14.2 Prostatitis, Epididymo-Orchitis & Fournier Gangrene

Prostatitis, Epididymo-Orchitis & Fournier Gangrene

Infections of the male genitourinary tract exhibit diverse clinical presentations, ranging from indolent chronic pelvic discomfort to rapidly lethal necrotizing soft-tissue infections. Mastering the anatomical fascial compartments, microbiological drivers, and emergency surgical decision-making is fundamental to achieving high pass rates on the European Board of Urology (FEBU) examination.

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1. NIH Classification of Prostatitis Syndromes

The National Institutes of Health (NIH) consensus classification delineates four distinct prostatitis categories based on clinical presentation, microbiological cultures, and leukocyte presence in expressed prostatic secretions.

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|                                 NIH PROSTATITIS CLASSIFICATION                                |
|                                                                                               |
|  CATEGORY I:   Acute Bacterial Prostatitis (ABP)                                              |
|                --> Severe systemic bacterial infection with acute fever, pelvic pain, dysuria,|
|                    and obstructive voiding; swollen, tender prostate on digital rectal exam   |
|                                                                                               |
|  CATEGORY II:  Chronic Bacterial Prostatitis (CBP)                                            |
|                --> Recurrent, relapsing UTIs caused by the identical bacterial pathogen;      |
|                    positive cultures in Expressed Prostatic Secretions (EPS) or VB3           |
|                                                                                               |
|  CATEGORY III: Chronic Pelvic Pain Syndrome (CPPS)                                            |
|                --> Genitourinary pain >= 3 months without documented bacterial infection      |
|                --> Category IIIa: Inflammatory CPPS (leukocytes present in EPS / VB3 / semen) |
|                --> Category IIIb: Non-Inflammatory CPPS (no leukocytes in EPS / VB3 / semen)  |
|                                                                                               |
|  CATEGORY IV:  Asymptomatic Inflammatory Prostatitis                                          |
|                --> No clinical symptoms; leukocytes discovered incidentally on semen analysis,|
|                    prostate biopsy histology, or expressed secretions                         |
+-----------------------------------------------------------------------------------------------+

Category I: Acute Bacterial Prostatitis (ABP)

• Pathophysiology & Microbiology: Ascending urethral infection or intraprostatic reflux of infected urine. The most frequent causative organism is Uropathogenic E. coli (65–80%), followed by Klebsiella, Proteus, Enterobacter, Pseudomonas aeruginosa, and Enterococcus faecalis.
• Clinical Presentation: Sudden onset of high spiking fevers, rigors, perineal and sacral pain, severe dysuria, frequency, urgency, and acute obstructive voiding difficulty.
• Physical Examination: Digital rectal examination (DRE) must be performed with extreme gentleness; the prostate is warm, exquisitely tender, swollen, and boggy.

• Diagnostic Workup & Prostatic Abscess: Midstream urine culture and blood cultures. Serum PSA is dramatically elevated during acute inflammation and must never be used to evaluate for prostate cancer; normalisation may take weeks or longer, so reassess an elevated PSA after recovery rather than interpreting it during infection. If fever and symptoms fail to improve after 48 to 72 hours of appropriate IV antibiotics, perform transrectal ultrasound (TRUS) or pelvic contrast-enhanced CT/MRI to diagnose a prostatic abscess, and guide treatment. Selected small abscesses may respond to antibiotics; larger, persistent or clinically significant collections often require image-guided drainage or transurethral unroofing.
• Pharmacological Treatment: Treat systemically ill ABP initially with an appropriate IV regimen, such as a third-generation cephalosporin or broad-spectrum penicillin, with an aminoglycoside in selected cases. Base coverage on illness severity, prior antibiotics/cultures and local resistance. Once infection parameters improve and oral treatment is feasible, use a susceptible oral agent with prostatic penetration, such as ciprofloxacin, levofloxacin or TMP-SMX. EAU recommends a total of 2–4 weeks for ABP; do not confuse this with the usual 4–6 weeks for CBP.

