10.
8. Risely PL: Physiology of the Male Accessory Organs. New
York: Pergamon 1963.
9. Kumazawa T, Mizumura K and Sato J: Response properties
of polymodal receptors studied using in vitro testes spermatic
nerve preparations of dogs. J Neurophysiol 1987; 57: 702.
10. Tamura R, Mizmura K, Sato J et al: Sequential distribution of
afferent neurons innervating the canine testis. J Auto Nerv Syst
1996; 58: 101.
11. Yenugu S, Hamil KG, French FS et al: Antimicrobial actions
of the human epididymis 2 (HE2) protein isoforms, HE2alpha,
HE2beta1 and HE2beta2. Reprod Biol Endocrinol 2004; 2: 61.
12. Bedford JM, Calvin HI and Cooper GW: The maturation of
spermatozoa in the human epididymis. J Reprod Fertil 1973;
18: 199.
13. Hoskins DD, Munsterman D and Hall ML: The control of
bovine sperm glycolysis during epididymal transit. Biol Reprod
1975; 12: 566.
14. Casillas ER, Elder CM and Hoskins DD: Adenylate cyclase
activity of bovine spermatozoa during maturation in the epididymis and the activation of sperm particulate adenylate cyclase
by GTP and polyamines. J Reprod Fertil 1980; 59: 297.
15. Orgebin-Crist MC: Studies on the function of the epididymis.
Biol Reprod 1969; 1: 155.
16. Rowley MJ, Teshima F and Heller CG: Duration of transit of
spermatozoa through the human male ductular system. Fertil
Steril 1970; 21: 390.
17. Johnson L and Varner DD: Effect of daily spermatozoan production but not age on transit time of spermatozoa through the
human epididymis. Biol Reprod 1988; 39: 812.
18. Amann RP: A critical review of methods for evaluation of
spermatogenesis from seminal characteristics. J Androl 1981;
2: 37.
19. Turner TT, Hartmann PK and Howards SS: In vivo sodium,
potassium, and sperm concentrations in the rat epididymis.
Fertil Steril 1977; 28: 191.
20. Robaire B and Hermo L: Efferent ducts, epididymis, and vas
deferens: structure, functions, and their regulation. In: The
Physiology of Reproduction. Edited by E Knobil and J Neill.
New York: Raven Press 1988; pp 999-1080.
21. Bedford JM: Effects of elevated temperature on the epididymis
and testis: experimental studies. Adv Exp Med Biol 1991;
286: 19.
121
22. Caroll BA and Gross DM: High-frequency scrotal sonography.
AJR Am J Roentgenol 1983; 140: 511.
23. Woodward PJ, Schwab CM and Sesterhenn IA: From the archives of AFIP: extratesticular scrotal masses: radiologicpathologic correlation. Radiographics 2003; 23: 215.
24. Stehr M and Boehm R: Critical validation of colour Doppler
ultrasound in diagnostics of acute scrotum in children. Eur J
Pediatr Surg 2003; 13: 386.
25. Ciftci AO, Senocak ME, Tanyel FC et al: Clinical predictors
for differential diagnosis of acute scrotum. Eur J Pediatr Surg
2004; 14: 333.
26. Keener TS, Winter TC, Nghiem HV et al: Normal adult epididymis: evaluation with color Doppler US. Radiology 1997;
202: 712.
27. Serra AD, Hricak H, Coakley FV et al: Inconclusive clinical
and ultrasound evaluation of the scrotum: impact of magnetic
resonance imaging on patient management and cost. Urology
1998; 51: 1018.
28. Cramer BM, Schlegel EA and Thueroff JW: MR imaging in
the differential diagnosis of scrotal and testicular disease. Radiographics 1991; 11: 9.
29. Yuon Z, Luo Q, Chen L et al: Clinical study of scrotum scintigraphy in 49 patients with acute scrotal pain: a comparison with
ultrasonography. Ann Nucl Med 2001; 15: 225.
30. Collins MM, Stafford RS, O’Leary MP et al: How common
is prostatitis? A national survey of physician visits. J Urol
1998; 159: 1224.
31. Moore CA, Lockett BL, Lennox KW et al: Prednisone in the
treatment of acute epididymitis: a cooperative study. J Urol
1971; 106: 578.
32. Nickel JC, Teichman JMH, Gregoire M et al: Prevalence, diagnosis, characterization and treatment of prostatitis, interstitial
cystitis, and epididymitis in outpatient urologic practice: the
Canadian PIE Study. Urology 2005; 66: 935.
33. Kaver I and Matzkin H: Epididymo-orchitis: a retrospective
study of 121 patients. J Fam Pract 1990; 30: 548.
34. Hoosen AA, O’Farrell N and van de Ende J: Microbiology of
acute epididymitis in a developing community. Genitourin Med
1993; 69: 361.
35. Hoppner W, Strohmeyer T, Hartmann Lopez-Gamarra D et al:
Surgical treatment of acute epididymitis and its underlying
diseases. Eur Urol 1992; 22: 218.
