TOC  | ID    Prostatitis 

RX:

• Cipro 500 mg bid x at least 2 weeks
• Septra DS/ Bactrim DS bid x at least 2 weeks
• Vibramycin 100 mg bid x at least 2 weeks

Prostatitis

Acute bacterial prostatitis is a generalized infection of the prostate gland and is associated with both lower urinary tract infection (UTI) and generalized sepsis.
Chronic bacterial prostatitis is associated with recurrent lower UTIs (i.e., cystitis) secondary to areas of focal uropathogenic bacteria residing in the prostate gland.
The most common cause of bacterial prostatitis is the Enterobacteriaceae family of gram-negative bacteria, which originate in the gastrointestinal flora.
The most common organisms are strains of Escherichia coli, which are identified in 65% to 80% of infections. Pseudomonas aeruginosa, Serratia species, Klebsiella species, and Enterobacter aerogenes are identified in a further 10% to 15%.

Gram-Positive Bacteria: Enterococci are believed to account for 5% to 10% of documented prostate infections.
The role of other gram-positive organisms, which are also commensal organisms in the anterior urethra, is controversial.
An etiologic role for gram-positive organisms such as Staphylococcus saprophyticus, hemolytic streptococci, Staphylococcus aureus, and other coagulase-negative staphylococci has been suggested by a number of authors. 

A common complication of UTI in men is prostatitis. Bacterial prostatitis is usually caused by the same gram-negative bacilli that cause UTI in females; 80% or more of such infections are caused by E. coli. The pathogenesis of this condition is poorly understood.  Antibacterial substances in prostatic secretions probably protect against such infections.

Etiologies of Prostatitis:

• Microbiologic Causes:
  Mainly Gram negative bacteria as E. Coli.  
• Altered Prostatic Host Defense:
  Risk factors that allow bacterial colonization or infection of the prostate with potentially pathogenic bacteria include intraprostatic ductal reflux; phimosis; specific blood groups; unprotected penetrative anal rectal intercourse; UTIs; acute epididymitis; indwelling urethral catheters and condom catheter drainage; and transurethral surgery, especially in men who have untreated, infected urine.
• Dysfunctional Voiding:
  Anatomic or neurophysiologic obstruction resulting in high-pressure dysfunctional flow patterns has been implicated in the pathogenesis of the prostatitis syndrome.
• Intraprostatic Ductal Reflux:
  Reflux of urine and possibly bacteria into the prostatic ducts has been postulated as one of the most important etiologic mechanisms involved in the pathogenesis of chronic bacterial and nonbacterial prostatic inflammation.
• Immunologic Alterations
• Chemically Induced Inflammation:
  may be simply due to a chemically induced inflammation secondary to the noxious substances in the urine that have refluxed into the prostatic duct.
• Neural Dysregulation/Pelvic Floor Musculature Abnormalities
• Interstitial Cystitis–like Cause:
  Interstitial cystitis is an ill-defined CPPS occurring primarily in females, and a number of investigators have hypothesized that chronic nonbacterial prostatitis may have a similar cause.
• Psychological Cause:
  Psychological factors have always been considered to play an important role in the development or exacerbation of both of the CP syndromes.
  Depression and psychological disturbances are common among Chronic Prostatitis patients.

A NIH expert consensus panel has recommended classifying prostatitis into three syndromes:

1. Category I: Acute Bacterial Prostatitis  
   Acute bacterial prostatitis, category I, is a rare but important lower urinary tract infectious disease.
   It is characterized by an acute onset of pain combined with irritative and obstructive voiding symptoms in a patient with manifestations of a systemic febrile illness. The patient typically complains of urinary frequency, urgency, and dysuria.  Obstructive voiding complaints including hesitancy, poor interrupted stream, strangury, and even acute urinary retention are common. The patient complains of perineal and suprapubic pain and may have associated pain or discomfort of the external genitalia. In addition, there are usually significant systemic symptoms including fever, chills, malaise, myalgia, nausea and vomiting, and even frank septicemia with hypotension. The combination and severity of symptoms in category I, acute bacterial prostatitis, are variable from patient to patient.  Approximately 5% of patients with acute bacterial prostatitis may progress to chronic bacterial prostatitis.  
   On physical examination, the prostate is found to be enlarged, tender, and indurated.
   Lab showed Pyuria & bacteriutia are present, and urine cultures generally grow E. coli or another typical uropathogen.
   - Acute bacterial prostatitis was diagnosed when prostatic fluid was clinically purulent, systemic signs of infectious disease were present, and bacteria were cultured from prostatic fluid.

