eMedicine Specialties > Emergency Medicine > Infectious Diseases

Prostatitis

Tarlan Hedayati, MD, Instructor of Clinical Emergency Medicine, Director of Observation Unit, Director of Chest Pain Unit, Department of Emergency Medicine, Los Angeles County/University of Southern California Medical Center
Molly Keegan, MD, Resident Physician, Department of Emergency Medicine, Los Angeles County and USC Medical Center

Updated: Jul 29, 2009

Introduction

Background

Prostatitis is an infection or inflammation of the prostate gland that presents as several syndromes with varying clinical features. The term prostatitis is defined as microscopic inflammation of the tissue of the prostate gland, which spans a broad range of clinical conditions.

The National Institutes of Health (NIH) has recognized and defined a classification system for prostatitis in 1999. The 4 syndromes of prostatitis are as follows: 

• I -Acute bacterial prostatitis
• II -Chronic bacterial prostatitis
• III - Chronic prostatitis and chronic pelvic pain syndrome (CPPS)
  • Inflammatory
  • Noninflammatory
• IV - Asymptomatic inflammatory prostatitis.

Acute and chronic bacterial prostatitis are defined by documented bacterial infections of the prostate. 

Chronic pelvic pain syndrome (CPPS) is characterized primarily by urological pain complaints in the absence of urinary tract infection. This syndrome includes several exclusion criteria, such as presence of active urethritis, urogenital cancer, urinary tract disease, functionally significant urethral stricture, or neurological disease affecting the bladder. It is subdivided into inflammatory and noninflammatory subtypes. Inflammatory CPPS is defined by the presence of white cells in the semen, expressed prostatic secretions, or voided bladder urine post-prostatic massage. Noninflammatory CPPS is defined by the absence of white cells.¹

Asymptomatic inflammatory prostatitis is characterized by the incidental discovery of prostatic inflammation without any genitourinary complaints. These patients do not present to the emergency department but rather are diagnosed while undergoing workup for infertility or elevated prostate-specific antigen (PSA) level.

Pathophysiology

In bacterial prostatitis, sexual transmission of bacteria is common, but hematogenous, lymphatic, and contiguous spread of infection from surrounding anatomy must also be considered. Although various routes have been postulated, none have been firmly substantiated.

A history of sexually transmitted diseases is associated with an increased risk for prostatitis symptoms. Prostatitis symptoms may increase a man's risk for benign prostatic hyperplasia (BPH), lower urinary tract symptoms, and prostate cancer.²

The presence of acute inflammatory cells in the glandular epithelium and lumens of the prostate, with chronic inflammatory cells in the periglandular tissue, characterizes prostatitis. However, the presence and quantity of inflammatory cells in the urine or prostatic secretions does not correlate with the severity of physical symptoms.

A nonspecific mixed inflammatory infiltrate that consists of lymphocytes, plasma cells, and histiocytes is typical in chronic bacterial prostatitis.

Viral and granulomatous prostatitis may be associated with HIV infection and is another cause of culture-negative disease. A common viral pathogen of prostatitis in HIV-infected patients is cytomegalovirus (CMV). Mycobacteria, such as Mycobacterium tuberculosis, and fungi, such as Candida albicans, have also been associated with culture-negative disease in this population.

Frequency

United States

Prostatitis is one of the most common diseases seen in urology practices in the United States, accounting for nearly 2 million outpatient visits per year, with chronic bacterial prostatitis and chronic pelvic pain syndrome being most frequently diagnosed. The diagnosis of prostatitis is made in approximately 25% of male patients presenting with genitourinary symptoms. Autopsy studies have revealed a histologic prevalence of prostatitis of 64-86%.

Approximately 8.2% of men have prostatitis at some point in their lives.¹  Of the 4 categories of prostatitis, the most common is chronic prostatitis/chronic pelvic pain syndrome, accounting for 90-95% of cases of prostatitis. Acute bacterial prostatitis and chronic bacterial prostatitis each make up another 2-5% of cases.

