A recent systematic review of atraumatic splenic rupture found there to be six major etiological groups: neoplastic processes (30.3%), infectious (27.3%), inflammatory (20.0%), iatrogenic (9.2%), mechanical (6.8%), and normal spleen (6.4%) [1]. ASR of the normal spleen is defined #GDC-0449 chemical structure randurls[1|1|,|CHEM1|]# by four criteria: no history of trauma, no evidence of extrasplenic disease known to affect the spleen, no perisplenic adhesions to suggest previous trauma, and normal spleen on gross and histologic

exam [3]. Clinical presentation of ASR mimics traumatic splenic rupture. Abdominal pain, especially in the left upper quadrant, or chest pain with radiation to the left shoulder, caused by subdiaphragmatic irritation, are classic symptoms of splenic pathology. There is often little or no clinical history to suggest splenic pathology, and the diagnosis is often made after imaging, which often includes ultrasonography or CT scan [4]. There are no definitive guidelines on management of ASR, although it is often modeled after that of traumatic splenic rupture. Treatment may include operative or non-operative therapy, depending

upon the patient’s hemodynamic stability and degree of splenic injury. The large amount of fluid within the abdomen could support operative evaluation with exploratory laparotomy. Factors favoring non-operative management in this case included total clinical TGF-beta inhibition stability, a soft abdomen, and duration of greater than 24 hours from the inciting event. The American Association for the Surgery of Trauma criteria for degree of splenic injury correlates with failure of conservative treatment. Given that a splenic etiology was not confirmed until the ultrasound after discharge, his injury could not be graded. At the time of follow-up, the subcapsular hematoma measured less than 10% of the surface area, consistent with a grade 1 injury [5]. Even in the setting of non-operative management, surgical teams

are often involved or are the primary team managing inpatient surveillance. Work-up in patients very with ASR should include studies to rule out the common causes, including neoplastic, infectious, and inflammatory processes. As this patient’s work-up was negative, we conclude that the patient had a normal spleen with ASR and associate the splenic rupture with cocaine use. Cocaine use remains epidemic and is associated with a wide range of medical complications. The well-studied physiologic effects of cocaine include increased norepinephrine reuptake with sustained alpha-adrenergic receptor stimulation and resultant vasoconstriction. Cocaine-associated vasoconstriction was shown to transiently reduce splenic volume on average by 20% [6]. This vasoconstriction transiently elevates blood pressure. In addition, increased abdominal venous pressure due to cough could suggest an inciting event for splenic hemorrhage in this patient.