Testicular infarction and spontaneous scrotal rupture secondary to acute epididymo-orchitis

Abstract

Epididymo-orchitis is a common cause of acute unilateral testicular pain. Both infectious or non-infectious causes have been proposed and, rarely, testicular abscess formation and even infarction can occur as a severe complication. We present here a case of acute epididymo-orchitis leading to testicular abscess formation, infarction and spontaneous rupture through the scrotal wall despite appropriate antibiotic treatments. Orchidectomy and partial scrotectomy were performed during surgical exploration for management of the non-viable testis and associated scrotal sinus. Clinical vigilance is important to prevent this complication by close clinical follow up with ultrasonography and even early surgical decompression to prevent testicular loss.

Background

Acute epididymo-orchitis is an inflammatory condition of the epididymis and testis. Patients usually present with an acute onset of epididymal and/or testicular pain with associated local features such as swelling and scrotal wall erythema. The common pathogens are those from anorectal and genitourinary system. In most instance, antibiotic management based on the local microbiological profile is adequate and leads to resolution. However, rarely, global testicular ischaemia and infarction can occur necessitating an orchidectomy at the time of surgical exploration. The postulated theories for this include inflammation and subsequent oedema causing compression of the spermatic cord, thrombosis secondary to venous congestion as well as a role of bacterial exotoxins.^{1 2} There is little available evidence to guide the management in these complicated infections to prevent them progressing to testicular loss, partly due to the low incidence of this sequelae. With only a small body of case reports on global testicular infarction following epididymo-orchitis available in the literature, it is hard to evaluate its incidence.³ We present here a case of severe epididymo-orchitis manifesting as spontaneous rupture of the testis and overlying scrotal skin, and review the literature on appropriate management of such cases.

Case presentation

A middle-aged man presented to the emergency department (ED) with a 3-day history of gradually worsening left testicular pain. He denied urethral discharge, dysuria, lower urinary tract symptoms or fevers/chills at presentation. He was sexually active. His medical history included hepatitis C carrier, psoriasis and left hip replacement. He reported intravenous drug use and heavy smoking history. His vitals, including temperature, were normal. In addition to psoriatic skin changes, the main finding on clinical examination was significant left testicular swelling with associated tenderness and erythema of ipsilateral scrotal wall and inguinal region. The left testis was firm and significantly enlarged.

Investigations

Laboratory investigations showed an elevated white blood cell count (WCC) of 15.0×10⁹/L and C reactive protein (CRP) of 162 mg/L. Urinalysis and screening for sexually transmitted infection (STI), that is, gonorrhoea and chlamydia, were negative. A clinical diagnosis of acute left epididymo-orchitis was supported by scrotal ultrasound scan (USS) that demonstrated a bulky and hypervascular left testis with thickening and vascularity within the left epididymis. There was also a complex left-sided hydrocele with internal density and septa (figure 1A–D). There was no sign of torsion or intratesticular focal mass. The right testis and epididymis appeared normal.

Figure 1.

Grayscale and colour doppler ultrasound of the left testicle showed progression from epididymo-orchitis to testicular abscess formation and rupture. (A–C) At initial emergency department presentation, the left testis was found to be slightly bulky and appears mildly hypervascular, with an associated mild-to-moderate complex hydrocele. (D) There was thickening and vascularity within the left epididymis. The right testis and epididymis appeared normal. The ultrasound scan (USS) diagnosis was moderate left-sided epididymo-orchitis with an associated mild-to-moderate complex hydrocele. (E–G) Two weeks later, repeated USS showed the left testicular morphology was completely deranged. Most of the left testis appeared occupied by a large irregular collection of complex fluid with surrounding oedema and hypervascularity, however reduced flow within the testis itself. The collection appeared to be discharging through a breach in the anterior aspect of the capsule, to the skin. There was marked oedema of the overlying scrotal wall. (H) Left epididymis was grossly enlarged and hyperaemic consistent with epididymitis. The right testis and epididymis were still normal. USS diagnosis was left testicular abscess and sinus, superimposed on acute left epididymitis.