International

The incidence of mycobacterial prostatitis, concomitant with disseminated disease, is increased in underdeveloped countries. Areas with widespread sexually transmitted disease (STD) rates and prostitution have a higher incidence of acute bacterial prostatitis.

Mortality/Morbidity

• Particularly susceptible patients include those with diabetes mellitus, patients on dialysis for chronic renal failure, patients who are immunocompromised, and postsurgical patients who have had urethral instrumentation. In these patients, prostatitis can lead to urosepsis with significant associated mortality. Do not overlook the prostate gland when searching for a source of sepsis in these patients.
• In the United States, the long-term prognosis of the first occurrence of acute bacterial prostatitis is good with antibiotic therapy in compliant patients.

Sex

• Prostatitis is a disease of men only.

Age

• In patients younger than 35 years, the most common variant of the syndrome is acute bacterial prostatitis.
• HIV-related disease is also predominantly seen in younger patients.
• Rare causes should be noted. According to case reports of Wegener granulomatosis in the fourth and fifth decades of life, prostatitis can be a presenting feature of Wegener granulomatosis and a clinical manifestation of relapse. Fungal infection with C albicans and Coccidioides immitis and mycobacterial infection with M tuberculosis have also been reported.

Clinical

History

• Acute bacterial prostatitis
  • Fever
  • Chills
  • Malaise
  • Arthralgias
  • Myalgias
  • Perineal prostatic pain
  • Dysuria
  • Obstructive urinary tract symptoms, including frequency, urgency, dysuria, nocturia, hesitancy, weak stream, and incomplete voiding
  • Low back pain
  • Low abdominal pain
  • Spontaneous urethral discharge
• Chronic bacterial prostatitis
  • Intermittent dysuria
  • Intermittent obstructive urinary tract symptoms
  • Recurrent urinary tract infections¹
  • Systemic symptoms typically absent 
• Chronic prostatitis and chronic pelvic pain syndrome
  • Pelvic pain or discomfort including perineal, suprapubic, coccygeal, rectal, urethral, and testicular/scrotal pain for more than 3 of the previous 6 months without documented urinary tract infections from uropathogens.¹
  • Obstructive urinary tract symptoms, including frequency, dysuria, and incomplete voiding
  • Ejaculatory pain
  • Erectile dysfunction
• Asymptomatic inflammatory prostatitis - This diagnosis is defined by its lack of symptoms.

Physical

• Acute bacterial prostatitis
  • Tender, nodular, hot, boggy, or normal-feeling gland on digital rectal examination
  • Suprapubic abdominal tenderness
  • Enlarged tender bladder due to urinary retention
• Chronic bacterial prostatitis
  • Normal examination findings between acute episodes
  • Tender, nodular, or normal gland on digital rectal examination
  • Suprapubic tenderness during acute episodes
• Chronic prostatitis and chronic pelvic pain syndrome
  • Mildly tender or normal prostate on digital rectal examination
  • Tight anal sphincter on digital rectal examination
• Asymptomatic inflammatory prostatitis - Normal or calcified prostate on digital rectal examination

Causes

• Consider Neisseria gonorrhoeae and Chlamydia trachomatis infection in any male younger than 35 years presenting with urinary tract symptoms.
• Acute bacterial prostatitis may be caused by the following:
  • Ascending infection through the urethra
  • Refluxing urine into prostate ducts
  • Direct extension or lymphatic spread from the rectum
  • Approximately 80% are gram-negative organisms (eg, Escherichia coli, Enterobacter, Serratia, Pseudomonas, Enterococcus, and Proteus species). Mixed bacterial infections are uncommon. One case report of prostatitis caused by methicillin-resistant Staphylococcus aureus was documented in a diabetic patient.
• Chronic bacterial prostatitis may be due to the following:
  • A primary voiding dysfunction, either structurally or functionally
  • E coli is responsible for 75-80% of chronic bacterial prostatitis cases. Enterococci and gram-negative aerobes such as Pseudomonas are usually isolated the remainder of the time.
  • C trachomatis, Ureaplasma species, Trichomonas vaginalis
  • Uncommon organisms, such as M tuberculosis and Coccidioides, Histoplasma, and Candida species , must also be considered. Tuberculous prostatitis may be found in patients with renal tuberculosis.
  • Human immunodeficiency virus
  • Cytomegalovirus
  • Inflammatory conditions such as sarcoidosis
• Chronic prostatitis and chronic pelvic pain syndrome
  • About 5-8% of men with this syndrome eventually have a bacterial pathogen isolated from their urine or prostatic fluid.

