An 11-year-old male with no past medical history, travel history, or family medical history presented with a 6-week history of gradually worsening periumbilical pain and two weeks of nonbilious vomiting, nonbloody diarrhea, and fever. History was negative for extra-intestinal symptoms such as joint pain or swelling, oral ulcers, eye pain, or skin rash. His physical exam was significant for diffuse abdominal tenderness but guarding or distention. Computerized tomography (CT) scan of abdomen and pelvis showed signs of inflammation in the ascending and transverse colon, and a contained bowel perforation (Figure 1). Laboratory investigation was significant for white blood cell count of 6 thou/cu mm (normal 4.5-13.5 thou/cu mm), hemoglobin of 9.9 g/dL (normal 11.5-15.5 g/dL), C-reactive protein of 221 mg/L (normal 0-5 mg/L), albumin of 2.5 g/dL (normal 3.5-5.2 g/dL), ferritin of 9 ng/mL (normal 24-336 ng/mL), and negative PCR stool studies for viral, bacterial, and parasitic infection. Fecal calprotectin was significantly elevated, at >1250 mug/g (normal 0-50 mug/g). We suspected a diagnosis of IBD versus a prior severe infectious colitis that was not detectable by stool PCR testing. Because the patient did not have free air in the abdomen or peritoneal signs, laparotomy was deferred and the patient received 14 days of broad-spectrum antibiotics, which lead to resolution of abdominal pain, vomiting, diarrhea, and fever.
After completing antibiotics, esophagogastroduodenoscopy (EGD) and colonoscopy revealed grossly normal intestinal mucosa, with biopsy findings of focal active ileitis and colitis, nonspecific and insufficient for diagnosis of IBD. Intestinal tuberculosis was considered, but QuantiFERON-TB test was negative, and imaging and histology did not support this diagnosis. 4th-generation IBD diagnostic test (commercial in US PROMETHEUS) which combines serologic, genetic, and inflammation markers including 9 serological markers: ASCA IgA, ASCA IgG, and proprietary markers anti-Fla-X, anti-A4-Fla2, anti-CBir1, anti-OMPC, and DNAse-sensitive pANCA that helps identify patients with IBD was negative for IBD, and repeat fecal calprotectin, serum inflammatory markers, complete blood count, and albumin had all normalized, without any treatment for IBD. The patient then developed daily bloody stools and was started on infliximab based on symptoms and ileal inflammation on MRE, though need for further testing with wireless capsule endoscopy was being planned to further solidify diagnosis. Several weeks after initiating treatment for IBD, the patient presented with worsening of abdominal pain and fever. A CT scan revealed signs suggestive of a 7.6 x 4.3 x 7 cm phlegmon adjacent to the bowel in the right lower abdomen.
With work-up not definitive for IBD, other causes for intra-abdominal abscess were considered, and concern for Meckel's diverticulum was raised. A technetium 99 m scan was obtained, and findings were consistent with Meckel's diverticulum (Figure 3). Nine months after this patient's onset of symptoms, laparoscopic exploration was performed, and a Meckel's diverticulum was identified. At the time of surgery, there was no abscess and no sign of perforation. The diverticulum was covered by a rind of inflammatory tissue, and the location of this inflammatory mass was concordant with the location of the phlegmon on the aforementioned CT scan. Another finding at the time of surgery was the presence of adhesions. Resection diverticulectomy with side-to-side anastomosis was performed. Histology confirmed this diagnosis. Patient's abdominal pain and hematochezia resolved after surgery. The patient was followed for 15 months after surgery and has remained asymptomatic since then.