Chronic Pelvic Pain in Males

Chronic pelvic pain is an important but underrecognized cause of morbidity in men. While there is abundant literature discussing female pelvic pain and the diagnostic role of imaging, much less attention has been given to imaging of non-gynecologic causes of chronic pelvic pain. Chronic pelvic pain in men is an important source of morbidity and health care expenditures, due to its prevalence and the difficulty of diagnosis and treatment. Historically, emphasis has been placed on the prostate gland as the primary source of chronic male pelvic pain, commonly referred to as prostatodynia. More recently, focus has shifted away from the prostate gland as the dominant source of male pelvic pain, and other terms, such as chronic pelvic pain syndrome (CPPS), have become more prevalent. CPPS refers to pain in or around the groin, genitalia, or perineum, with or without voiding symptoms, in the absence of urinary tract infection. CPPS has a worldwide prevalence between 2 and 16% and is the most common urologic disease in men below 50 years old.

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Chronic Pelvic Pain in Males Summary

Chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) and interstitial cystitis/bladder pain syndrome collectively referred to as urologic CPPS (UCPPS) is defined by the absence of identifiable bacterial infection as a cause for the chronic pain and urinary symptoms. Naturally, genitourinary pain should initially be regarded as a symptom of a possible underlying disorder, and every effort should be exerted to identify an organic source, but, when a pertinent causative disorder is effectively excluded from the differential diagnosis, chronic pain then becomes its own diagnosis. Chronic pain in the male genitourinary system is a distressing complaint for the patient, with only subtle objective anatomic and microanatomic findings, if any, and effective treatment options until recently have been limited.

Chronic Pain Pathophysiology

Genitourinary pain may be regarded as having either a neuropathic or a nociceptive cause. The term neuropathic pain implies that the peripheral nerves are involved in the primary disorder or have been directly damaged by infection, trauma, or surgery. The resultant pain usually develops in the sensory distribution of the affected peripheral nerve or nerves, and although the original insult has healed, the neurons acquire a pathologic level of activity to autonomously generate impulses in the absence of a stimulus. In contrast, non-neuropathic pain might include that of a persistent somatic nociceptive source, including inflammation of a wound, keloid formation, mass effect from aberrant anatomy such as a recurrent hernia, a foreign body such as a metallic vasectomy clip, or a chronic infection of the prostate or genitalia. There is evidence that additional pathophysiologic processes also contribute to the evolution of chronic pain, including neuroplasticity, afferent hypersensitivity, pain centralization, and deafferentation hypersensitivity, which if present may predispose a patient to treatment failure even if a neuropathic or nociceptive source is identified and corrected.

There is evidence that the peripheral and central nervous systems undergo a form of modulation following a long duration of painful stimuli, resulting in sensitization of the pain receptors. Other evidence suggests that, as peripheral nerves regenerate following injury, axons may rejoin erroneously with one another in the dorsal spinal cord such that a depolarization detected by an axon might propagate its signal to an inappropriate neuron proximally, and thus innocent stimuli may be perceived as inordinately noxious.

Prostatic Pain

The term prostatitis refers to a broad array of disease processes. The National Institutes of Health (NIH) developed a classification system for prostatitis in 1995 and proposed universal adoption at the International Prostatitis Collaborative Network workshop in 1998, in Washington, DC.

NIH prostatitis classification system

Category Type
I

Acute bacterial prostatitis

II

Chronic bacterial prostatitis

III

Chronic prostatitis/chronic pelvic pain syndrome (CPPS)

IIIA

Inflammatory

IIIB

Noninflammatory

IV

Asymptomatic inflammatory prostatitis

Prostatitis is a common genitourinary infection, with a lifetime prevalence of up to 16%. A proposed cause of acute bacterial prostatitis (ABP) involves the reflex of infected urine into the ejaculatory and prostatic ducts of the prostatic urethra. Other possible routes of infection include invasion of rectal bacteria through direct extension or hematogenous spread.8 Iatrogenic causes include cystoscopic manipulation of the prostate or bacterial seeding via transrectal biopsy. Risk factors for ascending infection include unprotected sexual intercourse, phimosis, indwelling catheter, and instrumentation. Anything leading to urinary stasis, such as distal urethral stricture and benign prostatic hyperplasia, is also a risk factor.