Bacterial prostatitis. Expressed prostatic fluid contains more than 10 white blood cells per high-power field, indicating prostatitis.

• Etiology is poorly understood but may result from an infectious or inflammatory initiator that results in neurologic injury and eventually results in pelvic floor dysfunction in the form of increased pelvic tone.¹
• Functional or structural bladder pathology, such as primary vesical neck obstruction, pseudodyssynergia (failure of the external sphincter to relax during voiding), impaired detrusor contractility, or acontractile detrusor muscle
• Ejaculatory duct obstruction
• Increased pelvic side wall tension
• Nonspecific prostatic inflammation
• Asymptomatic inflammatory prostatitis - Causes are similar to chronic inflammatory prostatitis without symptoms.

Differential Diagnoses

Workup

Laboratory Studies

• Complete blood count: A complete blood count (CBC) with differential and blood cultures are indicated in cases of acutely toxic patients or suspected septicemia.
• Urinalysis: Obtain quantitative values for the white blood count and bacterial count, presence of oval fat bodies, and lipid-laden macrophages.
• Urine culture: A urine culture can be used to identify the causative organism, if any.

Urine culture with greater than 100,000 colony-forming units (CFU) of Escherichia coli, the most common pathogen in acute and chronic prostatitis. Chronic bacterial prostatitis must be confirmed and diagnosed using a urine culture.

• Chemistry: Obtain electrolyte panel, including BUN and creatinine values, in patients presenting with urinary retention or obstruction.
• Prostate-specific antigen determination: Prostate inflammation can lead to elevation of serum prostate-specific antigen (PSA). PSA is used primarily as a cancer screening tool and should not be routinely used in the diagnosis of prostatitis.³

Imaging Studies

• Trans-abdominal ultrasonography or bladder scan to assess for volume of retained urine.¹
• Transrectal ultrasonography
  • Characteristic features are capsular thickening and prostatic calculi.
  • Hypoechoic halo in the periurethral region, heterogeneous echo pattern, and enlargement and thickening of the septa of the seminal vesicles may be seen.
  • Interpretation is highly subjective and therefore not very reliable; diagnosis requires clinical correlation and digital rectal examination.
• In acute prostatitis, a marked increase in color in the prostatic urethral site, around the ejaculatory ducts, and close to the seminal vesicles is visualized on color Doppler ultrasonography.
• Computed tomography (CT) studies of the pelvis may be useful in evaluation of prostatic abscess or suspected neoplasm.
• Cystoscopy is useful in follow-up of refractory cases to rule out neoplasm of the bladder or interstitial cystitis.
• Intravenous urography or voiding cystourethrography is appropriate for evaluation of the outlet system in patients with full renal function.

