A Series of Cases With Pain as a Symptom of a Serious and Unexpected Pathology


Pyogenic Hepatic Abscess Presenting With Abdominal Pain

Stephen Brawley, MD, PhD
Portsmouth Family Medicine, Portsmouth, Virginia

Katie Buel, DO
Camp Lejeune Naval Hospital, Camp Lejeune, North Carolina


A 27-year-old man presented initially to a family medicine clinic concerning a 1-week history of nausea, vomiting, diarrhea, fevers, and night sweats. He reported that intermittent diffuse abdominal pain had started several days prior, which had localized to his right lower abdomen and later to his right upper abdomen. He also reported fevers, decreased appetite, and mild diarrhea. He was otherwise healthy with no significant past medical history and no recent travel history.

Hepatic Abscess figure

Upon examination, the patient was afebrile and reported diffuse abdominal pain and pinpoint tenderness located in the epigastrium. Bowel sounds were hypoactive. Initial laboratory test results showed mild transaminitis and a white blood cell count of 15,900/µL. He was started on a regimen of ciprofloxacin, 500 mg twice daily, and metronidazole, 500 mg twice daily, for presumed colitis.

Five days later, he presented to an emergency department with continued nausea, vomiting, diarrhea, and increased fatigue. Laboratory tests performed then showed continued leukocytosis (15,400 cells/µL) and mild transaminitis. Computed tomography scanning of the abdomen and pelvis with oral and intravenous contrast was performed at that time (Figure). The radiology report showed a multiseptated cystic mass in the left hepatic lobe, measuring 9.3 × 7.8 × 8.0 cm, with no significant portal adenopathy or calcification of septations, and questionable dilated bile ducts seen at the anterior aspect of the second hepatic segment, which could have been related to mass effect.

Based on the patient’s history and physical examination findings, his condition was presumed to be a late presentation of a ruptured appendix followed by the development of hepatic pyogenic abscesses.

Discussion. Bacterial abscesses of the liver are relatively rare. Pyogenic abscesses, which are most often polymicrobial, account for 80% of liver abscess cases in the United States.1 Appendicitis had been the most common cause of liver abscesses, but as diagnosis and treatment of appendicitis has advanced, its frequency as a cause of liver abscesses has decreased to 10%.1 New diagnostic radiologic techniques and improvements in microbiologic identification, drainage techniques, and supportive care have reduced the mortality rate of liver abscess to 5% to 30%.1 Today, pyogenic liver abscesses are most often a result of biliary tract disease.1

In addition to including appendicitis, the differential diagnosis for hepatic cysts also includes hepatocellular carcinoma (HCC), cystic echinococcosis (CE), cystic hepatic metastases, and mucinous cystic neoplasms (MCNs).

HCC is a primary hepatic malignancy that most often develops in persons with underlying chronic liver disease and cirrhosis but can develop in persons with hepatitis B virus infection whose livers are not frankly cirrhotic.2 In contrast, in patients with hepatitis C virus infection, HCC almost invariably presents in association with cirrhosis.2

CE is caused by accidental infection with larvae of the 2- to 7-mm long parasitic tapeworm Echinococcus granulosus found in dogs, sheep, cattle, goats, and pigs. Although most human infections are asymptomatic, CE can cause slowly enlarging cysts in the liver, lungs, and other organs that can grow unnoticed for years.3,4

Cystic hepatic metastases can cause new cystic liver lesions. The internal cystic component of a cystic hepatic mass can be the result of necrosis that occurs as the tumor outgrows its blood supply, or it may it comprise mucinous content similar to that of the primary tumor.5 Typically, hepatic metastases arise from organs that can seed the liver via the portal vein, including the gastrointestinal tract and the pancreas.5 Because cystic metastases usually are much less well-marginated, they can be readily differentiated from hepatic cysts.5

MCNs are rare liver lesions whose radiologic features include internal septa or septal thickening.6 An estimated 20% of cases of MCN undergo malignant transformation.7

Outcome of the case. The patient was admitted to the hospital, was started on intravenous antibiotics, and underwent drainage of the abscess. Test results for hepatitis virus and human immunodeficiency virus were negative. Cultures of the cyst showed no bacterial growth, possibly as a result of his prior course of antibiotics. He completed a prolonged course of ciprofloxacin and metronidazole at home. 


