Case Presentation: 39-year-old female with a history of ulcerative colitis (UC), but not on therapy, presented with abdominal pain and hematochezia for two weeks, along with weight loss and night sweats. On admission, vital signs were notable for tachycardia and physical examination revealed a diffusely tender abdomen. Laboratory studies were remarkable for leukocytosis of 23,250/mm3. Due to presentation suggesting a UC flare, IV methylprednisolone was initiated. CT scan of abdomen revealed liver, splenic, and pancreatic abscesses, raising concern for disseminated infection or malignancy. Steroids were held and broad-spectrum antibiotics were initiated. After a few days, patient clinically worsened—developing fevers, vomiting, increased leukocytosis, and worsening hematochezia. Subsequently, antimicrobial regimen was broadened. Colonoscopy showed colitis but no malignancy. Despite follow-up imaging with MRI abdomen showing significant decrease in size of abscesses, patient continued to have multiple bloody stools, abdominal pain, nausea and vomiting. Cultures from a splenic abscess and pelvic free fluid sample were negative. Diagnostic testing revealed no infectious etiology, including sterile cultures and negative infectious work-up. After discussion with infectious disease and gastroenterology, IV methylprednisolone was restarted due to concern for aseptic abscesses (AA) as an extraintestinal manifestation of IBD. Patient had decreased bloody stool output and overall clinically improved. Two months later, CT abdomen showed resolution of liver and pancreatic abscesses and interval decrease of splenic abscesses.
Discussion: Extraintestinal manifestations of inflammatory bowel disease (IBD) include autoimmune hepatitis, primary sclerosing cholangitis, portal fibrosis/cirrhosis, and acute pancreatitis. Pyogenic liver abscesses occur in 114–297 per 100,000 patients with Crohn’s disease; even fewer case reports exist in UC. Our patient presented with AA which is a rare complication of IBD. Case reports have shown aseptic liver and splenic abscesses associated with IBD, but little data exists regarding pancreatic abscesses. Our patient was treated solely with broad-spectrum antimicrobials. After a negative infectious work-up, steroids were restarted, which is the standard of care for UC flare management. Patient showed further clinical improvement and resolution of abscesses. Her clinical presentation was mostly consistent with aseptic abscesses syndrome (AAS) characterized by abdominal pain, weight loss, fever, sterile abscesses, and lack of clinical improvement despite antibiotics. On antibiotics, she clinically worsened but her abscesses decreased in size, suggesting an unclear picture given that AAS does not respond to antibiotics. There are currently no guidelines regarding treatment of AA associated with IBD. Options of treatment from the literature range from corticosteroids and immunotherapy to splenectomy, with corticosteroids as the most effective treatment option. AA are often misdiagnosed as an infection and could lead to overuse of antimicrobials and delay of UC flare treatment.
Conclusions: Aseptic abscesses are a rare and serious extraintestinal manifestation in IBD. Hospitalists must consider AA when patients with IBD develop deep abscesses, regardless of the type of IBD. Future research should be geared toward developing guidelines to approaching and treating AA in UC to avoid unnecessary procedures and delayed care.