Aseptic Splenic Abscesses: Evaluating for Infectious versus Inflammatory Causes

Background: The development of splenic abscesses is a rare initial manifestation of Crohn’s disease. They can be multifocal and tend to occur in younger patients in the described literature. Differential diagnosis may include Behcet’s disease, primary infectious etiology, or rarely inflammatory bowel disease. About 50% of patients underwent splenectomy for management with improvement in symptoms. Several patients were maintained on targeted Crohn’s disease treatment following splenectomy to target mucosal healing. Methods: We report a 20-year-old female who presented for recurrent aseptic splenic abscesses of unclear etiology. She was initially hospitalized for LUQ abdominal pain and fever and was found to have large splenic abscesses and a small liver abscess. She was started on IV antibiotics with persistent fevers. Infectious disease evaluation was negative for endocarditis, toxoplasmosis, echinococcus, bartonella, anaplasma, babesia, ehrlichia, GI stool pathogens, HIV, and hepatitis. She required ICU care due to hemorrhagic shock following rupture of a splenic abscess. She underwent drainage of the abscesses without bacterial or fungal growth. She completed an extended course of antibiotics and outpatient immunodeficiency work-up was negative, including normal immunoglobulin levels, oxidative burst, and T cell studies. She felt well until 2 years later when she developed LUQ abdominal pain and imaging demonstrated recurrent splenic abscesses. Again, all infectious work-up was negative, and she improved with IV antibiotics. Results: Further work up with an MR enterography showed no evidence of inflammation in the small bowel or colon. EGD and colonoscopy showed numerous superficial ulcerations in the stomach and terminal ileum raising the possibility of early Crohn’s disease. Pathology demonstrated mild chronic inflammation in the antrum and body of the stomach; Normal esophageal mucosa; normal terminal ileum; focal acute colitis of the cecum, normal ascending and transverse colon, rare paneth cell metaplasia and focal cryptitis with crypt abscess of the descending colon without granulomas, normal sigmoid mucosa, and normal rectal mucosa. Video capsule endoscopy demonstrated numerous aphthous ulcers throughout the small bowel. Conclusions: The patient was diagnosed with Crohn’s disease of the small bowel and upper GI track. Although there was no evidence of penetrating disease, the occurrence of recurrent splenic abscesses may have formed in the setting of altered small bowel permeability due to ulceration leading to translocation of bacteria from the gut with local seeding. The patient was medically managed for her Crohn’s disease with vedolizumab. On 6-month follow up, there was not recurrence of abscesses. We discussed that splenectomy could be considered if biologic therapy was ineffective.