  1. Peralta R. Liver abscess. Medscape. http://emedicine.medscape.com/article/188802-overview. Updated June 20, 2016. Accessed March 21, 2017.
  2. Cicalese L. Hepatocellular carcinoma. Medscape. http://emedicine.medscape.com/article/197319-overview. Updated December 22, 2016. Accessed March 21, 2017.
  3. Brunetti E. Echinococcosis hydatid cyst. Medscape. http://emedicine.medscape.com/article/216432-overview. Updated April 8, 2015. Accessed March 21, 2017.
  4. Centers for Disease Control and Prevention. Parasites–echinococcosis. https://www.cdc.gov/parasites/echinococcosis. Updated December 12, 2012. Accessed March 21, 2017.
  5. Morgan MA. Cystic hepatic metastases. Radiopaedia. http://radiopaedia.org/articles/cystic-hepatic-metastases. Accessed March 21, 2017.
  6. Wahba R, Kleinert R, Dieplinger G, et al. Mucinous cystic neoplasm or non-parasitic liver cyst? A challenging diagnosis. Hepatogastroenterology. 2013;60(123):585-589.
  7. Grubor NM, Colovic RB, Atkinson HD, Micev MT. Giant biliary mucinous cystadenoma of the liver. Ann Hepatol. 2013;12(6):979-983.

NEXT: Hepatocellular Carcinoma Presenting With Knee Pain


Hepatocellular Carcinoma Presenting With Knee Pain

Fabiola Rios de Choudens, MD; Sowmya Nanjappa, MD; and Ebone Hill, MD
University of South Florida Morsani College of Medicine, Tampa, Florida


An otherwise healthy 18-year-old adolescent with no significant past medical history developed acute-onset pain in the anterior left knee after jogging. After experiencing ongoing pain for several weeks, he was evaluated at his local emergency department (ED), where he received a diagnosis of a knee sprain after the results of a radiograph of the knee were negative for fracture.

The knee pain persisted, and the patient was seen by an orthopedic surgeon, who presumptively diagnosed a torn meniscus. A few weeks later, the patient was reevaluated at a different ED, where repeat knee radiographs (Figure 1) revealed a pathologic fracture of the left femur. He was transferred to a cancer treatment center for further evaluation.

Hepatocellular Carcinoma figure 1
Figure 1. Radiograph showing a left proximal femur fracture.

He was a nonsmoker, and he denied the use of alcohol. His body mass index was normal, and he had no complaints of weight loss. He was taking no prescribed or over-the-counter medications or supplements, and he had no family history of cirrhosis or liver disease. Physical examination findings were unremarkable, and his vital signs were stable.

Computed tomography (CT) scanning with contrast of the abdomen was done to evaluate for primary malignancy, and the results revealed multiple hepatic masses, with the largest measuring 9.5 × 7.4 × 8.6 cm (Figure 2), as well as a destructive lesion in the left sacral ala; magnetic resonance imaging with contrast revealed an enhancing mass surrounding the proximal left femur (Figure 3). He underwent biopsy and intramedullary nailing of his left femur.

Hepatocellular Carcinoma figure 2
Figure 2. Contrast CT scan of the abdomen showing a left hepatic lobe tumor measuring 9.5 × 7.4 × 8.6 cm.

Hepatocellular Carcinoma figure 3
Figure 3. Contrast magnetic resonance imaging showing a left lytic femur lesion.