Other Tests

• Fractional urine examination
  • The use of fractional urine specimens may be useful in the diagnosis of prostatitis. Although not practical in most emergency departments, this technique is used by urologists if the diagnosis of prostatitis remains unclear.
  • The initial 10 mL of voided urine represents urine from the urethra and is termed voided urine 1 (V1). Elevated bacterial counts in V1 suggest urethritis. The next 200 mL of voided urine is discarded, and a midstream urine sample (V2) is collected, which represents bladder urine. Bacterial counts elevated in the midstream sample suggest cystitis without prostatitis. Next, the physician performs a prostatic massage and the expressed prostatic secretions (EPS) are collected from the urethral meatus. Finally, the 10 mL of voided urine following prostatic massage (V3) are collected. The bacterial findings of the EPS and V3 samples represent the microbiologic characteristics of the prostate gland.
  • Chronic bacterial prostatitis can be diagnosed if the culture of the EPS and V3 samples produce the same bacteria as the first-voided specimen and the colony count of the 2 cultures is at least 10 times as great as the first-void specimen.

Procedures

• Suprapubic catheterization: This may be warranted in severe obstruction and should be placed in consultation with a urologist.
• Needle biopsy or aspiration: In cases of prostatic abscess, the fluctuant site may be drained under local anesthesia through the perineal route, followed by insertion of a pigtail catheter.
• Urodynamic testing may be indicated.
• Cystoscopy may be performed to rule out bladder cancer and interstitial cystitis.

Treatment

Prehospital Care

No specific prehospital treatments of prostatitis exist; treatment should be tailored to symptoms and be supportive.

Emergency Department Care

• Individuals with acute bacterial prostatitis who appear acutely ill, have evidence of sepsis, or both require admission for parenteral antibiotics and supportive care.
  • Antibiotic therapy should initially include parental bactericidal agents such as broad-spectrum penicillin derivatives, third-generation cephalosporins with or without aminoglycosides, or fluoroquinolones.
  • Patients without a toxic appearance can be treated as outpatients with a 14- to 28-day course of oral antibiotics. Urologic follow-up is necessary to ensure eradication and to provide continuity of care to prevent relapse.
  • Urinary retention may complicate acute infection and warrant hospitalization. Suprapubic catheters are considered safer than urethral catheterization in severe obstruction and may be placed in consultation with a urologist.
  • Provide supportive measures such as antipyretics, analgesics, hydration, and stool softeners as needed.
  • Avoid serial examinations of the prostate to avoid seeding of the blood and subsequent bacteremia in acute bacterial prostatitis.
• Chronic bacterial prostatitis, chronic pelvic pain syndrome, and asymptomatic inflammatory prostatitis are probably best treated by or in consultation with a urologist.
  • A 4-week trial of antibiotic therapy is indicated in chronic bacterial prostatitis and chronic pelvic pain syndrome with inflammation, but no consensus exists regarding its use in chronic pelvic pain syndrome without inflammation and asymptomatic prostatitis.
  • Supportive measures such as analgesics (particularly nonsteroidal anti-inflammatory drugs [NSAIDs]), alpha-blocking agents, hydration, stool softeners, and sitz baths are often used.
  • Some evidence suggests pelvic floor training/biofeedback can be effective in controlling the symptoms of CP/CPPS.¹  
  • In cases where infected prostatic calculi serve as a nidus, transurethral resection or total prostatectomy may result in a cure.

For further information, the European Association of Urology has treatment guidelines available on chronic pelvic pain and prostatitis.^4,5

Consultations

• Consult a urologist.  
• Notify the health department, if reportable STD is cultured.
• Consult a psychiatrist, if psychosomatic disorder is suspected.

Medication

The different NIH prostatitic categories are treated with various medical therapies, depending on the underlying pathology.

Antibiotic therapy is essential in the treatment of acute bacterial prostatitis. If the patient is having systemic symptoms, then admission is warranted for intravenous antibiotics, hydration, and analgesia. If the patient has signs of urinary retention or obstruction, then placement of a Foley catheter is indicated.

Therapy for chronic bacterial prostatitis varies in regards to type and duration of antibiotics used as well as adjunctive medications. Treatment typically consists of 4-8 weeks of prostate-penetrating antibiotics, such a fluoroquinolone or trimethoprim-sulfamethoxazole.

