Traumatic injuries to the genitalia are relatively uncommon and rarely result in life-threatening circumstances [1]. In cases of testicular injury, blunt scrotal trauma is responsible for 75% of the reported cases; of these, most result from sports injuries, vehicle accidents and assault [1]. Regardless of the severity and mechanism of injury, immediate assessment of the genitalia is warranted to rule out testicular torsion or rupture. Other diagnoses of concern include urethral injuries, hematomas and epididymitis. One study looked at acute scrotal pain in boys under 17 years of age and found that testicular torsion, torsion of a testicular appendage, and epididymitis accounted for 94% of the diagnoses [2]. While most cases of epididymitis are the result of bacterial infection, some may present 2 to 3 days after trauma due to forceful compression of the testis against the pubic bones [3].
Once ultrasonography rules out the need for surgical intervention, scrotal injuries can be managed conservatively with ice, elevation, and analgesics [1]. In one study of external genital injuries during childhood, 66.5% involved the scrotum or its contents and 73.1% were managed with conservative treatment [4]. In our patient surgical intervention was never warranted because of the absence of torsion, significant hematoma, testis rupture, or abscess. It is generally believed that scrotal injuries are not life-threatening and are more concerning for their long-term complications [5]. In this case, despite conservative management and empiric antibiotics, our patient's condition worsened over the first days and progressed to SIRS requiring life-saving intervention.
SIRS, as defined by the American College of Chest Physicians and Society of Critical Care Medicine, requires that two or more of the following conditions are present: temperature >38°C or <36°C; heart rate >90 beats/minute; respiratory rate >20 breaths/minute or PaCO2 <32 torr; WBC >12,000 cells/mm3, <4000 cells/mm3, or >10% band forms. In the presence of proven infection, the term 'SIRS' becomes 'sepsis'. The difference in terminology arises from the observation that trauma patients with or without infections have similar outcomes, suggesting the body's overall response is more predictive of clinical course than the particular organism or mechanism of injury [6]. Noninfectious causes of SIRS include acute pancreatitis, burns, trauma, or major elective surgery [7].
Upon initial presentation our patient met four of the SIRS criteria, and while no culture evidence of bacteremia or abscess was found, it was difficult to distinguish between culture-negative SIRS versus noninfectious SIRS. Presently there is no specific or sensitive test to distinguish between the two diagnoses due to the expansive and overlapping systemic responses in infection and trauma [7], making medical management difficult and potentially delaying recovery. Our patient never showed symptoms of a urinary tract infection, did not have risk factors for sexually transmitted infections, and did not develop signs of an abscess, giving us no reason to suspect sepsis as opposed to SIRS.
Our patient's history of trauma without other underlying medical conditions led to the belief that his diagnosis of SIRS was the result of a cytokine storm released from direct trauma to the scrotum. Although the testis is an immune-privileged site, it is not completely protected from local and systemic activators of inflammation [8]. The theory behind cytokine storms lies in the ability of the immune system to control the response to injuries or infection. A cytokine storm is a potentially fatal immune reaction consisting of a positive feedback loop between cytokines and immune cells [9]. Cytokines, such as tumor necrosis factor-α, interleukin-1, and toll-like receptors, are highly involved in the activation and progression of the inflammatory response system [9]. Additionally, these same cytokines have been studied in the role of Leydig cell steroidogenesis, and thus are not only present in macrophages, T cells, and other circulating immune cells, but are also in Sertoli cells and developing germ cells of the testes [8]. Consequently, severe trauma to the scrotum and its contents can lead to a release of pro-inflammatory mediators with the potential to become overwhelming and systemic in nature. Testing for cytokines is not routinely performed and our patient was not tested. In view of the lack of laboratory confirmation of cytokine responses in our patient, the interpretation of cytokine storm cannot be made with certainty.
Current studies of immune regulation include potential therapies for combating SIRS before patients suffer severe complications. Mortality increases with increasing numbers of SIRS criteria present in a patient; in one study mortality doubled in patients with SIRS to 6% compared to those without, and increased to 17% in those matching four criteria [6]. Thus far, transcription factors such as nuclear factor-κB and activating protein have been targeted as possible treatment options for these patients [9]. However, these options are not currently available for therapeutic use. It may still be unwise to suppress the immune system, even without evidence of infection; thus we propose that the standard of care should include empiric antibiotics without immune suppression.