Pathology results of the biopsy revealed metastatic hepatocellular carcinoma (HCC) in noncirrhotic liver. Serologic test results for hepatitis B and C viruses were negative, his α1-fetoprotein level was 121,000 ng/mL, and the results of liver function tests were normal. He received radiation to his bone metastases, followed by chemotherapy with cisplatin, doxorubicin, fluorouracil, interferon alfa-2b, and leucovorin.

However, he was readmitted 3 weeks later with intractable nausea and vomiting as a result of gastric outlet obstruction due to compression from the large hepatic tumor. He underwent hepatic artery chemoembolization followed by chemotherapy.

Follow-up CT scans 2 months later showed decrease in the size of the liver metastases. He continued on chemotherapy for 4 months. Unfortunately, follow-up CT scans at 4 months showed progression of bony metastasis, and he began receiving palliative osseous radiation.

Discussion. Malignancies can arise in persons of any age, ranging from newborns to the geriatric population. However, adolescents with cancer have been stuck in limbo, because they are not grouped with either the pediatric group or the adult group of patients with cancer.

In the United States, older adolescents and young adults (15-44 years) with cancer are increasingly being approached as a distinct group owing to their unique medical and psychosocial needs. The most common malignancies in this age group, which accounts for 10% (or roughly 117,000) of all patients with cancer, are lymphoma, sarcoma, leukemia, and testicular cancer.1 Gastrointestinal tract tumors are rare and account for only 5% of cancers in the pediatric population.2

HCC is the most common primary cancer of the liver in adults, and its incidence is increasing.3 Cirrhosis is the major risk factor for the development of HCC, along with other viral, toxic, metabolic, and immune-related risk factors.3 In children, hepatoblastoma accounts for the majority of liver tumors, and HCC is the second most common; in adolescents, HCC is the most common primary hepatic malignancy.4,5 While underlying liver disease predisposes patients to the development of HCC, the majority of HCC cases in children and adolescents arise de novo and are usually not related to underlying liver cirrhosis,6 such as in our patient’s case.

In the adult population, HCC commonly presents as hepatomegaly with associated dull and aching epigastric pain. Symptoms may be accompanied by rapid weight loss and weakness.7 In children and adolescents, HCC can present differently, with symptoms ranging from asymptomatic abdominal mass to abdominal pain and constipation.

Laboratory studies may detect elevated levels of α1-fetoprotein, ferritin, and carcinoembryonic antigen; definitive diagnosis is achieved by way of biopsy.8

Our patient presented with an atypical case of lower extremity pain as a direct consequence of a rare malignancy in an adolescent: He had a pathologic fracture, had no predisposing factors to or family history of HCC, and had no gastrointestinal tract symptoms. This case illustrates the challenges encountered by health care providers when an adolescent presents with a common complaint such as left knee pain, and the possibility that the etiology unexpectedly could be a malignancy. Our patient was evaluated on multiple separate occasions, and it was not until a pathologic fracture was found that a malignancy was considered as the etiology of his knee pain.

Adolescents and young adults with malignancies are underrepresented in clinical trails of therapies that could impact survival, and their mortality rates have shown little improvement compared with those of the pediatric and adult populations. Mortality and survival trends in the US adolescents with cancer have lagged behind annual improvement in the 5-year survival rate compared with other age groups.9 Compared with pediatric patients, only approximately 5% of cancer patients aged 15 to 25 years are enrolled in clinical trials.10