Chronic prostatitis, chronic pelvic pain syndrome, and asymptomatic inflammatory prostatitis may be treated with alpha-blocking agents or diazepam with sitz baths. Some studies have shown that a longer course of antibiotics has been shown to result in a decrease in PSA values in patients with category IV prostatitis.

Antibiotics

Empiric antibiotics should be tailored toward treating gram-negative pathogens. STDs, where N gonorrhoeae and C trachomatis are the primary suspected pathogens, must also be considered, especially in patients younger than 35 years. 

In April 2007, the Centers for Disease Control and Prevention (CDC) updated treatment guidelines for gonococcal infection and associated conditions. Fluoroquinolone antibiotics are no longer recommended to treat gonorrhea in the United States. The recommendation was based on analysis of new data from the CDC's Gonococcal Isolate Surveillance Project (GISP). The data from GISP showed the proportion of gonorrhea cases in heterosexual men that were fluoroquinolone-resistant (QRNG) reached 6.7%, an 11-fold increase from 0.6% in 2001. The data were published in the April 13, 2007, issue of the Morbidity and Mortality Weekly Report.⁶ This limits treatment of gonorrhea to drugs in the cephalosporin class (eg, ceftriaxone 125 mg IM once as a single dose). Fluoroquinolones may be an alternative treatment option for disseminated gonococcal infection if antimicrobial susceptibility can be documented. For more information see, the CDC's Antibiotic-Resistant Gonorrhea Web site; CDC Updated Gonococcal treatment recommendations (April 2007); or Medscape Medical News on CDC Issues - New Treatment Recommendations for Gonorrhea.
 
For the treatment of chronic bacterial prostatitis, where Enterobacteriaceae, enterococci, and P aeruginosa are common pathogens, consider trimethoprim/sulfamethoxazole (Bactrim) or fluoroquinolones for 28 days or more as empiric agents.

For nonbacterial prostatitis caused by Chlamydia and Ureaplasma species, which are difficult to culture, an empiric trial of doxycycline or erythromycin should be instituted.

Levofloxacin (Levaquin)

Indicated to treat acute and chronic bacterial prostatitis due to E coli, E faecalis, or S epidermidis. Has good concentration in the prostate. This is the L stereoisomer of the D/L parent compound ofloxacin, the D form being inactive. Good monotherapy with extended coverage against Pseudomonas species, as well as excellent activity against pneumococcus. Agent acts by inhibition of DNA gyrase activity.

Dosing

Adult

500 mg PO qd for 14-28 d

Pediatric

<18 years: Not recommended
>18 years: Administer as in adults

Interactions

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; levofloxacin reduces therapeutic effects of phenytoin; probenecid may increase levofloxacin serum concentrations

Contraindications

Documented hypersensitivity; prolonged QT interval

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

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

Ofloxacin (Floxin)

Quinolone that is a pyridine carboxylic acid derivative with broad-spectrum bactericidal effect.

Dosing

Adult

400 mg PO once, then 300 mg PO bid for 14-28 d

Pediatric

<18 years: Not recommended
>18 years: Administer as in adults

Interactions

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; probenecid may increase serum concentrations; may increase toxicity of theophylline, caffeine, cyclosporine, and digoxin (monitor digoxin levels); may increase effects of anticoagulants (monitor PT)

Contraindications

Documented hypersensitivity; prolonged QT interval

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

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

Ciprofloxacin (Cipro, Cipro XR)

Fluoroquinolone that inhibits bacterial DNA synthesis and, consequently, growth, by inhibiting DNA gyrase and topoisomerases, which are required for replication, transcription, and translation of genetic material. Quinolones have broad activity against gram-positive and gram-negative aerobic organisms. Has no activity against anaerobes. Continue treatment for at least 2 d (7-14 d typical) after signs and symptoms have disappeared.