36. Ludwig M, Johannes S, Bergmann M et al: Experimental Escherichia coli epididymitis in rats: a model to assess the outcome
of antibiotic treatment. BJU Int 2002; 90: 933.
37. See W, Taylor T, Mack L et al: Bacterial epididymitis in the
rat: a model for assessing the impact of acute inflammation
on epididymal antibiotic penetration. J Urol 1990; 144: 780.
38. Jantos C, Baumgartner W, Durchfeld B et al: Experimental
epididymitis due to Chlamydia trachomatis in rats. Infect Immun 1992; 60: 2324.
39. Tracy CR and Costabile RA: The changing face of epididymitis
from 1965 to 2005. Presented at 53rd James C. Kimbrough
Urological Seminar, Savannah, Georgia, January 15-20, 2006.
40. Mittemeyer BT, Lennox KW and Borski AA: Epididymitis: a
review of 610 cases. J Urol 1966; 95: 390.
41. Berger RE, Alexander ER, Harnisch JP et al: Etiology, manifestations, and therapy of acute epididymitis: prospective study
of 50 cases. J Urol 1979; 121: 750.
122
42. Schmidt SS and Hinman F: The effect of vasectomy upon the
incidence of epididymitis after prostatectomy: an analysis of
810 operations. J Urol 1950; 63: 2.
43. Hawkins DA, Taylor-Robinson D, Thomas BJ et al: Microbiological survey of acute epididymitis. Genitourin Med 1986;
62: 342.
44. Scheibel JH, Anderson JT, Brandenhoff P et al: Chlamydia
trachomatis in acute epididymitis. Scand J Urol Nephrol 1983;
17: 47.
45. Pearson RC, Baumber CD, McGhie D et al: The relevance of
Chlamydia trachomatis in acute epididymitis in young men.
Br J Urol 1988; 62: 72.
46. Grant JFB, Costello CB, Sequeira PJ et al: The role of Chlamydia trachomatis in epididymitis. Br J Urol 1987; 60: 355.
47. Melekos M and Asbach H: Epididymitis: aspects concerning
etiology and treatment. J Urol 1987; 138: 83.
48. Eickhoff JH, Frimodt-Moller N and Frimodt-Moller C: A double blind randomized controlled multicentre study to compare
the efficacy of ciprofloxacin with pavampicillin as oral therapy
for epididymitis in men over 40 years of age. BJU Int 1999;
84: 827.
49. Somekh E, Gorenstein A and Serour F: Acute epididymitis
in boys: evidence of a post-infectious etiology. J Urol 2004;
171: 391.
50. Lau P, Anderson PA, Giacomantonio JM et al: Acute epididymitis in boys: are antibiotics indicated? Br J Urol 1997; 79: 797.
51. Ulbright TM, Amin MB and Young RH: Miscellaneous primary tumors of the testis, adnexa, spermatic cord, and scrotum.
In: Atlas of Tumor Pathology, fasc 25, ser 3. Edited by J Rosai
and LH Sobin. Washington, D.C.: Armed Forces Institute of
Pathology 1999; pp 235-366.
52. Heaton ND, Hogan B, Mitchell M et al: Tuberculous epididymo-orchitis: clinical and ultrasound observations. Br J Urol
1989; 64: 305.
53. Ferrie BG and Rundle JSH: Tuberculous epididymo-orchitis.
A review of 20 cases. Br J Urol 1983; 55: 437.
54. Cohen J and Powderly WG: Infectious Diseases, 2nd ed. New
York: Mosby 2004.
55. Al-Ghazo MA, Bani-Hani KE and Amarin ZO: Tuberculous
epididymitis and fertility in North Jordan. Saudi Med J 2005;
26: 1212.
56. Ryan DM, Lesser BA, Crumley LA et al: Epididymal sarcoidosis. J Urol 1993; 149: 134.
57. Burke BJ, Parker SH, Hopper KD et al: The ultrasonographic
appearance of coexistent epididymal and testicular sarcoidosis.
J Clin Ultrasound 1990; 18: 522.
58. Forte MD and Brant WE: Ultrasonographic detection of epididymal sarcoidosis. J Clin Ultrasound 1988; 16: 191.
59. Suzuki Y, Koike H, Tamura G et al: Ultrasonographic findings
of epididymal sarcoidosis. Urol Int 1994; 52: 228.
60. Rudin L, Megalli M and Mesa-Tejada R: Genital sarcoidosis.
Urology 1974; 3: 750.
61. Svetec DA, Waguespack RL and Sabanegh ES Jr: Intermittent
azoospermia associated with epididymal sarcoidosis. Fertil
Steril 1998; 70: 777.
62. Dewbury KC: Scrotal ultrasonography: an update. BJU Int
2000; 86: 143.
63. Pappas G, Akritidis N, Bostilkovski M et al: Brucellosis. N
Engl J Med 2005; 352: 2325.
