Updated: Sep 4, 2008
The epididymis is a coiled tubular structure located along the posterior aspect of the testis. It allows for the storage, maturation, and transport of sperm, connecting the efferent ducts of the testis to the vas deferens. Inflammation of the epididymis can be acute (<6 wk) or chronic and is most commonly caused by infection.
Under Investigation
Epididymitis most often is due to the retrograde extension of organisms from the vas deferens and is rarely the result of hematogenous spread. Bacterial infection results in the infiltration of white blood cells into the epididymal connective tissue, with resultant congestion and edema. This inflammation can rapidly spread to the tubules, with the risk of abscess formation and necrosis of the epididymis.3,4 The causative organism is identified in 80% of patients and varies according to the age of the patient.
In prepubertal males, the predominating sources are pathogens that cause bacteriuria (ie, coliform bacteria [Escherichia coli]). Workup should include a urologic evaluation for a genitourinary anomaly, which is present in as many as 50% of these patients.5,6 Epididymitis in this age group may also be secondary to a postinfectious inflammatory reaction to certain pathogens. Research has shown that boys with epididymitis had significantly elevated titers for Mycoplasma pneumoniae, enteroviruses, and adenoviruses when compared with control groups.7
In sexually active men (age 35 years has frequently been used as a parameter in research studies), the predominating sources are Chlamydia trachomatis and Neisseria gonorrhoeae, with C trachomatis being responsible for nearly two thirds of all cases. In homosexual men younger than 35 years, coliform bacteria are highly represented.
Epididymitis is the most common cause of intrascrotal inflammation. Incidence is less than 1 case in 1,000 males per year.
Infection of the epididymis can lead to the formation of an epididymal abscess. In addition, progression of the infection can lead to involvement of the testicle, causing epididymo-orchitis or a testicular abscess. Sepsis is a potential consequence of severe infection. Bilateral epididymitis may result in sterility due to occlusion of the ductules from peritubular fibrosis.
Epididymitis is primarily a disease of adults, most commonly affecting males aged 19-40 years.
The progression of epididymitis usually is gradual in nature, with symptoms often peaking within 24 hours of onset. Initially, the patient may note abdominal or flank pain because cellular inflammation typically begins in the vas deferens. As the inflammation descends to the lower segment of the epididymis, the patient notes discomfort localized to the scrotum. Younger patients or any patient with a sexually transmitted epididymitis may note symptoms related to urethritis. A recent history of endourethral instrumentation or urinary tract infection is more common in older patients. Symptoms include the following:
Hydrocele
Orchitis
Testicular Torsion
Urinary Tract Infection, Male
Epididymal cyst
Epididymal congestion following vasectomy
Spermatocele
Testicular tumor (hemorrhage into tumor)
Varicocele
The following laboratory studies may be indicated for suspected epididymitis:
Patients with testicle or scrotal pain require immediate evaluation in order to identify and quickly treat potential cases of testicular torsion. Although most cases of torsion occur in patients aged 12-18 years, testicular torsion should be considered in any patient aged 12-30 years who presents with a scrotal complaint.
Consult a urologist immediately if torsion is a possibility. Testicular torsion is a clinical diagnosis, and consultation should not be delayed for the performance of additional ancillary studies. Otherwise, most cases of epididymitis can be managed on an outpatient basis with follow-up with a urologist scheduled within 3-7 days. All pediatric cases of epididymitis require immediate consultation because of the high incidence of associated genitourinary anomalies.
Antibiotics should be used in all cases of epididymitis, regardless of a negative urinalysis or the urethral Gram stain result. Nonsteroidal anti-inflammatory agents or narcotic analgesics also generally are prescribed to patients with epididymitis.
Empiric coverage varies with the patient's age and sexual history.
Prepubertal patients and older men require empiric coverage for coliform bacteria (enteric gram-negative bacilli or Pseudomonas). Both of these patient populations may be treated with trimethoprim sulfamethoxazole (TMP-SMZ).