Dosing

Adult

500 mg PO bid for 14-28 d

Pediatric

<18 years: Not recommended
>18 years: Administer as in adults

Interactions

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; probenecid may increase serum concentrations; may increase toxicity of theophylline, caffeine, cyclosporine, and digoxin (monitor digoxin levels); may increase effects of anticoagulants (monitor PT); ciprofloxacin reduces therapeutic effects of phenytoin

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

A white crystalline precipitate located in superficial portion of corneal defect may occur (onset starts in 1-7 d); precipitate is usually cleared within 2 wk and does not adversely affect clinical course or outcome; do not use in ocular infections that may become systemic; superinfections may occur with prolonged or repeated antibiotic therapy

Trimethoprim/sulfamethoxazole DS (Bactrim)

Trimethoprim inhibits bacterial growth by inhibiting synthesis of dihydrofolic acid. Antibacterial activity of TMP-SMZ includes common urinary tract pathogens, except Pseudomonas aeruginosa.

Dosing

Adult

1 DS tab (160 mg TMP) PO bid for 10-28 d

Pediatric

<2 years: Not recommended
>2 years: 8-10 mg/kg/d trimethoprim divided bid

Interactions

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

Contraindications

Documented hypersensitivity; megaloblastic anemia due to folate deficiency

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

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, those with chronic alcoholism, elderly persons, those receiving anticonvulsant therapy, or those with malabsorption syndrome); hemolysis may occur in patients with G-6-PD deficiency; patients with AIDS 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

Ceftriaxone (Rocephin)

Third-generation cephalosporin with broad-spectrum, gram-negative activity; lower efficacy against gram-positive organisms; higher efficacy against resistant organisms. Bactericidal activity results from inhibiting cell wall synthesis by binding to one or more penicillin-binding proteins. Exerts antimicrobial effect by interfering with synthesis of peptidoglycan, a major structural component of bacterial cell wall. Bacteria eventually lyse due to the ongoing activity of cell wall autolytic enzymes while cell wall assembly is arrested.
Highly stable in presence of beta-lactamases, both penicillinase and cephalosporinase, of gram-negative and gram-positive bacteria. Approximately 33-67% of dose excreted unchanged in urine, and remainder secreted in bile and ultimately in feces as microbiologically inactive compounds. Reversibly binds to human plasma proteins, and binding has been reported to decrease from 95% bound at plasma concentrations <25 mcg/mL to 85% bound at 300 mcg/mL.

Dosing

Adult

250 mg IM once (in conjunction with doxycycline 100 mg PO for 10 d)

Pediatric

Neonates >7 d: 25-50 mg/kg/d IV/IM; not to exceed 125 mg/d
Infants and children: 50-75 mg/kg/d IV/IM divided q12h; not to exceed 2 g/d

Interactions

Probenecid may increase ceftriaxone levels; coadministration with ethacrynic acid, furosemide, and aminoglycosides may increase nephrotoxicity

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Adjust dose in severe renal insufficiency (high doses may cause CNS toxicity); superinfections and promotion of nonsusceptible organisms may occur with prolonged use or repeated therapy; caution in breastfeeding women

Doxycycline (Bio-Tab, Doryx, Vibramycin)

Inhibits protein synthesis and, thus, bacterial growth by binding to 30S and possibly 50S ribosomal subunits of susceptible bacteria. May block dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest.
Used to treat nonbacterial prostatitis caused by Chlamydia species. Chlamydia and Ureaplasma are difficult to culture; therefore, an empiric trial of doxycycline should be instituted.

Dosing

Adult

100 mg PO bid for 10 d (used in conjunction with ceftriaxone 250 mg IM once)

Pediatric

<8 years: Not recommended
>8 years: 100 mg PO bid for 10 d

Interactions

Bioavailability decreases with antacids containing aluminum, calcium, magnesium, iron, or bismuth subsalicylate; tetracyclines can increase hypoprothrombinemic effects of anticoagulants

Contraindications

Documented hypersensitivity; severe hepatic dysfunction

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

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

Alpha-adrenergic antagonists

These agents are used in the treatment of benign prostatic hypertrophy.