By definition, ABP has a rapid onset. Patients typically present with a combination of pelvic pain and lower urinary tract symptoms (LUTS). The pain is often described as pelvic, perineal, genital, or a combination.In addition to pain, patients may show a wide array of lower urinary tract symptoms. Symptoms may be irritative (urgency, frequency) or obstructive (weakened stream, intermittent stream, acute urinary retention). Patients may also have dysuria. High-grade fever and other signs and symptoms of systemic illness are often present.

In a retrospective analysis of 614 patients diagnosed with ABP by Milan and colleagues, the most common complications in these patients were acute urinary retention (9.7%), prostatic abscess (2.7%), and recurrent infection (12.7%). Patients with ABP secondary to genitourinary tract manipulation also fared much worse overall. Specifically, the investigators noted a higher risk of prostatic abscess, recurrent infections, and infections involving atypical organisms in this group. Patients with ABP are at significant risk of progressing to chronic bacterial prostatitis (CBP).

Diagnosis Of Acute Prostatitis

Unlike chronic prostatitis, ABP is diagnosed primarily by clinical history, physical examination, and urine culture alone. Given the interconnectivity of the genitourinary tract, a complete urologic physical examination should be performed, including costovertebral angle percussion and palpation of the abdomen, bladder, testicles, and epididymides to rule out associated infectious/inflammatory processes. A gentle palpation of the prostate should be performed as well. The prostate is often described as being tender to palpation and often warm and boggy. Vigorous prostatic massage should be avoided because of the theoretic risk of bacteremia. Therefore, the 2-glass and 4-glass tests used in the diagnosis of chronic prostatitis should be avoided (discussed later).

Urine cultures generally grow out typical uropathogens, with Escherichia coli isolated up to 87% of the time. Other organisms include Pseudomonas, Serratia, Klebsiella, and Enterobacter.10 Chlamydia trachomatis is rarely isolated. Recent literature has shown an increasing prevalence of fluoroquinolone-resistant and extended spectrum b-lactamase–producing bacteria in all patients with prostatitis, but especially in those with prostatitis associated with transrectal prostate biopsy.

Treatment Of Acute Prostatitis

Medical

If the patient is febrile or systemically ill, treatment should be with a high-dose, broad spectrum parenteral antibiotic, such as a broad-spectrum penicillin derivative, third generation cephalosporin, or a fluoroquinolone until fevers and systemic symptoms have resolved. When clinically stable, the condition can be treated with oral fluoroquinolone or trimethoprim/sulfamethoxazole, if tested susceptible.18 Treatment duration of 4 weeks is recommended.

Along with treatment of the causative organism, medical management directed at patient symptoms should be considered. Treat concomitantly with nonsteroidal anti inflammatory medicines for symptomatic pain relief. Treatment with a-blockers has been shown to improve LUTSs in men with prostatic inflammation and should be considered in men in whom LUTSs are an issue. Temporary catheterization may be necessary to relieve acute urinary obstruction.

Surgical

Most patients who present with ABP are adequately treated with medical therapy alone; however, a small subset of patients require surgical intervention. In patients who fail to respond rapidly to medical therapy, consider transrectal ultrasonography or computed tomography scan to assess for abscess.Prostatic abscesses smaller than 1 cm can be treated conservatively with antibiotics, whereas larger abscesses benefit from drainage.23 Percutaneous perineal drainage, transrectal ultrasonography– guided drainage, and transurethral unroofing are all viable methods of treating a prostatic abscess with no clear data recommending one rather than the other.

Chronic Bacterial Prostatitis

Clinical Presentation

To be chronic, symptoms must be present for more than 3 months. It is the most frequent cause of recurrent urinary tract infection in young to middle-aged men, with 25% to 43% of patients diagnosed with CBP having recurrent urinary tract infection as shown by the 4-glass test.Symptoms are indistinguishable from those of chronic pelvic pain syndrome, which is described in detail later.

Diagnosis

From 4.2% to 7% of men with chronic prostatitis/pelvic pain syndrome have a chronic bacterial infection, as shown by the 4-glass or 2-glass tests.24 The 4-glass test, the current gold standard, developed in 1968 by Meares and Stamey, is used to distinguish between infections of the urethra, prostate, and bladder.