2. Category II: Chronic bacterial prostatitis
   Chronic bacterial prostatitis is a clinically more occult disease and may be manifested only as recurrent bacteriuria (UTI) or variable low-grade fever with back or pelvic discomfort. Urinary symptoms usually relate to the reintroduction of infection into the bladder, with both pyuria and bacteriuria being present; a chronic prostatic focus is the most common cause of recurrent UTI in men.
   - Chronic bacterial prostatitis was diagnosed when pathogenic bacteria were recovered in significant numbers from a purulent prostatic fluid in the absence of a concomitant UTI or significant systemic signs.
   
   The most important clue in the diagnosis of category II, chronic bacterial prostatitis, is a history of documented recurrent UTIs.
   Patients may be relatively asymptomatic between acute episodes, or they may present with a long history of a CPPS (chronic pelvic pain syndrome).
   The prevalence of bacterial prostatitis ranges from 5% to 15% of prostatitis cases. In one of the largest and most comprehensive clinical series, Weidner and associates (1991b) found significant bacteriuria (with uropathogenic organisms) in 4.4% of patients with symptoms of CP (chronic prostatitis).

3. Category III: Chronic pelvic pain syndrome (CPPS) /  Chronic "Abacterial" prostatitis
   CPPS describes the large group of men who present with minimal signs on physical examination but have a variety of irritative or obstructive voiding symptoms; perineal, pelvic, or back pain; and sexual dysfunction. These men can be divided into those with and those without inflammation (defined as > 10 white blood cells per high-power field in expressed prostatic secretions). The etiology and appropriate management in these patients, regardless of inflammatory status, is unknown. 
   The predominant symptom in all these studies was pain or discomfort, which was most commonly localized to the perineum, suprapubic area, and penis but can also occur in the testes, groin, or low back. Pain during or after ejaculation is one of the most prominent, important, and bothersome feature in many patients ( Shoskes et al, 2004 ). Irritative and obstructive voiding symptoms including urgency, frequency, hesitancy, and poor interrupted flow are associated with this syndrome in many patients. Erectile dysfunction and sexual disturbances have been reported in patients with CPPS ( Mehik et al, 2001 ; Liang et al, 2004 ; Zaslau et al, 2005) but are not pathognomonic features of this syndrome. By definition, the syndrome becomes chronic after 3 months' duration. The symptoms tend to wax and wane over time; approximately one third of patients improve over 1 year (usually patients with shorter duration and fewer symptoms)
    
   Patients with the inflammatory subtype of chronic prostatitis/chronic pelvic pain syndrome have leukocytes in their expressed prostatic secretions, postprostate massage urine, or semen. In contrast, patients with the noninflammatory subtype have no evidence of inflammation.
   * A primary component of this syndrome and 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).
   - Prostatodynia was diagnosed in the remaining patients who had persistent pain and voiding complaints as in the previous two categories but who had no significant bacteria or purulence in the prostatic fluid.
   Rx:  Consider antibiotics, alpha-blockers, NSAID, Biofeedback & progressive muscle relaxation & strengthening exercise.
   
   
4. Category IV: Asymptomatic Inflammatory Prostatitis
   The patients present with BPH, an elevated prostate-specific antigen (PSA) level, prostate cancer, or infertility.
   Subsequent microscopy of EPS or semen, and histologic examination of BPH chips, prostate cancer specimens, or prostate biopsies disclose evidence of prostatic inflammation.
   Asymptomatic inflammatory prostatitis is diagnosed in patients who have no history of genitourinary tract pain complaints. Such patients are usually diagnosed during evaluation for other genitourinary tract issues. For example, many men undergo prostate biopsy for evaluation for possible prostate cancer because of an elevated serum PSA prostate-specific antigen level. Prostatitis is the most common noncancer diagnosis (based on histological criteria) in these men. Other asymptomatic patients undergo evaluation for infertility. Excess concentrations of leukocytes in the seminal fluid are a common finding in such patients.
   - Nonbacterial prostatitis was diagnosed when significant numbers of bacteria could not be cultured from prostatic fluid, but the fluid consistently revealed microscopic purulence.