Studies suggest that combining alpha-blockers with antibiotics may reduce the risk of prostatitis recurrence in chronic prostatitis. Alpha-blockers improve bladder outlet obstruction and thus improves voiding dysfunction that may be associated with the pathogenesis of prostatitis.

Alpha-blockers may also have role in chronic pelvic pain syndrome to improve symptoms.

Terazosin (Hytrin)

Quinazoline compound that counteracts alpha1-induced adrenergic contractions of bladder neck, facilitating urinary flow in presence of prostate inflammation.

Dosing

Adult

1 mg PO qhs; increase slowly to effect; not to exceed 10 mg/d

Pediatric

Not established

Interactions

Effects decrease with coadministration of NSAIDs; effects increase with coadministration of diuretics and antihypertensive medications

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in renal impairment; may cause marked hypotension following first dose and coadministration with beta-blockers

Tamsulosin (Flomax)

An alpha-adrenergic blocker, specifically targeting the A1 receptors. Has the advantage of causing relatively less orthostatic hypotension, and it requires no gradual up-titration from the initial introductory dosage. On the other hand, a higher incidence of ejaculatory dysfunction exists with this medication (8.4-18.1%).

Dosing

Adult

0.4-0.8 mg PO qd

Pediatric

Not established

Interactions

Cimetidine may significantly increase plasma concentrations; tamsulosin may increase toxicity of warfarin

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Not for use as antihypertensive drug; may cause orthostasis; avoid situations that may result in injuries if syncope occurs; rule out presence of carcinoma or cancer before initiating treatment

Follow-up

Further Inpatient Care

• Carefully treat associated septicemia in acutely ill patients.
• Carefully monitor for bladder outlet obstruction and renal failure.

Further Outpatient Care

• After primary management and stabilization, care of the patient is appropriately transferred to a urologist, as aggressive treatment of acute prostatitis can lessen the chance of developing chronic prostatitis.
• After initial improvement with parental antibiotics, acute bacterial prostatitis may be managed with outpatient care with a 2- to 4-week course of oral antibiotics and urologic follow-up.
• Management strategies for category II prostatitis, chronic bacterial prostatitis, include intraprostatic antibiotic injection, transurethral resection of the prostate (TURP), and long-term antimicrobial suppression.
• Additional therapeutic modalities studied for category III prostatitis include anti-inflammatories, phytotherapy, biofeedback, thermal therapy, and pelvic floor exercises.
• Although no clear connection between elevated PSA level in prostatitis and cancer have been established, patients found to have elevated PSA levels should be followed up by their primary care-physicians, urologists, or both.

Deterrence/Prevention

• Protection against STDs also provides protection against many of the organisms associated with acute bacterial prostatitis, development of chronic prostatitis, and suspected causes of nonbacterial prostatitis.
• Psychological stress has been associated with men who report symptoms of chronic prostatitis. Recognition of underlying psychosomatic disease in chronic cases and appropriate psychiatric referral and treatment lessens the recurrence rate.

Complications

• Chronic prostatitis - Approximately one third of patients with chronic bacterial prostatitis experience recurrence following initial treatment.
• Bladder outlet obstruction/urinary retention
• Abscess - Typically in immunocompromised patients
• Infertility due to scarring of the urethra
• Recurrent cystitis
• Pyelonephritis
• Renal damage
• Sepsis

Prognosis

• The prognosis of the first occurrence of acute bacterial prostatitis is good with aggressive antibiotic therapy and good patient compliance.
• In cases of recurrent chronic prostatitis that may present with acute exacerbations, causative underlying factors must be determined to affect outcome.

Patient Education

• For excellent patient education resources, visit eMedicine's Prostate Health Center. Also, see eMedicine's patient education article Prostate Infections.