Category II: Chronic Bacterial Prostatitis (CBP)

• Clinical Presentation: Recurrent, relapsing episodes of symptomatic cystitis separated by asymptomatic intervals, persistently caused by the same bacterial strain. Between flares, patients report low-grade perineal aching, scrotal or testicular discomfort, and dysuria.
• Diagnostic Gold Standard: The Meares-Stamey Four-Glass Test:
  • VB1 (Voided Bladder 1): Initial 10 mL of urine (urethral flush).
  • VB2 (Voided Bladder 2): A midstream urine sample representing bladder urine.
  • EPS (Expressed Prostatic Secretions): Secretions obtained via gentle prostatic massage.
  • VB3 (Voided Bladder 3): Initial 10 mL of urine voided immediately following prostatic massage.
  • Diagnostic Interpretation: CBP is formally diagnosed when the colony count of bacteria in EPS or VB3 exceeds the count in VB1 and VB2 by at least 10-fold (1 log10).
• Therapy: Lipophilic antimicrobials capable of crossing the acidic lipid barrier of the prostatic epithelium. Oral fluoroquinolones (Ciprofloxacin or Levofloxacin) for 4 to 6 weeks achieve bacteriological eradication in 60% to 75% of cases. Macrolides (azithromycin) or doxycycline may be used if atypical pathogens (Chlamydia, Ureaplasma) are isolated.

Category III: Chronic Pelvic Pain Syndrome (CPPS)

CPPS represents over 90% of symptomatic men presenting to prostatitis clinics. Patients experience non-malignant pelvic pain (perineum, suprapubic, testicles, or penis) for at least 3 of the previous 6 months in the complete absence of uropathogenic bacteria.

• Multimodal UPOINT Phenotype-Directed Management: EAU recommends multimodal, phenotype-directed care. UPOINT is one studied framework for organizing the relevant domains; no single treatment reliably benefits every patient:
  1. U - Urinary Symptoms (storage/voiding LUTS): Treated with selective alpha-blockers (Tamsulosin, Silodosin).
  2. P - Psychosocial Dysfunction (catastrophizing, depression, anxiety): Treated with Cognitive Behavioral Therapy (CBT), SSRIs, or tricyclic antidepressants.
  3. O - Organ-Specific Findings (prostate tenderness, leukocyturia): Treated with anti-inflammatory phytotherapies (quercetin, pollen extract Cernilton) or NSAIDs.
  4. I - Infection: Treat a documented pathogen appropriately. For treatment-naïve primary prostate pain syndrome lasting <1 year, EAU supports one ≥6-week quinolone or tetracycline course; move to other options after an unsuccessful course and avoid repeated unnecessary antibiotics.
  5. N - Neurological / Systemic Conditions (central sensitization, fibromyalgia, irritable bowel): Consider individualized pain-specialist treatment. Neuromodulators may suit selected neuropathic pain, but pregabalin has not shown efficacy for unselected primary prostate pain syndrome.
  6. T - Tenderness of Pelvic Floor Muscles (spasm, myofascial trigger points): Treated with specialized pelvic floor physical therapy and myofascial release with relaxation and down-training for an overactive pelvic floor; avoid indiscriminate strengthening that increases symptoms.

Category IV: Asymptomatic Inflammatory Prostatitis

Incidental finding of inflammatory cells (leukocytes) in semen or prostate biopsy specimens without symptoms. No treatment is required for asymptomatic inflammation alone. Before procedures breaching urinary mucosa, obtain a urine culture and manage bacteriuria/prophylaxis according to the procedure; leukocytes in semen alone do not establish infection.

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2. Scrotal Infections: Acute Epididymitis & Epididymo-Orchitis

Acute epididymitis is an inflammatory infection of the epididymis that frequently extends to the adjacent testicle (epididymo-orchitis). Pathophysiology involves retrograde canalicular migration of infected urine or urethral pathogens via the ejaculatory duct and vas deferens.

Etiology, Testing and Risk-Directed Treatment

Obtain a midstream urine culture and first-void urine NAAT for C. trachomatis and N. gonorrhoeae. Young age or a negative sexual history alone cannot reliably identify or exclude an STI. Enterobacterales also occur in young men; instrumentation, obstruction and urinary abnormalities increase enteric-pathogen risk.

+--------------------------------------------------------------------------------------------------------------+
| ACUTE EPIDIDYMITIS: EAU PATHOGEN-RISK APPROACH                                                               |
|                                                                                                              |
| LIKELY GONORRHOEA / URETHRAL DISCHARGE                                                                       |
|   Ceftriaxone 1 g IM or IV once, plus doxycycline 200 mg initially then 100 mg BID for 10–14 days.           |
|   Test, notify and manage sexual contacts under local public-health policy; avoid sex until cleared.         |
|                                                                                                              |
| LOW GONORRHOEA RISK: COVER CHLAMYDIA AND ENTEROBACTERALES WHEN RELEVANT                                      |
|   Levofloxacin 500 mg daily for 10–14 days, or doxycycline plus TMP-SMX as an alternative.                   |
|   Non-sexually active men: enteric coverage guided by cultures and local susceptibility.                     |
|   Fluoroquinolones do not provide reliable gonorrhoea treatment. Adjust to results and response.             |
|                                                                                                              |
| CHILDREN AND VIRAL ORCHITIS                                                                                  |
|   Prepubertal epididymitis is often non-bacterial; first exclude torsion and assess urinary causes.          |
|   Mumps may cause orchitis after puberty, usually unilateral, with risk of testicular atrophy.               |
|   Traditional 20–30% orchitis estimates mainly reflect unvaccinated cases; rates are lower after vaccination.|
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Clinical Presentation & Diagnostic Differentiation