  • The first 10 mL of urine represent the urethral specimen (voided bladder 1[VB1]).
  • The second specimen is the midstream urine collection, and assesses thebladder for infection (VB2).
  • The third specimen is the prostatic secretions collected at the urethra during vigorous massage (expressed prostatic secretion [EPS]).
  • The last specimen contains the first 10 mL of voided urine after a vigorous prostatic massage and further assesses the prostate (VB3)

The 2-glass test assesses for bladder infection versus prostate infection and is much less complicated and costly.

  • It involves a midstream urine collection to assess the bladder and the first 10 mL of urine after a vigorous prostatic massage to assess the prostate.
  • It has been shown to be a viable alternative to the 4-glass test, and less costly and complicated.

The diagnosis of CBP is made when there is a 10-fold increase in bacteria in the EPS or VB3 specimen compared with the VB1 and VB2 specimens on a 4-glass test. Alternatively a 10- fold increase in bacteria in the post–prostatic massage specimen in the 2-glass test is also diagnostic. In addition, providers should consider obtaining uroflowmetry and postvoid residuals to rule out bladder outlet obstruction as a contributor. Bacterial isolates are similar to those in ABP. In patients with immunodeficiency, consider atypical organisms such as fungus, Staphylococcus, Mycobacterium tuberculosis, and Mycobacterium avium.

Treatment

Fluoroquinolone antibiotics are considered to be the drugs of choice for CBP because prostate concentrations of these drugs have been shown to reach efficacious doses. Bactrim also has proven efficacy. Ultimately, treatment should be tailored appropriately based on culture results. a-Blockers have also been shown to improve symptoms and reduce recurrence in men with CBP. Treatment course should be at least 4 to 6 weeks. If symptoms fail to resolve at 6 weeks, consider prostate imaging to assess for abscess, because this requires drainage, as discussed earlier.

Chronic Non Bacterial Prostatitis/chronic Pelvic Pain Syndrome (cpps)

Clinical Presentation

Chronic nonbacterial prostatitis (CP)/chronic pelvic pain syndrome (CPPS) is a commondisease process affecting around 10% to 16% of men. It is most prevalent in men between 36 and 50 years old and accounts for approximately 8% of visits to urologists and 1% of primary care visits in the United States. The cause is currently unknown and may involve several simultaneous mechanisms. Nickel and colleagues showed no differences in positive cultures in EPS in men with CPPS versus controls. Multiple other studies have failed to show a link between CPPS and sexually transmitted diseases.

Presenting symptoms in patients with IIIA and IIIB disease are essentially indistinguishable. As mentioned previously, they are similar to those with CBP. The most common symptom in these patients is perineal, suprapubic, or penile pain; however, pain can also occur in the testes, groin, or lower back. Pain associated with ejaculation is also common and very concerning to patients and is associated with more severe and refractory symptoms. Other symptoms possibly seen in these patients include obstructive or irritative voiding symptoms, erectile dysfunction, and sexual disturbances. The NIH Prostatitis Cohort Study reported that more than half of men had pain related to sexual climax.

Along with physical symptoms, psychological symptoms are common in this patient demographic. Depression, stress, or a history of abuse is common in these patients and their presence may exacerbate primary disease symptoms.

Diagnosis

Symptoms must be present for 3 months to be considered chronic. Physical examination in patients with CP/CPPS is often unremarkable except for pain. Examination and palpation of the external genitalia, groin, perineum, coccyx, external anal sphincter, and internal pelvic floor and sidewalls is essential to look for particular areasof pain because this may facilitate directed treatment.

As with CBP, a 2-glass or 4-glass test is important in diagnosis, mainly ruling out CBP given that the NIH Chronic Prostatitis Cohort Study suggested no significant clinical difference between patients in category IIIA and IIIB.

  • Category IIIA CP/CPPS is diagnosed when uropathogenic bacteria are not cultured, but more than 5 to 10 white blood cells (WBCs) per high power field are noted on microscopic analysis of the EPS and/or VB3 specimen.18
  • Category IIIB CP/CPPS is diagnosed when no uropathogenic bacteria are cultured and fewer than 5 to 10 WBCs per high power field are noted on microscopic analysis.