Traditional Classification of Prostatitis Syndromes:

Acute bacterial prostatitis was diagnosed when prostatic fluid was clinically purulent, systemic signs of infectious disease were present, and bacteria were cultured from prostatic fluid.

Chronic bacterial prostatitis was diagnosed when pathogenic bacteria were recovered in significant numbers from a purulent prostatic fluid in the absence of a concomitant UTI or significant systemic signs.

Nonbacterial prostatitis was diagnosed when significant numbers of bacteria could not be cultured from prostatic fluid, but the fluid consistently revealed microscopic purulence.

Prostatodynia was diagnosed in the remaining patients who had persistent pain and voiding complaints as in the previous two categories but who had no significant bacteria or purulence in the prostatic fluid. This clinical differentiation of the prostatitis syndromes is now referred to as the traditional classification system ( Table below ).

Classification System for the Prostatitis Syndromes

Traditional	National Institutes of Health	Description
Acute bacterial prostatitis	Category I	Acute infection of the prostate gland
Chronic bacterial prostatitis	Category II	Chronic infection of the prostate gland
	Category III Chronic Pelvic Pain Syndrome (CPPS)	Chronic genitourinary pain in the absence of uropathogenic bacteria localized to the prostate gland employing standard methodology
Nonbacterial prostatitis	Category IIIA (Inflammatory CPPS)	Significant number of white blood cells in expressed prostatic secretions, post–prostatic massage urine sediment (VB3), or semen
Prostatodynia	Category IIIB (Noninflammatory CPPS)	Insignificant number of white blood cells in expressed prostatic secretions, post–prostatic massage urine sediment (VB3), or semen
	Asymptomatic Inflammatory Prostatitis (AIP)	White blood cells (and/or bacteria) in expressed prostatic secretions, post–prostatic massage urine sediment (VB3), semen, or histologic specimens of prostate gland

* Prostatic pain is usually secondary to inflammation with secondary edema and distention of the prostatic capsule. Pain of prostatic origin is poorly localized, and the patient may complain of lower abdominal, inguinal, perineal, lumbosacral, and/or rectal pain. Prostatic pain is frequently associated with irritative urinary symptoms such as frequency and dysuria, and, in severe cases, marked prostatic edema may produce acute urinary retention.

Physical Examination in Prostatitis Evaluation

Physical examination is an important part of the evaluation of a prostatitis patient, but it is usually not helpful in making a definitive diagnosis or further classifying a prostatitis patient. It assists in ruling out other perineal, anal, neurologic, pelvic, or prostate abnormalities and is an integral part of the lower urinary tract evaluation by providing prostate-specific specimens.

In category I, acute bacterial prostatitis, the patient may be systemically toxic, that is, flushed, febrile, tachycardic, tachypneic, and even hypotensive. The patient usually has suprapubic discomfort and perhaps has clinically detectable acute urinary retention. Perineal pain and anal sphincter spasm may complicate the digital rectal examination.
The prostate itself is usually described as hot, boggy, and exquisitely tender. The expression of prostatic fluid secretion (EPS) is believed to be totally unnecessary and perhaps even harmful.

The physical examination of a patient with category II, chronic bacterial prostatitis, and category III CPPS is usually unremarkable (except for pain).
Careful examination and palpation of external genitalia, groin, perineum, coccyx, external anal sphincter (tone), and internal pelvic floor and side walls may pinpoint prominent areas of pain or discomfort. The digital rectal examination should be performed after the patient has produced pre–prostatic massage urine specimens (see later). The prostate may be normal in size and consistency, and it has also been described as enlarged and boggy (loosely defined by the author as softer than normal). The degree of elicited pain during prostatic palpation is variable and is unhelpful in differentiating a prostatitis syndrome. The prostate should be carefully checked for prostatic nodules before a vigorous prostatic massage is performed to produce prostate-specific specimens (EPS - the expressed prostatic secretion and post–prostatic massage urine sample).