  1. Bleyer A, Budd T, Montello M. Adolescents and young adults with cancer: the scope of the problem and criticality of clinical trials. Cancer. 2006;107(7 suppl):1645-1655.
  2. Subbiah V, Varadhachary G, Herzog CE, Huh WW. Gastric adenocarcinoma in children and adolescents. Pediatr Blood Cancer. 2011;57(3):524-527.
  3. Gomaa AI, Khan SA, Toledano MB, Waked I, Taylor-Robinson SD. Hepatocellular carcinoma: epidemiology, risk factors and pathogenesis. World J Gastroenterol. 2008;14(27):4300-4308.
  4. Walther A, Tiao G. Approach to pediatric hepatocellular carcinoma. Clin Liver Dis (Hoboken). 2013;2(5):219-222.
  5. Litten JB, Tomlinson GE. Liver tumors in children. Oncologist. 2008;13(7):​812-820.
  6. Czauderna P, Mackinlay G, Perilongo G, et al; Liver Tumors Study Group of the International Society of Pediatric Oncology. Hepatocellular carcinoma in children: results of the first prospective study of the International Society of Pediatric Oncology group. J Clin Oncol. 2002;20(12):2798-2804.
  7. Czauderna P. Adult type vs. childhood hepatocellular carcinoma—are they the same or different lesions? Biology, natural history, prognosis, and treatment. Med Pediatr Oncol. 2002;39(5):519-523.
  8. Otte J-B. Progress in the surgical treatment of malignant liver tumors in children. Cancer Treat Rev. 2010;36(4):360-371.
  9. Ferrari A, Montello M, Budd T, Bleyer A. The challenges of clinical trials for adolescents and young adults with cancer. Pediatr Blood Cancer. 2008;50(5 suppl):1101-1104.
  10. Bleyer WA. Cancer in older adolescents and young adults: epidemiology, diagnosis, treatment, survival, and importance of clinical trials. Med Pediatr Oncol. 2002;38(1):1-10.

NEXT: Leiomyoma Presenting With Pain, Dyspnea, and Fever


Leiomyoma Presenting With Pain, Dyspnea, and Fever

Ingrid Jones-Ince, MD, and Charles P. Murrah, MD
Tallahassee Memorial HealthCare, Tallahassee, Florida


A 56-year-old woman presented to the emergency department (ED) with a 3-day history of fever, chills, myalgia, progressive dyspnea, right-sided pleuritic chest pain, and a dry cough on a background of a 4-month history of dyspnea and malaise. She denied weight loss, nausea, vomiting, diarrhea, hemoptysis, wheezing, or upper respiratory tract symptoms.

She had no sick contacts and no recent travel history. She was a nonsmoker who denied the use of illicit drugs and alcohol. Her medical history was significant for hypertension and gastroesophageal reflux. Her family history was pertinent for cancer of unknown primary origin. She worked as a home health assistant. Her symptoms had worsened, prompting her visit to the ED.

Physical examination. Her vital signs were stable except for a pulse of 112 beats/min, a respiratory rate of 24 breaths/min, a temperature of 38.3°C, and an oxygen saturation as measured by pulse oximetry (Spo2) of 92%.

Examination of the respiratory system revealed moderate respiratory distress, increased vocal fremitus in the right lower lung field, egophony in the right lower lung base, and dullness to percussion in the right lower lung base with bronchial breath sounds. During the initial examination, she developed sudden-onset dyspnea with persistent tachycardia and pain in the right leg. Pulmonary embolism (PE) was considered as a differential diagnosis, because her Wells score was 6 points (≤ 6 indicates a moderate probability of PE; > 6 indicates a high probability). Thus she underwent helical computed tomography (CT) scan of the chest.

Diagnostic tests. Laboratory test results showed leukocytosis (12,400 white blood cells/µL) without bandemia. Tests results for influenza A and B were negative. Results of blood cultures and sputum cultures were noncontributory. Results of arterial blood gas testing on room air were pertinent for acute respiratory alkalosis with hypoxemia, a pH of 7.59, and an Spo2 of 89%. Hemoglobin and hematocrit levels, basic metabolic panel results, and serial cardiac enzyme levels were unremarkable.

Chest radiographs demonstrated a right lower lobe infiltrate consistent with pneumonia. Helical CT scan of chest demonstrated a questionable endobronchial lesion involving the right lower lobe, measuring 15 × 10 mm.

Once the patient’s pneumonia had resolved on a 7-day course of ceftriaxone and azithromycin (intravenous and then oral), an elective bronchoscopy was performed, the results of which revealed an almost perfectly spherical, 3 × 2-cm, whitish gray, rubbery, glistening, encapsulated lesion at the stoma of the right lower lobe bronchus that was fairly or minimally vascular.