• Symptoms: Acute unilateral scrotal swelling, severe aching pain radiating along the spermatic cord into the ipsilateral groin, fever, dysuria, and urethral discharge.
• Physical Signs:
  • Prehn's Sign: Elevation of the affected hemiscrotum historically alleviates pain in epididymitis (positive Prehn's sign) while worsening or not altering pain in testicular torsion. However, Prehn's sign is unreliable and cannot be used to rule out torsion.
  • Cremasteric Reflex: Usually preserved in epididymitis and often absent in torsion; examine it as part of the clinical assessment rather than using it alone to exclude torsion.
• Imaging Workup: Color Doppler Scrotal Ultrasound assists diagnosis when it will not delay urgent exploration for suspected torsion:
  • Epididymo-orchitis: Markedly enlarged, hypoechoic epididymal head/tail with intense hyperemia and increased vascular flow (often a low-resistance flow pattern), thickened scrotal skin, and reactive inflammatory hydrocele.
  • Testicular Torsion: Absent or markedly diminished intratesticular arterial blood flow, high resistive indices, or twisting of the spermatic cord ("whirlpool sign"). Persistent arterial flow can occur in early, partial or intermittent torsion. If clinical suspicion remains, arrange immediate surgical exploration regardless of reassuring flow; imaging must not delay treatment.

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3. Fournier Gangrene

Fournier gangrene is a life-threatening, rapidly progressive necrotizing fasciitis involving the external genitalia, perineum, and perianal region. Characterized by synergistic polymicrobial infection, it triggers microvascular thrombosis and widespread soft-tissue necrosis.

Pathophysiological Synergy & Microbiology

Fournier gangrene is driven by a virulent synergistic interaction between aerobic and anaerobic microorganisms:

• Aerobic / Facultative Organisms: Escherichia coli, Klebsiella pneumoniae, Pseudomonas aeruginosa, Proteus mirabilis, Enterococcus faecalis, and Streptococcus pyogenes (Group A Strep).
• Anaerobic Organisms: Bacteroides fragilis, Clostridium perfringens, Peptostreptococcus, and Fusobacterium.
• Mechanistic Synergy: The aerobic bacteria consume tissue oxygen and produce collagenases, hyaluronidases, and heparinases. The resulting low tissue oxygen tension fosters the rapid proliferation of obligate anaerobes. Anaerobes synthesize potent endotoxins and cytolytic enzymes that induce obliterative endarteritis and microvascular thrombosis in nutrient arterioles, resulting in full-thickness necrosis of the overlying skin and subcutaneous fat. Tissue destruction can propagate at an astounding rate of 2 to 3 cm per hour.

Fascial Anatomy: Pathways of Extension

The infectious necrosis travels within the superficial fascial envelopes of the pelvis and abdominal wall:

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|                             FOURNIER GANGRENE: FASCIAL ANATOMY                                |
|                                                                                               |
|                     Scarpa's Fascia (Anterior Abdominal Wall)                                 |
|                                        ^                                                      |
|                                        |                                                      |
|                       Colles' Fascia (Perineum) <--------> Dartos Fascia (Scrotum & Penis)    |
|                                        |                                                      |
|                                        v                                                      |
|                           Perianal & Ischiorectal Fossa                                       |
|                                                                                               |
|  KEY CLINICAL PEARL: THE TESTES ARE PRESERVED!                                                |
|  --> The dartos tunic and scrotal skin derive blood from the superficial external pudendal    |
|      and perineal vessels, which undergo rapid thrombotic occlusion.                          |
|  --> Conversely, the TESTES derive their arterial supply directly from the ABDOMINAL AORTA via|
|      the internal spermatic (testicular) arteries within the retroperitoneum, and their venous|
|      drainage empties into the IVC/left renal vein.                                           |
|  --> Consequently, the testes are typically anatomically preserved and viable, even when the  |
|      entire scrotum, perineum, and lower abdominal wall are completely gangrenous!            |
+-----------------------------------------------------------------------------------------------+