The patient was admitted to urology department for 48 hours of intravenous antibiotics (ceftriaxone +gentamicin) per local guideline. He was also given 1 g single dose of azithromycin in ED for STI coverage and discharged, with a plan of oral ciprofloxacin 500 mg two times per day for 2 weeks and one further dose of azithromycin in a week, after symptoms initially improved. He was advised to see his general practitioner (GP) in 1-week time.

Two weeks later, the patient was referred to ED by his GP due to purulent discharge from the left scrotal wall. His scrotal pain and swelling had been worsening until the night before representation when the scrotal skin was noted to have broken down with pus draining spontaneously. There were no other new symptoms. On examination, he remained afebrile and haemodynamically stable. The left testicular swelling had significantly reduced but there was a sinus (1×1 cm) in the overlying left scrotal wall expressing purulent discharge. Laboratory investigations showed normal WCC and decreased CRP (20 mg/L). Microscopy, culture and sensitivity (MCS) of the swab from the scrotal discharge showed moderate growth of mixed skin and enteric flora while urine MCS showed no growth with unremarkable urinalysis. Scrotal USS showed the left testicular morphology was completely deranged with formation of abscess in addition to acute left epididymitis (figure 1E–H). The right testis remained normal in size and vascularity.

Differential diagnosis

The patient was diagnosed with left testicular abscess formation and scrotal rupture subsequent to epididymo-orchitis at this time. Other differentials include testicular torsion, spermatic vein thrombosis, testicular vasculitis, testicular tumours and segmental/global testicular infarction.

Treatment

The patient underwent emergent scrotal exploration. Intraoperative finding confirmed the rupture of left testis with visible seminiferous tubules through the defect (figure 2). The testicular abscess communicated through the overlying sinus within the indurated scrotal wall. A left orchidectomy with resection of scrotal wall sinus was performed. Histological examination showed a left testicular infarction with significant amount of paratesticular abscess and fibrosis (figure 2). The tunica vaginalis was disrupted with extrusion of necrotic tissues. Some vessels in the spermatic cord contained occlusive organising thrombi.

Figure 2.

Intraoperative and macroscopic findings. (A–B) Urgent scrotal exploration was performed with resection of the non-viable left testis and overlying discharging scrotal sinus. (C) Necrotic tissue and seminiferous tubules were seen through the defect in the tunica albuginea adherent to the scrotal wall. (D) On the posterolateral view, grossly enlarged spermatic cord and epididymis were seen. (E) Macroscopic longitudinal histological section view showed infarcted testis (*), surrounding fibrotic tissues (arrow) and significant amount of paratesticular abscess draining through the defect in the anterior tunica vaginalis (arrow head).

Outcome and follow-up

The patient recovered well postoperatively and was discharged with 2 weeks of ciprofloxacin. He was reviewed 8 weeks later at urology outpatient clinic and the wound healed well with palpable normal right testis.

Discussion

Due to anatomical proximity, epididymitis often occurs together with orchitis and thus termed as epididymo-orchitis. Acute epididymo-orchitis is relatively common and can occur in all age groups and tends to be unilateral. The most commonly affected is the 20–59 years-old age group (43% in men aged 20–39 years-old), and sexually transmitted organisms are the most common pathogens in this group. In contrast, coliform bacteria are the primary pathogens in other age groups (29% in men aged 40–59 years-old).⁴ Interestingly, rates of epididymitis diagnosis in hospital admission and ED presentations are found to be on the rise.⁵ The current Australian Therapeutic Guidelines (https://www.tg.org.au) recommend empirical therapy with single dose of ceftriaxone plus azithromycin (repeated 1 week later) for suspected sexually transmitted pathogens; and 2 weeks of either trimethoprim, cefalexin or ciprofloxacin for suspected urinary tract pathogens.⁶ This empirical antibiotic regimen is deemed adequate to cover most of the common pathogens unless there are multidrug-resistant bacteria involved or for cases with septic shock. However, atypical pathogens, like Pseudomonas aeruginosa and Staphylococcus aureus, have also been reported in acute suppurative epididymo-orchitis and thus consideration of their coverage may be worthwhile in patients with risk factors for such organisms.⁷