Bronchial cytology test results were negative for malignancy. The histopathology report of the right lower lobe bronchial mass showed benign bronchial mucosa overlying a benign spindle cell proliferation (Figure), a finding compatible with leiomyoma, and clinical correlation was advised. Of note, a pelvic sonogram revealed a 1.7 × 1.6 × 1.7-cm hypoechoic region in the uterine fundus, consistent with a small fibroid.

Figure. Low-power view of smooth, whorled fascicles of muscle bundles, actin positive, with overlying ciliated pseudostratified columnar epithelium with goblet cells, consistent with endobronchial leiomyoma.

A right lower lobectomy was performed with the idea that distal atelectasis would be a persistent problem in light of her 4-month history of respiratory symptoms and her 87% occlusion of the right lower lobe bronchus. No mitoses or cytologic atypia were found, and nuclei were bland. Immunohistochemistry results revealed the spindle cells to be 4+ positive for desmin, negative for CD34, negative for CD117, and positive for actin, with no evidence of gastrointestinal stromal tumor.

Discussion. Endobronchial leiomyomas are rare, benign tumors that account for 33% to 45% of all pulmonary leiomyomas.1 In a case series, Kwon and colleagues2 described cough, dyspnea, and fever as the major symptoms in pulmonary leiomyomas. Our patient demonstrated this clinical presentation.

CT is an excellent tool for delineating endobronchial tumors in the bronchial tree. Its sensitivity to detect obstructive lesions ranges from 60% to 100%.3 Leiomyomas have an attenuation of 25 to 46 Hounsfield units on unenhanced CT and 46-85 Hounsfield units on contrast-enhanced CT.1 However, “iceberg” tumors (small endoluminal component, large extraluminal component) have been documented in 15% of leiomyoma cases, the differential diagnosis of which includes carcinoid and mucoepidermoid carcinomas.1,3 Most benign endobronchial tumors produce nonspecific masses in the wall of the airways, except for lipomas, which can show fat, and cartilaginous tumors, which can show calcium. Four cases of leiomyomas with calcification have been reported.4

Bronchial leiomyomas are benign tumors that predominantly occur in the fourth decade of life, with a female preponderance. They are thought to arise from the smooth muscle cells of the bronchial wall and the interstitium of the arterioles. The definitive diagnosis can be made via bronchoscopy, which enables visualization of the lesion and sampling for histopathologic diagnosis. Histologic criteria, including cellularity, mitotic activity, and pleomorphism, have been proposed to differentiate benign from malignant smooth muscle neoplasms, but the principle criterion is mitotic activity being less than 5 mitoses per 50 high-power fields.5

The optimal management of such tumors remains undefined, although bronchoscopy, local excision, and partial tracheal resection have been performed. The aim of treatment is complete resection to prevent recurrence.6 Fiberoptic bronchoscopy is the best modality for the examination of the endoluminal and mucosal lesions of the respiratory tract, but it is limited in determining the extraluminal component and airway patency distal to the involved area of bronchial stenosis.

Novel noninvasive modalities that can assist in visualization from multiple angles include virtual bronchoscopy and 3-dimensional reconstruction of high-resolution CT.3,4 Historically, surgical management has been considered the standard treatment modality; however, less-invasive procedures have been reported as safe alternatives, including simple bronchoscopic removal with or without laser, bronchoplasty, or bronchotomy utilizing sleeve resection of the involved bronchus while sparing distal lobectomy. Parenchymal resection is appropriate if there is a solitary parenchymal nodule or end-stage infection distal to the obstruction.7 However, a few case series and a single case have been published illustrating the use of bronchoscopic techniques, including electrocautery, snare excision, Nd:YAG laser, and cryotherapy.8

A retrospective study2 documented treatment methods and outcomes of 10 patients with tracheobronchial leiomyoma who underwent bronchoscopic intervention between 2000 and 2007 at a single center—9 patients underwent Nd:YAG laser surgery, and 1 underwent flexible bronchoscopy. Two patients later underwent surgical resection due to late tumor recurrence. In the remaining 8 of 10 patients who were successfully treated with bronchoscopic intervention, clinical outcome was good during the median follow-up period of 24.5 months. There were no procedure-related mortalities or late complications.