The NIH Chronic Prostatitis Symptom Index (NIH-CPSI) is a validated patient questionnaire that is invaluable in helping to guide therapy specific to the patient’s symptoms. It consists of 9 questions that address 3 domains: pain, urinary function, and quality of life. In a complex disease such as CPPS, this tool is invaluable in helping direct treatment. Along with the NIH-CPSI, the NIH Third International Collaborative Network recommends a urinary flow rate and postvoid residual test be performed on every patient with CPPS to help classify symptoms to aid in more directed treatment.

Proposed causes of persistent irritative and obstructive voiding symptoms, often associated with CP/CPPS, include detrusor internal/external sphincter dyssynergia, proximal or distal urethral obstruction, and bladder neck fibrosis/hypertrophy. Kaplan and colleagues showed that men with a diagnosis of CP/CPPS had symptoms of voiding dysfunction, including 54% with primary bladder neck obstruction, 24% with functional membranous urethral obstruction, 17% with impaired bladder contractility, and 5% with an acontractile bladder. Because of this, videourodynamics may be of some value in selected patients who fail directed therapy, with a component of voiding dysfunction.

In patients who fail appropriate antibiotic therapy, transrectal ultrasonography may play a role in diagnosis of medial prostatic cysts, prostatic abscesses, and seminal vesicle obstruction in patients who present with prostatitislike symptoms. Cystoscopy should be performed in all patients presenting with gross hematuria and in those with persistent microscopic hematuria despite appropriate treatment of prostatitis. It should also be considered in patients who fail treatment, to rule out another cause of symptoms, or if the diagnosis is unclear.

Treatment Of Chronic Pelvic Pain Syndrome (cpps)

CP/CPPS encompasses a broad array of patients and symptoms. Because of this, clinicians are often frustrated in choosing the correct treatment modality for these patients. Numerous treatments have shown efficacy in the treatment of this disease spectrum and can be used selectively based on patient symptom domains. Although patients with CP/CPPS do not grow out bacteria from prostate cultures, by definition, it is thought that bacteria may be the prime cause of patient symptoms in at least a subset of these patients. Nickel and colleagues showed a 45% to 65% NIH-CPSI score in patients with category II, IIIa, and IIIb with treatment of ofloxacin alone, regardless of disease category, suggesting bacteria may play a role even in culture-negative patients. Later studies showed that patients with long-standing symptoms and multiple previous treatments do not benefit from further antibiotic treatment. It is reasonable, therefore, to consider antibiotic treatment in a patient newly diagnosed with CP/CPPS, without previous antibiotic treatment.

Given the significant LUTSs experienced in many individuals with CP/CPPS, therapy targeted at this domain is of benefit to patients. Pseudodyssynergia (contraction of the external sphincter during voiding) is one proposed method leading to LUTSs in CP/CPPS patients. This dysfunctional voiding is thought to lead to reflux of urine into the prostatic ducts, leading to inflammation and pain. a-Adrenergic blockade is known to improve outflow obstruction, by causing relaxation of the bladder neck. There are currently 4 randomized controlled trials showing the efficacy of a-adrenergic blockade in treatment of patients with urinary symptoms, as defined by the NIH-CPSI.

Category IIIA CP/CPPS involves prostatic inflammation, therefore modulation of prostatic inflammation is another possible treatment modality in these patients. Nonsteroidal antiinflammatory medications have been shown to cause rapid improvement in inflammatory symptoms, such as dysuria, stranguria, and painful ejaculation. High-dose cyclooxygenase-2 inhibitors have also shown efficacy. Oral corticosteroid formulations have not shown efficacy in treatment of CP/CPPS at this time.

Some clinicians have proposed pelvic floor dysfunction as a potential cause of CP/ CPPS. Clinical data regarding these use of muscle relaxants have been conflicting. One prospective double-blind study showed a significant improvement in patients treated with baclofen compared with placebo, whereas other studies have shown no improvement compared with placebo. At present, data are conflicting. In patients in whom pelvic floor dysfunction is a possible cause for CP/CPPS, use of a striated muscle relaxant is reasonable.

Other possible treatments include hormonal therapy with 5 alpha-reductase inhibitors, phytotherapeutic agents, gabapentinoids, allopurinol, prostatic massage, pudendal nerve entrapment therapy, biofeedback, acupuncture, and psychological support. Each of these modalities has some supporting research, although it is limited and conflicting. More research is needed in these areas.