In patients presenting with category I, acute bacterial prostatitis,
a urine culture is the only laboratory evaluation of the lower urinary tract required.
It has been suggested that the vigorous prostatic massage necessary to produce EPS can exacerbate the clinical situation, although such fears have never been substantiated in the literature. A midstream urine specimen will show significant leukocytosis and bacteriuria microscopically, and culturing usually discloses typical uropathogens. Blood cultures may show the same organism.

Although the classical 1968 Meares & Stamey four-glass urine collection test (technique) remains the gold standard diagnostic evaluation to distinguish urethral, bladder, and prostate infections of prostatitis patients, numerous surveys have confirmed that clinicians have more or less abandoned this time-consuming and expensive rigorous evaluation.

Technique and interpretation of the Meares-Stamey four-glass lower urinary tract localization test for chronic prostatitis/chronic pelvic pain syndrome.

1. The voided bladder-1 (VB1) specimen includes the first 10 mL of urine and represents the urethral specimen.
2. The voided bladder-2 (VB2) specimen is similar to a midstream urine collection and represents the bladder urine.
3. EPS (the expressed prostatic secretion) should be collected directly into a sterile container during prostatic massage.
4. The voided bladder-3 (VB3) specimen, the first 10 mL of urine voided after prostatic massage, includes any EPS trapped in the prostatic urethra. The three urine specimens are centrifuged for 5 minutes and the sediment examined under high power for leukocytes (including aggregates of leukocytes), macrophages, oval fat bodies, erythrocytes, bacteria, and fungal hyphae. A wet mount of a drop of EPS (the expressd prostatic secreetion) can be examined under a coverslip in a similar manner. In fact, the NIH Chronic Prostatitis Cohort Study suggested that leukocyte determination did not appear to add significant clinical information to the assessment of a patient with CP/CPPS. All four specimens are sent to the laboratory for quantitative culturing.

Category II, chronic bacterial prostatitis, is diagnosed if there is a 10-fold increase in bacteria in the EPS or VB3 specimen compared with the VB1 and VB2. In a patient who has acute cystitis, this localization is impossible; and in this case, patients can be treated with a short course (1 to 3 days) of therapy with antibiotics such as nitrofurantoin, which penetrates the prostate poorly but eradicates the bladder bacteriuria. Subsequent localization of bacteria in the post–prostatic massage urine or EPS is then diagnostic of category II prostatitis.

Category IIIA CPPS (chronic nonbacterial prostatitis) is diagnosed when no uropathogenic bacteria are cultured, but excessive leukocytosis (usually defined as more than 5 to 10 WBCs per high-power field [HPF]) is noted in the prostate-specific specimens (EPS or VB3 or both).

Category IIIB CPPS (prostatodynia) is diagnosed when no uropathogenic bacteria are cultured and there is no significant leukocytosis noted on microscopic examination of EPS or the sediment of VB3.

Table -- Suggested Evaluation of a Man with CPPS

Mandatory

• History
• Physical examination, including digital rectal examination
• Urinalysis and urine culture

Recommended

• Lower urinary tract localization test
• Symptom inventory or index (NIH-CPSI)
• Flow rate
• Residual urine determination
• Urine cytology

Optional

• Semen analysis and culture
• Urethral swab for culture
• Pressure flow studies
• Video urodynamics (including flow electromyography)
• Cystoscopy
• Transrectal ultrasound
• Pelvic imaging (ultrasound, CT, MRI)
• Prostate-specific antigen

Treatment of uncomplicated UTI in men:
Even when seemingly uncomplicated UTI does occur, men should never be treated with short-course therapy, because of a high rate of early relapse.
Fluoroquinolone (as: Cipro 500 mg bid) or with TMP-SMX  (Bactrim-DS  or Septra-DS1 tab bid) for 7 to 14 days,
assuming the organisms are susceptible.