Shigematsu and colleagues9 described the removal of a 60-year-old woman’s tracheal tumor by flexible bronchoscopy with electrocautery using a wire snare. Postoperative bronchoscopy results showed complete opening of her trachea and subsequent improvement in pulmonary function.

Cryosurgery is a promising treatment modality for benign airway neoplasms. Tan and colleagues10 reported a first-ever case of complete bronchoscopic cryosurgical resection of a leiomyoma in a 55-year-old Chinese male nonsmoker who presented with chronic cough, left-sided pleuritic chest pain, and weight loss. This technique illustrated the cryopreservation of the tumor’s histologic morphology. Surveillance bronchoscopy performed 6 months later revealed no tumor recurrence.

Take-home message. Solitary pulmonary nodules may present symptomatically, and one should probe the etiology behind recurrent pathology such as recurrent pneumonia or persistent atelectasis.

Our patient continues to thrive, and she is in good health with no evidence of recurrence to date.


  1. Kim YK, Kim H, Lee KS, et al. Airway leiomyoma: imaging findings and histopathologic comparisons in 13 patients. AJR Am J Roentgenol. 2007;​189(2):​393-399.
  2. Kwon YS, Kim H, Koh W-J, et al. Clinical characteristics and efficacy of bronchoscopic intervention for tracheobronchial leiomyoma. Respirology. 2008;13(6):908-912.
  3. Finkelstein SE, Schrump DS, Nguyen DM, Hewitt SM, Kunst TF, Summers RM. Comparative evaluation of super high-resolution CT scan and virtual bronchoscopy for the detection of tracheobronchial malignancies. Chest. 2003;124(5):1834-1840.
  4. Ko SM, Han SB, Lee SK, et al. Calcified endobronchial leiomyoma. Br J Radiol. 2007;80(953):e91-e93.
  5. Swarnakar R, Sinha S. Endobronchial leiomyoma: a rare and innocent tumour of the bronchial tree. Lung India. 2013;30(1):57-60.
  6. Macchiarini P. Primary tracheal tumors. Lancet Oncol. 2006;7(1):83-91.
  7. Cárdenas-Garcia J, Lee-Chang A, Chung V, Shim C, Factor S, Tibb A. Bronchial leiomyoma, a case report and review of literature. Respir Med Case Rep. 2014;12:59-62.
  8. Bharadwaj SC, Unruh HW. Leiomyoma of the trachea. Ann Thorac Surg. 2012;93(2):669-670.
  9. Shigematsu H, Andou A, Rai K, Higashi R. Leiomyoma of the trachea. Eur J Cardiothorac Surg. 2008;34(3):674.
  10. Tan JHY, Takano AM, Hsu AAL. Resection with preserved histologic morphology of a rare tumour via bronchoscopic cryosurgery. J Thorac Dis. 2016;8(10):2964-2967.

NEXT: Epididymo-orchitis Complicated by Testicular Infarction Presenting With Scrotal Pain


Epididymo-orchitis Complicated by Testicular Infarction Presenting With Scrotal Pain

Eiyu Matsumoto, MB; Ryan L. Steinberg, MD; and Elizabeth B. Takacs, MD
University of Iowa Carver College of Medicine, Iowa City, Iowa

Jennifer R. Carlson, PA-C, and Mack H. Longmire, MD
Iowa City Veterans Affairs Health Care System, Iowa City, Iowa


A 69-year-old man with history of hypertension and diabetes presented to the emergency department (ED) with 3-day history of left scrotal pain. He denied fever, chills, back pain, or dysuria. He was not sexually active.

