Pediatric emergency care · 2025
Pediatric Epididymitis With Atypical Evolution: A Case of Testicular Necrosis and Review of Management Strategies.
СтатьяКлинический случайОбзорНазвание и аннотация: Перевод в очереди
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Jaime Dávila Rodolfo, Cornelio Ramos José Isabel, Galván Hernández Fernando, Mata Rodrigo Romero, González Adrián Gutiérrez
Аннотация
INTRODUCTION: Acute epididymitis (AE) in children usually responds to conservative therapy. However, in rare cases (1% to 2%), it may progress to severe complications such as testicular infarction or necrosis due to vascular compromise. We report a case of progressive segmental testicular necrosis following presumed post-infectious AE after a recent viral respiratory illness.
METHODS: An 8-year-old boy presented with a 2-day history of left testicular pain, swelling, and erythema. Initial Doppler ultrasound revealed epididymal enlargement, hyperemia, and reactive hydrocele without signs of torsion. Urine culture was collected, and empirical ibuprofen and trimethoprim-sulfamethoxazole were prescribed.
RESULTS: Six days later, symptoms worsened with increased swelling and pain. Repeat Doppler ultrasound demonstrated hypoechoic avascular areas and reduced flow, consistent with necrosis. Urine, blood, and smegma cultures were negative. Surgical exploration revealed extensive testicular necrosis without torsion, leading to simple orchiectomy. Histopathology confirmed ischemic necrosis secondary to an inflammatory process. The observed evolution supports the concept of TCS, in which rising intratesticular pressure due to venous congestion and extraluminal compression within the noncompliant tunica albuginea leads to impaired microcirculatory perfusion and ischemic necrosis.
CONCLUSIONS: Testicular necrosis is an exceedingly uncommon but serious complication of AOE in children. Persistent pain, increasing testicular size, or poor clinical response should prompt early Doppler reassessment and consideration of surgical exploration. Recognition of TCS as a possible pathophysiological mechanism may help guide timely diagnosis and intervention to prevent irreversible ischemic injury.
METHODS: An 8-year-old boy presented with a 2-day history of left testicular pain, swelling, and erythema. Initial Doppler ultrasound revealed epididymal enlargement, hyperemia, and reactive hydrocele without signs of torsion. Urine culture was collected, and empirical ibuprofen and trimethoprim-sulfamethoxazole were prescribed.
RESULTS: Six days later, symptoms worsened with increased swelling and pain. Repeat Doppler ultrasound demonstrated hypoechoic avascular areas and reduced flow, consistent with necrosis. Urine, blood, and smegma cultures were negative. Surgical exploration revealed extensive testicular necrosis without torsion, leading to simple orchiectomy. Histopathology confirmed ischemic necrosis secondary to an inflammatory process. The observed evolution supports the concept of TCS, in which rising intratesticular pressure due to venous congestion and extraluminal compression within the noncompliant tunica albuginea leads to impaired microcirculatory perfusion and ischemic necrosis.
CONCLUSIONS: Testicular necrosis is an exceedingly uncommon but serious complication of AOE in children. Persistent pain, increasing testicular size, or poor clinical response should prompt early Doppler reassessment and consideration of surgical exploration. Recognition of TCS as a possible pathophysiological mechanism may help guide timely diagnosis and intervention to prevent irreversible ischemic injury.