Our current case first came for medical attention on day 3 of symptoms at which time he had most of the common clinical features of acute epididymo-orchitis, for example, testicular swelling, scrotal pain with radiation to the groin (spermatic cord), erythema of scrotal skin and reactive hydrocele on USS (figure 1). He was admitted overnight for intravenous antibiotics and was discharged with oral ciprofloxacin given negative STI screening and presumed enteric organism origin (urine MCS was not performed given the negative urinalysis). Despite his history of intravenous drug use, he did not receive antibiotics to cover methicillin-resistant S. aureus given the complexity in treatment regimens for this organism. Unfortunately, he had progressive worsening of scrotal swelling and pain and came to the hospital for the second time 2 weeks later when there was rupture of the testicular contents through the scrotum. Same day emergency decompression of the necrotic testis led to relief of symptoms and improvement in inflammatory markers, but orchidectomy was needed as the testis was non-viable (figure 2).

In patients who are immunocompetent, severe complication such as abscess formation is uncommon, especially with the availability of broad-spectrum antibiotics. There are only a small number of case reports describing progression to abscess formation and global testicular infarction/loss from epididymo-orchitis.1–3 8–15 Rarely, testicular infarction could involve both testes.^{8 14} Even more infrequently, there have been reports of spontaneous scrotal skin rupture with purulent discharge.^{16 17} Similar to the findings of Chia et al, we found extrusion of testicular contents (seminiferous tubules) intraoperatively.¹⁷ Given the small body of literature, there is lack of data on the incidence of testicular infarction following acute epididymo-orchitis. In 1966, Mittemeyer et al reviewed 610 consecutive cases of epididymitis and reported 19 patients (3%) had suppurative orchitis with abscess formation on orchidectomy.¹⁸ Desai et al reviewed 33 men with epididymitis and only one orchidectomy done due to suspicion of tumour demonstrated an infarcted testis (3%).¹⁹ Therefore, this current case would add awareness to this uncommon but serious complication of acute epididymo-orchitis.

The cause of testicular infarction after epididymo-orchitis is not fully understood, but may be multifactorial, with a mixed arterial and venous insufficiency. Inflammation of the epididymal head is likely to cause initial testicular venous congestion.¹¹ When the intratesticular pressure due to ongoing inflammatory processes overcomes the arterial perfusion pressure, a further arterial insufficiency can arise.²⁰ As the testes receive a joint blood supply from the testicular artery, deferential artery and the cremasteric artery, this risk of global testicular infarction is low unless the inflammatory infiltration is causing compression at the level of spermatic cord, similar to testicular torision.²¹ Clinically, this can be manifested as cord induration at the level of the scrotal neck and superficial inguinal ring.¹⁹ It is also possible a grossly inflamed and enlarged testis is more prone to torsion especially with predisposed bell clapper deformity. Otherwise, segmental infarction is more likely in upper pole as the anterior epididymal artery flow has higher chance to be impaired.²² However, the management of segmental infarction remains controversial as testicular salvage is not always achievable. Indeed, a reversal of diastolic blood flow on colour Doppler has been suggested as a sign of impending infarction.¹² Focal orchitis can also promote abscess/pyocele formation, which might further compromise regional vascular sufficiency due to mass effects. Similar mass effects can also arise from acute reactive hydroceles. Another possible explanation is endothelial damage imposed by endotoxins released from gram negative bacteria that could impair the local vasculature.¹⁰ This can partially explain why urinary tract pathogens were more commonly found in those with complications than STI pathogens.²¹

One important clinical feature of our current case is the rapid progression to testicular infarction and spontaneous rupture in the scrotal wall within 2 weeks despite being systemically well and on appropriate antibiotic treatments. To date, there was only one similar case report in literature, in which a 50-year-old male patient had spontaneous scrotal rupture despite a 3-week course of oral antibiotics.¹⁷ But that patient presented with more severe symptoms including macroscopic haematuria and dysuria in addition to scrotal pain. He also reported squeezing a pimple where the scrotum defect developed 2 days later. More remotely in 1989, Slavis et al reported two cases of spontaneous rupture of testis secondary to suppurative epididymo-orchitis. However, both cases were initially treated with scrotal incision to drain the pyoceles and later the necrotic testicular tissue/seminiferous tubules were noted to be extruding from the incision sites. In contrast, there was no clear history of scrotal trauma or instrumentation in our case. The spontaneous breakthrough of underlying abscess suggests a severe localised inflammatory process.