Urinalysis results were positive for large leukocyte esterase and nitrite, 2+ positive for bacteria, and had a white blood cell count of more than 100 per high-power field. Point-of-care ultrasonography showed an enlarged left epididymis with increased vascular flow on color Doppler imaging. Blood flow to the left testicle seemed sustained, and there was no hydrocele.

The patient received a diagnosis of epididymitis presumed to be from enteric organisms. Trimethoprim-sulfamethoxazole (TMP-SMX) was prescribed. Urine cultures grew Escherichia coli susceptible to TMP-SMX.

Eight days after the initial visit, however, the patient returned to the ED with persistent left scrotal pain.

Physical examination. On evaluation at this ED visit, his vital signs were as follows: blood pressure, 160/84 mm Hg; heart rate, 85 beats/min; respiratory rate, 18 breaths/min; temperature, 36.6°C; and oxygen saturation, normal.

Physical examination revealed an uncircumcised penis and a right testicle without swelling or masses. The left hemiscrotum was erythematous and swollen and blanched to palpation, with the patient reporting mild pain. The left testicle was not definitively palpable. The prostate was normal in size and shape on digital rectal examination.

Scrotal ultrasonography revealed a large, complex hydrocele with thick scrotal skin tissue (Figure 1). Doppler color flow was increased to the surrounding scrotal soft tissue (Figure 2). The left testicle measured 4.1 × 2.2 × 2.9 cm, with no blood flow indicated by color flow and spectral Doppler imaging.

Epididymo-orchitis figure 1

Epididymo-orchitis figure 2

Outcome of the case. Urgent surgical exploration was performed. Intraoperative findings consisted of a scrotal pyocele containing purulent drainage, along with extensive peritesticular and spermatic cord inflammation with resultant massive testicular infarction and twisting of the cord. A diagnosis of severe epididymo-orchitis complicated by pyocele and testicular infarction was made. Left scrotal orchiectomy with drain placement was subsequently performed, after which the patient’s condition improved.

Discussion. Acute epididymitis is a clinical syndrome comprising pain, swelling, and inflammation of the epididymis that lasts less than 6 weeks.1 Epididymitis is common in all age groups, occurs with equal frequency in either testicle, and has no racial predilection.2

Patients with epididymitis often present with a painful scrotum with unilateral swelling developing over a few days.3 Many patients have dysuria, urethral discharge, fever, an erythematous swollen scrotum that is tender, and leukocytosis. One study reported that urine bacterial cultures were positive in only 24% of patients with epididymo-orchitis, of whom 35% were younger than 30 years of age.4 For this reason, empiric antibiotic treatment is indicated. Frequently, concomitant orchitis and inflammatory hydrocele develop.4

Presumably, epididymitis occurs secondary to retrograde flow of infected urine into the ejaculatory duct.1 Up to 80% of epididymitis cases may be bacterial in origin. In men younger than 35 years, sexually transmissible pathogens such as Chlamydia trachomatis and Neisseria gonorrhoeae are the most common culprits.5 In older men aged 35 years and older, the coliform organisms that cause urinary tract infections are predominant, with E coli being most common, followed by Klebsiella and Pseudomonas species.5,6

When evaluating scrotal pain, it is essential to differentiate testicular torsion from acute epididymitis, because testicular torsion has a high risk of testicular infarction if surgical treatment is delayed. Typically, a patient with testicular torsion will present with a more sudden onset of pain.7 Scrotal ultrasonography with color Doppler imaging is the study of choice in evaluating the acute scrotum.8 In a study of patients with acute scrotal pain, color Doppler imaging had a sensitivity of 70% and a specificity of 88% in the diagnosis of epididymitis.9 Sensitivity was 82% and specificity was 100% in the diagnosis of testicular torsion.9 Urine cultures and polymerase chain reaction techniques are vital for identifying causative pathogens.