Predisposing Risk Factors

• Diabetes Mellitus: Present in 60% to 75% of patients (impaired phagocytosis, microvascular disease, high tissue glucose).
• Chronic Alcohol Abuse & Liver Cirrhosis: Immunosuppression and malnutrition.
• Systemic Immunocompromise: Chemotherapy, HIV infection, end-stage renal disease (ESRD).
• Pharmacological Factor: Sodium-Glucose Cotransporter-2 (SGLT2) Inhibitors (e.g., Empagliflozin, Dapagliflozin, Canagliflozin). SGLT2 inhibitors induce substantial glucosuria, creating a favorable perineal environment for fungal and polymicrobial bacterial proliferation; regulators have issued safety warnings about reported Fournier gangrene during SGLT2 inhibitor treatment. If suspected, stop the drug, arrange alternative glycemic management and start urgent infection treatment.
• Portals of Entry: Colorectal pathology (perianal abscess, ischiorectal fistula, rectal perforation, 30–50%), urogenital pathology (urethral stricture, traumatic Foley catheterization, periurethral extravasation, 20–40%), or cutaneous trauma/scrotal hidradenitis.

Clinical Presentation & The Fournier Gangrene Severity Index (FGSI)

• Clinical Signs: Severe, unrelenting perineal pain that is initially out of proportion to physical examination findings, accompanied by high fever and tachycardia. Rapidly progresses to scrotal erythema, dusky purple-to-black cutaneous bullae, foul-smelling "dishwater" purulent discharge, and subcutaneous crepitus (palpable gas in 50–60% of cases, produced by Clostridium or E. coli fermentation).
• FGSI Scoring: Calculates mortality risk using 9 physiological variables (temperature, heart rate, respiratory rate, serum sodium, potassium, creatinine, bicarbonate, hematocrit, and leukocyte count). In the original FGSI cohort, scores >9 were associated with about 75% mortality, while scores ≤9 predicted about 78% survival. Use the score for risk assessment; it must not delay resuscitation or surgery.

Emergency Management Protocol

Fournier gangrene is a surgical emergency where every hour of delay significantly increases mortality.

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| FOURNIER GANGRENE: RESUSCITATION, ANTIBIOTICS AND SURGERY IN PARALLEL                                    |
|                                                                                                          |
| 1. IMMEDIATE RESUSCITATION                                                                               |
|    Assess airway and circulation; give IV crystalloid with frequent reassessment and monitor perfusion.  |
|    Treat shock, electrolyte disturbance and acidosis; norepinephrine for persistent hypotension.         |
|    Establish safe urinary drainage; select urethral versus suprapubic diversion for the actual injury.   |
|                                                                                                          |
| 2. PROMPT BROAD-SPECTRUM IV ANTIBIOTICS                                                                  |
|    Example: piperacillin-tazobactam 4.5 g every 6–8 hours or meropenem 1 g every 8 hours,                |
|    plus MRSA coverage such as vancomycin with weight/renal/exposure-guided dosing.                       |
|    Add clindamycin 600–900 mg IV every 8 hours for suspected toxin-mediated streptococcal disease;       |
|    documented group A streptococcal infection is treated with penicillin plus clindamycin.               |
|    Obtain operative cultures and narrow treatment; one fixed triple regimen is not mandatory for all.    |
|                                                                                                          |
| 3. URGENT COMPLETE DEBRIDEMENT                                                                           |
|    Excise all necrotic skin, subcutaneous tissue and fascia to viable margins; do not delay for imaging. |
|    Preserve viable testes and other deeper structures; protect exposed testes while planning coverage.   |
|    Thigh pouches are one option in extensive scrotal loss, not a required step for every patient.        |
|                                                                                                          |
| 4. EARLY REPEAT EXPLORATION                                                                              |
|    Plan return to theatre, commonly within 24–36 hours, and repeat debridement until no necrosis remains.|
|    Re-explore sooner if deterioration or ongoing necrosis requires it.                                   |
|                                                                                                          |
| 5. DIVERSION AND WOUND CARE                                                                              |
|    Consider fecal diversion for sphincter disruption or uncontrolled wound contamination.                |
|    Tailor urinary diversion, dressings and later graft/flap reconstruction to the wound and patient.     |
|    NPWT may assist selected wounds, but survival benefit is unproven and it cannot replace debridement.  |
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Summary Reference Tables: Prostatitis & Scrotal Emergencies

Table 1: NIH Prostatitis Classification, Diagnostic Workup & Therapeutics

Table 2: Scrotal Emergencies: Acute Epididymo-Orchitis vs. Testicular Torsion vs. Fournier Gangrene