One recent modality that has shown promise is intraprostatic botulinum toxin injection. It is known that its injection leads to apoptosis and atrophy of the prostate gland. It also results in release of multiple pain mediators, leading to relief of nociceptive pain. One double-blinded randomized controlled trial showed significant NIH-CPSI scores in the treatment group. Although not currently approved in this patient group, it may represent a treatment alternative in refractory and severe disease.

Upoint Classification For Treatment Of Cpps

CP/CPPS is a challenging disease with a broad spectrum of symptoms. Pinpointing the correct area to treat can be challenging for any clinician. One new 6-point clinical classification system, called UPOINT (urinary, psychosocial, organ specific, infection, neurologic/systemic, and tenderness of skeletal muscles), classifies patients into domains and was designed to help physicians tailor therapy to these complex patients and has proved efficacious.

The treatment of CP/CPPS is often multimodal and complex. The goal of UPOINT is to better characterize the broad array of symptoms with which patients may present in order to develop a better treatment plan that addresses all of the patient’s symptoms. Online tools have been developed and validated to assist in classifying patients into UPOINT domains and to assess disease severity.

Table

a Therapies listed are not necessarily evidence based but are suggested on the best available evidence, interpretation of clinical trial data, and clinical experience. Therapies should be targeted against specific symptom or clinical assessment within a particular phenotype. Some treatments are effective only in a subcategory of a specific phenotype and are not effective in others.

b This category does not include patients with category II CBP, defined as men with recurrent uri- nary tract infections (usually same organism) with identical organism identified in prostate-specific specimens between episodes of infection (see text). These patients have the requirements for in- clusion in the category III CP/CPPS: genitourinary and/or pelvic pain with no history of recurrent uri- nary tract infections.

(From Nickel JC. Prostatitis and related conditions, orchitis, and epididymitis. In: Wein AJ, Kavoussi LR, Novick AC, et al. Campbell-Walsh Urology. 10th edition. Philadelphia: Elsevier Saunders; 2012. p. 353;)

Asymptomatic Inflammatory Prostatitis

Asymptomatic inflammatory prostatitis is asymptomatic. Patients typically present with another complaint, such as benign prostatic hyperplasia (BPH), prostate cancer, or infertility, and the semen analysis or histologic examination of the prostate shows evidence of inflammation. Because prostatitis is a recognized cause of male infertility, its incidental finding during infertility could necessitate treatment.

Inguinal Pain (inguinodynia)

The single most common identifiable predisposing factor in the literature associated with chronic inguinal pain is inguinal herniorrhaphy. By one estimate, up to 27% of all men in the industrialized world may undergo inguinal herniorrhaphy in their lifetimes, and so, even though the procedure might incur an overall low rate of complications, many men might subsequently present annually with persistent postoperative inguinal pain. Although regional practice patterns vary, in North America inguinal hernia repair is most often a procedure performed by general surgeons, and therefore patients who experience postoperative inguinodynia are likely to present to the surgeon who performed their herniorrhaphy. Much of the literature on inguinodynia is likewise written from a general surgical perspective. Inguinodynia of a principally surgical or traumatic cause is discussed later in the article, although other causes might include diabetic neuropathy, herpes zoster infection, and drug-related neuropathy, as can be the case with certain chemotherapy regimens.

Diagnosis

The iliohypogastric, ilioinguinal, and genitofemoral nerves have been collectively dubbed the border nerves by some anatomists, based on their cutaneous innervation of the region between the abdomen and anterior thigh. Surgical incisions in the lower abdomen, even when deliberately made parallel to the Langer lines, risk injury to these nerves, and the resultant neuropathy that follows presents with inguinal pain with possible radiation to the scrotum or medial thigh. Damage to these nerves can occur intraoperatively or postoperatively. Intraoperatively, nerves can be damaged by surgical manipulation but also by stretching; crushing; electrical/thermal damage; partial or complete transection; becoming entrapped in suture during an open repair; or entrapment in tacks, suture, or fixation used during a laparoscopic repair. Postoperatively, nerves can become damaged by envelopment within an inflammatory pseudocapsule surrounding implanted mesh, irritation secondary to an excessive fibrotic reaction, or inflammatory processes such as granuloma or neuroma formation. For the remainder of this article, the term inguinodynia is used to refer to chronic postoperative inguinal pain.