Sexually active men need empiric coverage for C trachomatis and N gonorrhoeae, usually with ceftriaxone and doxycycline or azithromycin.
Fluoroquinolones are no longer recommended to treat gonorrhea in the United States. This recommendation was based on an analysis of data from the CDC's Gonococcal Isolate Surveillance Project (GISP). The data from GISP shows an 11-fold increase in the proportion of fluoroquinolone-resistant gonorrhea (QRNG) in heterosexual men, increasing from 0.6% in 2001 to 6.7% in 2006.9 This limits treatment of gonorrhea to drugs in the cephalosporin class. Fluoroquinolones may be an alternative treatment option for disseminated gonococcal infection if antimicrobial susceptibility can be documented.
Third-generation cephalosporin that has broad gram-negative spectrum, lower efficacy against gram-positive organisms, and higher efficacy against resistant organisms.
By binding to one or more of the penicillin-binding proteins, it arrests bacterial cell wall synthesis and inhibits bacterial growth.
250-1000 mg IM once
Infants and children: 50-75 mg/kg/d IV divided q12h; not to exceed 2 g/d
Probenecid may increase ceftriaxone levels; coadministration with ethacrynic acid, furosemide, and aminoglycosides may increase nephrotoxicity
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Adjust dose in renal impairment; caution in breastfeeding women and those allergic to penicillin
Inhibits protein synthesis and bacterial growth by binding with the 30S and, possibly, the 50S ribosomal subunits of susceptible bacteria.
100 mg PO bid for 10-14 d
<8 years: Not recommended
>8 years: 2-5 mg/kg/d in 1-2 divided doses; not to exceed 200 mg/d
Bioavailability decreases with antacids containing aluminum, calcium, magnesium, iron, or bismuth subsalicylate; tetracyclines can increase hypoprothrombinemic effects of anticoagulants; tetracyclines can decrease effects of oral contraceptives, causing breakthrough bleeding and increased risk of pregnancy
Documented hypersensitivity; severe hepatic dysfunction
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Photosensitivity may occur with prolonged exposure to sunlight or tanning equipment; reduce dose in renal impairment; consider drug serum level determinations in prolonged therapy; tetracycline use during tooth development (last one half of pregnancy through age 8 y) can cause permanent discoloration of teeth; Fanconilike syndrome may occur with outdated tetracyclines
Used to treat mild-to-moderate infections caused by susceptible strains of microorganisms. Indicated for chlamydial and gonorrheal infections of the genital tract.
1 g PO once
<6 months: Not established
>6 months: 10 mg/kg PO day 1; 5 mg/kg PO qd days 2-5
May increase toxicity of theophylline, warfarin, and digoxin; effects are reduced with coadministration of aluminum and/or magnesium antacids; nephrotoxicity and neurotoxicity may occur when coadministered with cyclosporine
Documented hypersensitivity; hepatic impairment
Sudden death may occur when azithromycin is taken concurrently with pimozide
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Site reactions can occur with IV route; bacterial or fungal overgrowth may result with prolonged antibiotic use; may increase hepatic enzymes and cholestatic jaundice; caution in patients with impaired hepatic function, prolonged QT intervals, or pneumonia; caution in hospitalized, geriatric, or debilitated patients
Inhibits bacterial synthesis of dihydrofolic acid by competing with para-aminobenzoic acid. This results in the inhibition of bacterial growth.
The antibacterial activity of TMP-SMZ includes common urinary tract pathogens, except Pseudomonas aeruginosa.