Treatment of Acute Bacterial Prostatitis:
Fluoroquinolone (as: Cipro 500 mg bid) for 2 weeks or with TMP-SMX  (Bactrim-DS  or Septra-DS1 tab bid) for at least 4 weeks,
assuming the organisms are susceptible.
Recurrence is common and usually connotes a sustained focus in the prostate that has not been eradicated.
The prostate may harbor calculi, which can block drainage of portions of the prostate gland or act as foreign bodies in which persistent infection can reside. An enlarged (and inflamed) prostate gland can cause bladder outlet obstruction, resulting in pools of stagnant urine in the bladder that are difficult to sterilize.

Treatment of Chronic Bacterial Prostatitis:
Fluoroquinolone (as: Cipro 500 mg bid) for 2 weeks or with TMP-SMX  (Bactrim-DS  or Septra-DS1 tab bid) for at least 4 to 6weeks,
assuming the organisms are susceptible.  
Prolonged treatment with any of these drugs has a greater than 60% probability of eradicating infection. Most therapeutic failures result from either anatomic factors or infection by Enterococcus faecalis or P. aeruginosa; these two organisms are particularly likely to cause relapse after treatment with the antimicrobial agents currently recommended. Relapses should be treated for 12 weeks. If this therapy fails, long-term antimicrobial suppression or repeated treatment courses for each relapse are often needed.

Medical Therapy of Prostatitis

1. Antimicrobial Agents
   Fluoroquinolone of TMP-SMX antibiotics for 4-6 weeks
   The fluoroquinolones have demonstrated improved therapeutic results, especially in CP caused by E. coli and other members of the Enterobacteriaceae but not necessarily in prostatitis due to P. aeruginosa or enterococci.
   It appears that longer-duration therapy (90 days) provides the best clinical results. Trimethoprim-sulfamethoxazole is less effective, both in bacterial eradication and cost-effectiveness, when compared with the newer fluoroquinolones.
   Except for the well-studied fluoroquinolones, most antibiotics (including minocycline, cephalexin, and carbenicillin) do not demonstrate significant clinical efficacy in clinical studies in which patients were followed for sufficient time. One notable exception has been the macrolides, erythromyci, azithromycin, and clarithromycin, particularly when C. trachomatis is implicated.
2. Alpha-Adrenergic Blocker Therapy
   The lessons learned from these very well designed and implemented studies were that ?-adrenergic blockers provided significant symptom amelioration only after more than 6 weeks of therapy in less heavily treated patients with recent onset of moderate to severe symptoms.
3. Anti-inflammatory Agents and Immune Modulators
   Nonsteroidal anti-inflammatory drugs, corticosteroids, and immunosuppressive drugs theoretically should improve the inflammatory parameters within the prostate and possibly result in a reduction of symptoms.
4. Hormone Therapy (Proscar/Finasteride) - the anti-androgens 5 Alpha-reductase inhibitors
   Six months of finasteride resulted in a numerical but not statistically significant reduction in symptoms compared with the symptom reduction noted in the placebo group.
   Finasteride cannot be recommended as a monotherapy except perhaps in men with associated BPH.
   Theoretically, anti-androgens (including 5?-reductase inhibitors) could result in regression of prostatic glandular tissue (inflammation is believed to begin at the level of the ductal epithelium), improved voiding parameters (especially in older patients with BPH and prostatitis), and reduced intraprostatic ductal reflux
5. Prostate Massage
   Some patients do appear to improve with prostatic massage, but a panel of North American “prostatitis experts” could not come to a consensus on the potential overall benefit or even the mechanism of achieving that benefit if it does occur.

* Multimodal therapy employing multiple concurrent treatment strategies may offer the best results at this time ( Shoskes et al, 2003 ). However, a number of well-controlled prospective studies did not demonstrate increased efficacy by combining ?-adrenergic blockers and antibiotics ( Alexander et al, 2004 ) or Alpha-adrenergic blockers and anti-inflammatory agents ( Batstone et al, 2005). The explanation for this difficulty in treating CP may be that the patients become peripherally and centrally sensitized and treatment targeted to the initiators of the process may not work as well when the condition becomes chronic ( Yang et al, 2003 ).