The diagnosis of inguinal pain remains largely based on subjective findings. Efforts to define inguinodynia by quantifying the degree of neuralgia in patients with inguinal pain have shown poor sensitivity. Quantifiable electromyographic abnormalities are present in only 60% of men with proven ilioinguinal or iliohypogastric nerve entrapment, and in fewer than 40% of men with probable entrapment. Diagnosis of inguinal neuralgia is thus made principally on symptoms, although in the absence of an obvious inciting factor, such as herniorrhaphy, other associated disorders, such as zoster infection, should be clinically excluded.

Medical treatment of postoperative inguinodynia

Commonly prescribed acute pain regimens in the immediate perioperative period following herniorrhaphy typically include acetaminophen and nonsteroidal antiinflammatory drugs followed by low-dose opioids for breakthrough pain. Although this seems to suffice for uncomplicated patients, some patients complain of pain that persists beyond the anticipated convalescence period. The extent of pain at 1 week and 4 weeks postherniorrhaphy correlates with the incidence of ongoing pain after 1 year. Although historically surgeons might have addressed these requests by reordering more prescription narcotics, published consensus guidelines from both the International Association for the Study of Pain and the Neuropathic Pain Special Interest Group have firmly established that opioids do not have a role in first-line treatment of chronic neuropathic pain.

Instead, first-line medications for evolving chronic genitourinary pain include antidepressants and gamma-aminobutyric acid analogues. Secondary amine tricyclic antidepressants (TCAs), including nortriptyline and desipramine, are inexpensive and feature convenient dosing schedules relative to other agents. Their sedative and anticholinergic side effects can limit patient compliance but may become more tolerable with time and are less severe than for tertiary amine TCAs such as amitriptyline. The efficacy of TCAs is optimized by ensuring that an adequate 6-week to 8-week trial is performed.

GABA analogues have been studied for their potential role not only in treatment of postoperative pain but also in the preoperative setting to mitigate the risk of developing chronic neuropathic pain. An elegant meta-analysis confirmed that perioperative administration of a single dose of either pregabalin or gabapentin 1 hour before surgery effectively reduced the risk of chronic postsurgical pain more than placebo in several surgical populations, including inguinal herniorrhaphy. Participants in the treatment arms experienced reduced incidence and severity of chronic pain with 6 months’ follow-up. Used over the longer term, these medications can produce dose-related dizziness and sedation that can be ameliorated by starting with low dosages and titrating cautiously.

Guidelines for the treatment of chronic pain describe the use of transdermal medications to assist in regional pain control. However, specific to postoperative inguinodynia, lidocaine patch treatment did not reduce combined resting and dynamic pain ratings compared with placebo in patients with severe, persistent inguinal postherniorrhaphy pain.

Interventional treatment of postoperative inguinal pain

Many regional pain specialists and general surgeons have endeavored to treat postherniorrhaphy pain by targeting the causative peripheral nerve. Although intellectually promising, the results of regional interventions have been mixed. High-level evidence is lacking regarding the interventional and surgical treatment of inguinodynia. Efforts even to inject a temporary local analgesic into the nerves of the groin have had limited results: a double-blinded placebo-controlled study showed no statistical difference between the pain relief of men who received ultrasonography-guided ilioinguinal and iliohypogastric nerve blocks with lidocaine compared with those who received placebo injections. This finding may indicate that peripheral neuropathy has a more complex pathophysiology than can be addressed by a neuroablative approach.

A triple neurectomy procedure has been described whereby the ilioinguinal nerve, the iliohypogastric nerve, and the genital branch of the genitofemoral nerve are individually identified and ligated proximal to the site of the previous herniorrhaphy incision. Importantly, specific risks of neurectomy procedures include permanent sensory deficits, because the nerves involved all provide cutaneous sensory innervation. In addition, the variable loss of motor innervation of the oblique muscles may result in abdominal wall laxity. Patients who elect to proceed with neurectomy for inguinodynia must make it their goal to feel numbness rather than to feel pain; for this reason, critics of neurectomy have condemned its indiscriminate use.