There might be several explanations with regards to the rapid testicular abscess formation and infarction in our current case. First, on initial presentation, the inflamed epididymis was already significantly enlarged and could have impaired the testicular blood supply by compression of other spermatic cord contents. Second, resistant or atypical pathogens (brucella, tuberculosis, filariasis, cytomegalovirus) might be involved and thus not responsive to empirical antibiotic regime.^{15 23} Therefore, investigations for atypical pathogens should be performed when there is refractory epididymo-orchitis.²⁴ However, even though epididymo-orchitis is considered an infectious process, urine cultures are often negative.²⁵ Additionally, there may be underlying anatomical variations, that is, bell clapper anomaly that could predispose him to testicular infarction after infection. However, it is hard to prove these hypotheses retrospectively.

The major lesson from this current case is increasing awareness of testicular abscess formation, infarction or even rupture as a rare complication of commonly encountered epididymo-orchitis to GPs, ED physicians and urologists. One area of potential improvement is close clinical follow-up and reassessment with USS within 1 week of commencement of antibiotics for patients with high risks features, such as significant epididymal and testicular swelling posing risks to vascularity, severe inflammation manifested as induration of the spermatic cord, coexistent bacterial urinary infection, comorbidities like immune deficiency conditions or intravenous drug use.^{19 24} Routine grey scale USS has been suggested as a good predictor of complicated epididymitis requiring orchiectomy.²⁶ Colour Doppler, power Doppler and more recent advances like contrast-enhanced USS has been recommended as a low-risk, bedside examination that can evaluate tissue viability in cases where there is concern of evolving ischaemia.²⁷ Contrast-enhanced USS, despite not being widely available, is especially worthwhile if doppler sonography findings are equivocal. Before the advent of effective antibiotics, surgical decompressive procedures, for example, testicular/spermatic cord fasciotomy, epididymotomies and epididymectomies were in fact quite common to salvage the compromised vasculature.10 19 28 29 Witherington et al described their epididymotomy techniques over 40 years ago, which resulted in a testicular salvage rate of 86% (12/14) in select cases of progressive epididymo-orchitis. This involved an anterior scrotal incision through the parietal tunica vaginalis to expose the testicle, and then either a shallow vertical incision or multiple transverse incisions over the epididymis, with care to avoid the epididymal tubules.²⁸ In this day and age, this would rarely be required but should be in the urologist’s armamentarium for cases that do not respond to conventional treatment and show progressive worsening of vascularity on USS. Prompt adjustment of antibiotics regime based on microbiological findings by GP or infectious disease input without being delayed by repeat ultrasound are appropriate especially when symptoms persist or worsening over the week. The value of other medical treatments like anticoagulation (eg, pampiniform plexus thrombosis) need to be validated in further clinical trials.

Patient’s perspective.

I had symptoms after having sex. I don’t remember that I ever injured my testis. I knew something must be wrong when I noticed the discharge. I wish I would have come to the hospital earlier to avoid surgery.

Learning points.

• We hereby presented a rare case of testicular infarction with abscess and testicular rupture through the scrotal skin in a middle age man after acute acute epididymo-orchitis within 2 weeks.

• Empirical antibiotic regime (intravenous ceftriaxone +gentamicin, and oral azithromycin +ciprofloxacin) failed to prevent the rapid progression to abscess formation and infarction due to the severity of vascular comprise.

• Simple orchidectomy and partial scrotectomy were performed with good effect.

• Patient education is indispensable to return for medical care in the absence of clinical improvement

• Further management guidance is required in preventing testicular loss in severe infections. Early clinical follow-up within 1 week and reassessment with doppler/contrast-enhanced ultrasound scan should be considered in patients with high-risk features (compromise to testicular vascularity and low compliance/non-adherent to oral medications) to prevent this severe complication.

Ethics statements

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Consent obtained directly from patient(s).