Others:

• Balloon Dilatation:
  This treatment effect has never been substantiated, and balloon dilatation has not been routinely employed in clinical practice.
• Microwave Hyperthermia and Thermotherapy:
  Heat therapy appears to be a promising therapeutic approach but, until larger-scale studies are performed, should be restricted to patients with refractory or end-stage symptoms.
• Surgery
  A developing prostate abscess, best detected with transrectal ultrasonography or computed tomography (CT) ( Rovik and Doehlin, 1989 ), in patients who fail to respond quickly to antibiotics is optimally drained by the transurethral incision route.
  Surgery does not have an important role in the treatment of most CP syndromes unless a specific indication is discovered during the evaluation of the patient .
  Radical transurethral resection of the prostate has not been advocated for category III CPPS, but open radical prostatectomy has been shown anecdotally to benefit a few patients with symptoms of nonbacterial prostatitis or prostatodynia, or both. No definitive clinical series or long-term follow-up has ever been presented, and this type of surgery should not be encouraged or recommended at this time.
  

Medical Therapy for Chronic Prostatitis and Chronic Pelvic Pain Syndrome

    2008  

*  As a rule, only symptomatic UTI requires therapy.

* Asymptomatic Bacteriuria

Bacteriuria detected in the absence of symptoms referable to the urinary tract does not warrant antimicrobial therapy except in specific settings. These include during pregnancy, before surgery or instrumentation of the urinary tract, and after renal transplantation. Treatment of asymptomatic bacteriuria in patients who are immunosuppressed because of transplantation other than renal (i.e., other solid organ or bone marrow) or because of neutropenia has not been well studied and is not currently recommended as standard practice.

In women with diabetes and asymptomatic bacteriuria, a large randomized trial of antimicrobial treatment versus no antimicrobials found no difference in the time to first symptomatic UTI between the groups. The authors conclude that there is no benefit to screening for asymptomatic bacteriuria or treating it in women with diabetes.

* Catheter-Associated UTI

UTIs are the most common nosocomial infections, representing 40% of all such infections. Most nosocomial UTIs are related to bladder catheterization. Catheter-associated UTIs are associated with increased mortality and costs.  Multiple risk factors for catheter-associated UTIs have been identified, including the duration of catheterization, lack of systemic antibiotic therapy, female sex, age older than 50 years, and azotemia.57 Risk factors for bacteremia related to catheter-associated UTI are not well established.

Several guidelines can be followed to minimize the occurrence of catheter-related infection [see Table 5]. Most important, the catheter should be inserted with strict aseptic technique by trained persons. In addition, a closed system should be used at all times. Even with optimal care, however, catheter use for 1 month or longer will eventually result in bladder infection. Apparently, little additional protection is provided by antibiotic rinses for the bladder, antibiotic ointments applied to the urethral meatus, and instillation of disinfectants such as hydrogen peroxide into the urinary collection bag. Although systemic antibiotics are of no value when the closed system is to be in place for an extended period, antibiotics may be protective when the catheter is in place for only a few days.  However, this advantage should be balanced against the risk of selecting for resistant flora if catheterization must be prolonged unexpectedly. In patients who require urethral catheterization for 2 to 10 days, use of a silver alloy-coated urinary catheter or a nitrofurazone-impregnated catheter may offer some protection against gram-negative organisms infections.

Treatment of catheter-associated UTI depends on the clinical circumstances.
Symptomatic patients (e.g., those with fever, chills, dyspnea, and hypotension) require immediate antibiotic therapy [see Complicated UTI, above]. In addition, it may be useful to remove and replace the urinary catheter if it has been in place for a week or longer. This eliminates difficult-to-eradicate organisms in the biofilm on the catheter. In an asymptomatic patient, therapy should be postponed until the catheter can be removed. Patients with persistent asymptomatic bacteriuria and those with lower urinary tract symptoms who have had the catheter removed respond well to short-course therapy.61

Patients with long-term indwelling catheters seldom become symptomatic unless the catheter is obstructed or is eroding through the bladder mucosa. In patients who do become symptomatic, appropriate antibiotics should be administered, and the catheter should be changed. Therapy for asymptomatic catheterized patients leads to the selection of increasingly antibiotic-resistant bacteria.56,57,60 Thus, although long-term bladder catheterization carries a significant risk of chronic pyelonephritis (10% or more if the catheter is in place for more than 90 days), there is no way to avoid this event other than by catheter removal.62