1 tab PO bid for 10-14 d
<2 months: Do not administer
>2 months: 8 mg/kg TMP and 40 mg/kg SMZ qd
May increase PT when used with warfarin (perform coagulation tests and adjust dose accordingly); coadministration with dapsone may increase blood levels of both drugs; coadministration of diuretics increases incidence of thrombocytopenia purpura in elderly persons; phenytoin levels may increase with coadministration; may potentiate effects of methotrexate in bone marrow depression; hypoglycemic response to sulfonylureas may increase with coadministration; may increase levels of zidovudine
Documented hypersensitivity; megaloblastic anemia due to folate deficiency
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Discontinue at first appearance of skin rash or sign of adverse reaction; obtain CBCs frequently; discontinue therapy if significant hematologic changes occur; goiter, diuresis, and hypoglycemia may occur with sulfonamides; prolonged IV infusions or high doses may cause bone marrow depression (if signs occur, give 5-15 mg/d leucovorin); caution in folate deficiency (eg, chronic alcoholics, elderly persons, those receiving anticonvulsant therapy, or those with malabsorption syndrome); hemolysis may occur in G-6-PD deficient individuals; AIDS patients may not tolerate or respond to TMP-SMZ; caution in renal or hepatic impairment (perform urinalyses and renal function tests during therapy); give fluids to prevent crystalluria and stone formation
An alternative to Septra DS; a bactericidal antibiotic that inhibits bacterial DNA synthesis, and, consequently, growth, by inhibiting DNA-gyrase in susceptible organisms.
Indicated for pseudomonal infections and those that are due to multi-drug-resistant gram-negative organisms. Duration of treatment depends upon severity of infection. Generally, continue therapy for at least 2 d after the signs and symptoms of infection have disappeared. Usual treatment duration is 7-14 d.
500 mg PO bid for 10-14 d
Not established
Antacids, iron salts, and zinc salts may reduce serum levels; administer antacids 2-4 h before or after taking fluoroquinolones; cimetidine may interfere with metabolism of fluoroquinolones; ciprofloxacin reduces therapeutic effects of phenytoin; probenecid may increase ciprofloxacin serum concentrations
May increase toxicity of theophylline, caffeine, cyclosporine, and digoxin (monitor digoxin levels); may increase effects of anticoagulants (monitor PT)
Documented hypersensitivity
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
In prolonged therapy, perform periodic evaluations of organ system functions (eg, renal, hepatic, hematopoietic); adjust dose in renal function impairment; superinfections may occur with prolonged or repeated antibiotic therapy
Complications of epididymitis may include the following:
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epididymitis, epididymo-orchitis, intrascrotal inflammation, Escherichia coli, Chlamydia trachomatis, Neisseria gonorrhoeae, chemical epididymitis, epididymal abscess, testicular abscess, sterility, peritubular fibrosis, sexually transmitted epididymitis, urethritis, scrotal pain, scrotal edema, urinary frequency, urinary urgency, dysuria, urinary retention, urethral discharge, scrotal abscess, Prehn sign, candidal epididymitis
Catherine Tubridy, MD, Staff Physician, Combined Residency Program for Emergency Medicine and Internal Medicine, State University of New York Downstate/Kings County Hospital Centers
Catherine Tubridy, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, and Medical Society of the State of New York
Disclosure: Nothing to disclose.
Richard Sinert, DO, Associate Professor of Emergency Medicine, Clinical Assistant Professor of Medicine, Research Director, State University of New York College of Medicine; Consulting Staff, Department of Emergency Medicine, Kings County Hospital Center
Richard Sinert, DO is a member of the following medical societies: American College of Physicians and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Robert M McNamara, MD, FAAEM, Chair and Professor, Department of Emergency Medicine, Temple University School of Medicine
Robert M McNamara, MD, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, American Medical Association, Pennsylvania Medical Society, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.
Richard Sinert, DO, Associate Professor of Emergency Medicine, Clinical Assistant Professor of Medicine, Research Director, State University of New York College of Medicine; Consulting Staff, Department of Emergency Medicine, Kings County Hospital Center
Richard Sinert, DO is a member of the following medical societies: American College of Physicians and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Barry E Brenner, MD, PhD, FACEP, Program Director, Professor, Department of Emergency Medicine, Professor, Internal Medicine, University Hospitals, Case Western Reserve School of Medicine
Barry E Brenner, MD, PhD, FACEP is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Chest Physicians, American College of Emergency Physicians, American College of Physicians, American Heart Association, American Thoracic Society, Arkansas Medical Society, New York Academy of Medicine, New York Academy of Sciences, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.