Miscellaneous

Medicolegal Pitfalls

• Failure to consider diagnosis in sexually active adolescents
• Performing prostatic massage in patients with acute bacterial prostatitis
• Failure to recognize acute urinary retention

Special Concerns

• Acute bacterial prostatitis is a recognized complication after sclerotherapy for rectal prolapse.
• Nursing home patients with indwelling urethral catheters may be at increased risk.
• Patients with an elevated PSA value must be referred to their primary care physician or a urologist for PSA recheck and follow-up.
• Chronic prostatitis and asymptomatic inflammatory prostatitis have not been scientifically linked to prostate cancer.

Multimedia

Media file 1: Bacterial prostatitis. Expressed prostatic fluid contains more than 10 white blood cells per high-power field, indicating prostatitis.

Media file 2: A nonspecific mixed inflammatory infiltrate that consists of lymphocytes, plasma cells, and histiocytes is typical in chronic bacterial prostatitis.

Media file 3: Urine culture with greater than 100,000 colony-forming units (CFU) of Escherichia coli, the most common pathogen in acute and chronic prostatitis. Chronic bacterial prostatitis must be confirmed and diagnosed using a urine culture.

References

1. Murphy AB, Macejko A, Taylor A, Nadler RB. Chronic prostatitis: management strategies. Drugs. 2009;69(1):71-84. [Medline].

2. Krieger JN, Lee SW, Jeon J, Cheah PY, Liong ML, Riley, et al. Epidemiology of Prostatitis. Int J Antimicrob Agents. Feb 2008;Suppl 1:85-90. [Medline].

3. Loeb S, Gashti SN, Catalona WJ. Exclusion of inflammation in the differential diagnosis of an elevated prostate-specific antigen (PSA). Urol Oncol. Jan-Feb 2009;27(1):64-6. [Medline].

4. [Guideline] Grabe M, Bishop MC, Bjerklund-Johansen TE, et al. Prostatitis and chronic pelvic pain syndrome. Guidelines on the management of urinary and male genital tract infections. Arnhem, The Netherlands: European Association of Urology (EAU). Mar 2008;79-88. [Full Text].

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Keywords

prostatitis, acute bacterial prostatitis, chronic bacterial prostatitis, nonbacterial prostatitis, prostatodynia, prostate gland, bacterial prostatitis, chronic pelvic pain syndrome, CPPS, asymptomatic inflammatory prostatitis, prostatic inflammation

Contributor Information and Disclosures

Author

Tarlan Hedayati, MD, Instructor of Clinical Emergency Medicine, Director of Observation Unit, Director of Chest Pain Unit, Department of Emergency Medicine, Los Angeles County/University of Southern California Medical Center
Tarlan Hedayati, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

Molly Keegan, MD, Resident Physician, Department of Emergency Medicine, Los Angeles County and USC Medical Center
Disclosure: Nothing to disclose.

Medical Editor

David S Howes, MD, Residency Program Director, Professor of Medicine, Section of Emergency Medicine, University of Chicago/Pritzker School of Medicine
David S Howes, MD is a member of the following medical societies: American College of Emergency Physicians, American College of Physicians-American Society of Internal Medicine, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Eddy Lang, MDCM, CCFP (EM), CSPQ, Assistant Professor, Department of Family Medicine, McGill University; Consulting Staff, Department of Emergency Medicine, The Sir Mortimer B Davis-Jewish General Hospital
Eddy Lang, MDCM, CCFP (EM), CSPQ is a member of the following medical societies: American College of Emergency Physicians
Disclosure: Nothing to disclose.

CME Editor

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.

Chief Editor

Robert E O'Connor, MD, MPH, Professor and Chair, Department of Emergency Medicine, University of Virginia Health System
Robert E O'Connor, MD, MPH is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Physician Executives, American Heart Association, American Medical Association, Medical Society of Delaware, National Association of EMS Physicians, Society for Academic Emergency Medicine, and Wilderness Medical Society
Disclosure: Nothing to disclose.

The authors and editors of eMedicine gratefully acknowledge the contributions of previous author, David S Kwon, MD, to the development and writing of this article.

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