The appearance of Candida in the urine is an increasingly common complication of indwelling catheterization, particularly for patients in the intensive care unit, on broad-spectrum antimicrobials, or with underlying diabetes mellitus.63C. albicans is still the most common isolate, although C. glabrata and other non-albicans species are also frequently isolated. The clinical presentation can vary from an asymptomatic laboratory finding to sepsis. In asymptomatic patients, removal of the urethral catheter results in resolution of the candiduria in as many as one third of cases. For patients with symptomatic candiduria (fever with or without cystitis symptoms), oral fluconazole, 200 mg/day for 7 to 14 days, has been shown to be highly effective. This regimen was even effective for non-albicans species of Candida that had reduced susceptibility to fluconazole, possibly because of the high concentrations achieved in the urine. For more severely ill patients, the possibility of pyelonephritis and candidemia should be evaluated, and systemic antifungal therapy with fluconazole, 6 mg/kg/day, or amphotericin, 0.6 mg/kg or more a day, should be instituted.

    2008

Endoscopy (Cystoscopy)

Clinical experience (rather than controlled clinical studies) suggests that lower urinary tract endoscopy (i.e., cystoscopy) is not indicated in the majority of men presenting with CP/CPPS. However, cystoscopy is indicated in patients in whom the history (e.g., hematuria), lower urinary tract evaluation (e.g., VB1 urinalysis), or ancillary studies (e.g., urodynamics) indicate the possibility of a diagnosis other than CP/CPPS. In these patients, occasionally lower urinary tract malignancy, stones, urethral strictures, bladder neck abnormalities and so forth that can be surgically corrected are discovered. Cystoscopy can probably be justified in men refractory to standard therapy.

Transrectal Ultrasonography of Prostate

Transrectal ultrasonography has become one of the best radiologic methods to evaluate prostate disease and has become an especially helpful clinical tool for the assessment of prostate volume and ultrasound guidance of biopsy needles. The diagnostic value of ultrasonography in differentiating benign from malignant prostate disease is controversial, and the further differentiation of the various benign conditions of the prostate is even more so.

Transrectal ultrasonography can be valuable in diagnosing medial prostatic cysts in patients with prostatitis-like symptoms, diagnosing and draining prostatic abscesses, or diagnosing and draining obstructed seminal vesicles. It is not required in all cases of acute bacterial prostatitis but rather only in those patients who are failing appropriate antimicrobial therapy ( Horcajada et al, 2003 ).

Prostate Biopsy

Occasionally, because of an elevated PSA level or abnormal digital rectal examination, prostate biopsy is indicated. Some clinicians will consider starting patients with elevated screening PSA levels and a history of prostatitis or symptoms of CPPS on antibiotics, but this practice is really only rational in patients with acute or chronic bacterial prostatitis, conditions that invariably lead to elevated PSA levels. The diagnosis of CP/CPPS should only be used as a reason against a prostate biopsy if the clinician is looking for an excuse not to biopsy.

Out of desperation, urologists sometimes resort to prostate biopsy in an attempt either to demonstrate histologic evidence of prostatic inflammation or to culture an organism that cannot be cultured employing the standard approach. The importance and interpretation of prostate biopsies in CP performed for reasons other than prostate cancer screening is unclear.

Hematospermia

Hematospermia refers to the presence of blood in the seminal fluid. It almost always results from nonspecific inflammation of the prostate and/or seminal vesicles and resolves spontaneously, usually within several weeks. It frequently occurs after a prolonged period of sexual abstinence, and we have observed it several times in men whose wives are in the final weeks of pregnancy. Patients with hematospermia that persists beyond several weeks should undergo further urologic evaluation, because, rarely, an underlying etiology will be identified. A genital and rectal examination should be done to exclude the presence of tuberculosis, a prostate-specific antigen (PSA) and a rectal examination done to exclude prostatic carcinoma, and a urinary cytology done to exclude the possibility of transitional cell carcinoma of the prostate. It should be emphasized, however, that hematospermia almost always resolves spontaneously and rarely is associated with any significant urologic pathology.   

(REF: Wein: Campbell-Walsh Urology, 9th ed. 2007)