64. Troy SB, Rickman LS and Davis CE: Brucellosis in San Diego:
epidemiology and species-related differences in acute clinical
presentations. Medicine (Baltimore) 2005; 84: 174.
65. Lubani MM, Dudin KI, Sharda DC et al: A multicenter therapeutic study of 1100 children with brucellosis. Pediatr Infect
Dis J 1989; 8: 75.
66. Ozturk A, Ozturk E, Zeyrek F et al: Comparison of brucella and
non-specific epididymo-orchitis: grey scale and color Doppler
ultrasonographic features. Eur J Radiol 2005; 56: 256.
67. Solera J, Geijo P, Largo J et al: A randomized, double-blind
study to assess the optimal duration of doxycycline treatment
for human brucellosis. Clin Infect Dis 2004; 39: 1776.
68. Williams PB, Henderson RJ, Sanusi ID et al: Ultrasound diagnosis of filarial funiculoepididymitis. Urology 1996; 48: 644.
69. Cho YH, Lee KH, Band D et al: Clinical features of patients
with Behcet’s disease and epididymitis. J Urol 2003; 170: 1231.
70. Greene HL, Graham EL, Werner JA et al: Toxic and therapeutic
effects of amiodarone in the treatment of cardiac arrhythmias.
J Am Coll Cardiol 1983; 2: 1114.
71. Gasparich JP, Mason JT, Greene HL et al: Amiodarone-associated epididymitis: drug-related epididymitis in the absence of
infection. J Urol 1985; 133: 971.
72. Nickel CJ, Siemens RD, Nickel KR et al: The patient with
chronic epididymitis: characterization of an enigmatic syndrome. J Urol 2002; 167: 1701.
73. Davis BE and Noble MJ: Analysis and management of chronic
orchalgia. AUA Update Series 1992; XI: lesson 2.
74. Padmore DE, Norman RW and Millard OH: Analyses of indications for and outcomes of epididymectomy. J Urol 1996;
156: 95.
75. Leung ML, Gooding GA and Williams RD: High-resolution
sonography of scrotal contents in asymptomatic subjects. AJR
Am J Roentgenol 1984; 143: 161.
76. Holden A and List A: Extratesticular lesions: a radiological
and pathological correlation. Australas Radiol 1994; 38: 99.
77. Bostwick DG: Spermatic cord and testicular adnexa. In: Urologic Surgical Pathology. Edited by DG Bostwick and JN Eble.
St Louis, Missouri: Mosby 1997; pp 647-674.
78. Johnson KA and Dewbury KC: Ultrasound imaging of the
appendix testis and appendix epididymis. Clin Radiol 1996;
51: 335.
79. Billesbolle P and Nielsen K: Papillary cystadenoma of the
epididymis. J Urol 1988; 139: 1062.
80. Kuhn MT and MacLennan GT: Benign neoplasms of the epididymis. J Urol 2005; 174: 723.
81. Jones MA, Young RH and Scully RE: Adenocarcinoma of the
epididymis: a report of four cases and review of the literature.
Am J Surg Pathol 1997; 21: 1474.
82. Goldstein M: Surgical management of male infertility and other
scrotal disorders. In: Campbell’s Urology, 8th ed. Edited by
PC Walsh, AB Retik, ED Vaughan et al. Philadelphia: WB
Saunders Co. 2002; pp 1556-1557.
83. Hinman F Jr: Atlas of Urologic Surgery, 2nd ed. Philadelphia:
WB Saunders Co. 1998; pp 406-410.
84. Goldstein M and Waterhouse K: When to use the Chevassu
maneuver during exploration of intrascrotal masses. J Urol
1983; 130: 1199.
123
Study Questions Volume 26 Lesson 12
1. Which artery does not directly supply the epididymis?
a. Cremasteric
b. Deferential
c. Inferior epigastric
d. Testicular
e. External spermatic
2. The best antibiotic to treat a 23-year-old sexually active male
with pyuria and swollen, tender epididymis is
a. Trimethoprim
b. Doxycycline
c. Tequin
d. Sulfamethoxazole
e. Amoxicillin
3. The process that can involve epididymis and commonly lead
to infertility is
a. Brucellosis
b. Chlamydia
c. Lupus
d. Sarcoidosis
e. Ureaplasma
4. The best antibiotic to treat a 50-year-old male with acutely
swollen, tender epididymis and normal urinalysis is
a. Ciprofloxin
b. Doxycycline
c. Trimethoprim
d. Amoxicillin
e. Erythromycin
5. The most common bilateral epididymal masses in a 40-yearold man with renal cell carcinoma, cerebral hemangioblastoma and hypertension are
a. Metastatic renal cell
b. Angiomas
c. Ectopic pancreatic tissue
d. Papillary cystadenomas
e. Adenocarcinoma
Fill in answers on answer sheets provided or take this test online at http://www.auanet.org/eforms/cme/