Testicular Pain (chronic Orchalgia)

Pain in the scrotum has presented a long-standing conundrum to urologists and pain experts. Acute pain in the scrotum should initially be evaluated to rule out testicular torsion, acute epididymitis and/or orchitis, and scrotal trauma, as well as pain from a referred source such as a ureteral stone. Testicular cancer rarely manifests with orchalgia and is more commonly painless, but this too is important to exclude because tumors with internal or external hemorrhagen may manifest with pain. Scrotal Doppler ultrasonography is a crucial test in the initial work-up for orchalgia to rule out torsion, neoplasm, and genital trauma. However, scrotal ultrasonography is otherwise an inherently insensitive and nonspecific test: ultrasonic abnormalities such as epididymal cysts or varicoceles may be present in asymptomatic men as well as in those with orchalgia, whereas some men with debilitating orchalgia may manifest with a normal scrotal ultrasonography scan. Furthermore, some patients with orchalgia have some identifiable abnormalities on ultrasonography, but the locus of the pain may be something separate from the appreciable cyst or varicocele, and the ultrasonic anomalies may be incidental and unconnected to the patient’s symptoms.

More than 2% to 3% of all outpatient urology office visits are devoted to chronic scrotal and testicular pain, defined as testicular discomfort lasting more than 3 months and of a magnitude sufficient to significantly affect the man’s quality of life. Roughly half of these men have no history of trauma or infection to explain the onset of pain, and patients have variable presentations in terms of timing, severity, reproducibility, and radiation.

A unique subset of men who develop chronic testicular pain have a history of vasectomy; patients who undergo vasectomy incur at least a 1%to 2% chance of developing significant chronic scrotal pain after the procedure. Because of inconsistencies in the accrual of such data, the likelihood of any chronic discomfort after a vasectomy is not clear but may be as low as 0.1% or as high as 54%. Chronic discomfort has been attributed to obstruction and congestion of the epididymal ducts, nerve entrapment by scar tissue, or formation of an inflammatory sperm granuloma following the initial contact between the immune system and sperm cells. Of the men who develop chronic discomfort, some develop the pain instantly after the vasectomy, whereas others heal quickly from the initial procedure and then progress to chronic pain only years later.

Physical examination in patients with orchalgia is geared toward the exclusion of associated disorders, including neoplasm, cysts, varicoceles, and inguinal hernias. Acute intense focal tenderness of the epididymis is suggestive of an active infection, and may merit an empiric 10-day to 20-day course of a fluoroquinolone or trimethoprim-sulfamethoxazole followed by a period of convalescence before arriving at the conclusion that the patient’s pain is chronic and does not have an infectious cause. Note that infectious epididymitis cannot occur de novo in a patient after vasectomy, unless the pathogen ascended into the epididymis before or during the procedure.

Spermatic cord block (Genitofemoral nerve block)

A helpful diagnostic step is the option of a spermatic cord block with local anesthesia. Although by definition a local anesthetic provides only temporary analgesia at best, the efficacy of the block may help to localize the patient’s complaint to the branchesof the genitofemoral and ilioinguinal nerves within the spermatic cord, and may help to prognosticate the efficacy of future surgical efforts to mitigate neuropathic pain in a particular patient. In addition, it provides the patient with a reasonable simulation of the result that can be obtained with pulsed radiofrequency ablation or surgery to denervate the spermatic cord.

Surgical treatment of chronic scrotal pain

Historically, the ultimate definitive surgical treatment of orchalgia is orchiectomy. Surgical removal of the testis carries the risk of inadequate androgen synthesis as well as a non-negligible psychological burden. Not only is orchiectomy an intellectually unsatisfying treatment modality from the physician’s perspective, orchiectomy also does not guarantee relief of scrotal pain, with up to 45% of men noting incomplete resolution of pain.

Microsurgical denervation of the spermatic cord may not always be successful. In a patient who has had unsuccessful treatment with a microdenervation, alternative pathways may exist for the depolarization to propagate to the CNS. Plausible explanations include a more proximal locus of the painful stimulus on the peripheral nerve (as illustrated), persistent intact afferent nerve fibers located too close to the vital lymphovascular structures to safely permit dissection and ligation, formation of a neuroma at the point of nerve ligation, or pain centralization within the brain.

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Dr Murli Krishna

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