Treatment of uncomplicated epididymitis consists of empiric antibiotic and supportive measures such as nonsteroidal anti-inflammatory drugs, scrotal elevation, cold packs, and analgesics. For presumed sexually acquired epididymitis, single doses of ceftriaxone and azithromycin or doxycycline for 10 days in combination are used. The patient’s sexual partners also should be treated. For older populations, coverage for enteric organisms can be achieved with fluoroquinolones for 10 days.1,3

Acute epididymitis usually resolves rapidly. However, complications such as intratesticular and epididymal abscess, testicular infarction, testicular atrophy, and systemic infection/sepsis can occur.3 Abscess formation is rare and occurs in less than 3% of cases.10 Severe epididymitis is thought to lead to testicular ischemia due to inflammatory involvement of the cord and extrinsic compression of the testicular blood vessels by an edematous epididymis.11 Testicular hypoperfusion, shown by nuclear scanning or Doppler imaging, has been used to identify testicular ischemia to select patients for surgical exploration.12

Complication rates are higher in older men with bacteriuria and those with urologic abnormalities.10,13 No improvement after 3 days of treatment should prompt reassessment.3 Features suggesting a lack of response include sepsis, pronounced scrotal edema, severe testicular pain, and scrotal wall fixation.14

Although culture results showed infection with E coli susceptible to TMP-SMX, the clinical efficacy of this antibiotic when used for epididymo-orchitis has not been established; its use, along with the patient’s risk factors of age and bacteriuria, may have contributed to treatment failure in this case.


  1. Tracy CR, Steers WD, Costabile R. Diagnosis and management of epididymitis. Urol Clin North Am. 2008;35(1):101-108.
  2. Mittemeyer BT, Lennox KW, Borski AA. Epididymitis: a review of 610 cases. J Urol. 1966;95(3):390-392.
  3. Luzzi GA, O’Brien TS. Acute epididymitis. BJU Int. 2001;87(8):747-755.
  4. Kaver I, Matzkin H, Braf ZF. Epididymo-orchitis: a retrospective study of 121 patients. J Fam Pract. 1990;30(5):548-552.
  5. De Jong Z, Pontonnier F, Plante P, et al. The frequency of Chlamydia trachomatis in acute epididymitis. Br J Urol. 1988;62(1):76-78.
  6. Berger RE, Alexander ER, Harnisch JP, et al. Etiology, manifestations and therapy of acute epididymitis: prospective study of 50 cases. J Urol. 1979;121(6):750-754.
  7. Jefferson RH, Perez LM, Joseph DB. Critical analysis of the clinical presentation of acute scrotum: a 9-year experience at a single institution. J Urol. 1997;158(3):1198-1200.
  8. Herbener TE. Ultrasound in the assessment of the acute scrotum. J Clin Ultrasound. 1996;24(8):405-421.
  9. Wilbert DM, Schaerfe CW, Stern WD, Strohmaier WL, Bichler KH. Evaluation of the acute scrotum by color-coded Doppler ultrasonography. J Urol. 1993;​149(6):1475-1477.
  10. Eickhoff JH, Frimodt-Møller N, Walter S, Frimodt-Møller C. A double-blind, randomized, controlled multicentre study to compare the efficacy of ciprofloxacin with pivampicillin as oral therapy for epididymitis in men over 40 years of age. BJU Int. 1999;84(7):827-834.
  11. Owen ER, Kitson JL, Green B. Venous infarction of the testis secondary to acute epididymitis. Br J Urol. 1990;65(1):107-108.
  12. Rencken RK, du Plessis DJ, de Haas LS. Venous infarction of the testis—a cause of non-response to conservative therapy in epididymo-orchitis: a case report. S Afr Med J. 1990;78(6):337-338.
  13. Krishnan R, Heal MR. Study of the seminal vesicles in acute epididymitis. Br J Urol. 1991;67(6):632-637.
  14. Witherington R, Harper WM IV. The surgical management of acute bacterial epididymitis with emphasis on epididymotomy. J Urol. 1982;128(4):722-725.