Case Presentation: A 19-year-old man with past medical history of recently incompletely treated H. pylori presented to the ED with severe abdominal pain, nausea, and vomiting for 20 days. Vital signs were normal, and physical exam was unremarkable. CT abdomen/pelvis showed diffuse gastric wall thickening with mucosal enhancement and mesenteric, gastrohepatic ligament, and para-aortic adenopathy. The differential included diffuse gastritis, Zollinger-Ellison syndrome, gastric lymphoma, and infiltrating adenocarcinoma. The patient received doxycycline, metronidazole, pantoprazole, and bismuth subsalicylate quadruple therapy for H. Pylori but failed to improve. EGD 6 days after admission showed diffuse severe mucosal changes characterized by congestion, erythema, erosion, and friability throughout the stomach and duodenal bulb. Pathology from the esophagus, stomach, and duodenum revealed significant enteritis, neutrophils, and no H. pylori. The final diagnosis made based on pathology was phlegmonous enteritis. The patient was continued on quadruple therapy and started on daptomycin and cefepime for broad-spectrum antibiotic coverage. The patient gradually became PO tolerant, advancing to a bland regular diet with no subsequent vomiting and minimal nausea. Follow-up EGD 6 days after initiation of broad-spectrum antibiotics showed significant improvement in inflammation grossly and on pathology. The patient was discharged on pantoprazole and symptomatic antiemetic medications with GI follow-up. Follow-up EGD 7 weeks after discharge showed an inactive body and antral gastritis and duodenal mucosa without diagnostic abnormalities.

Discussion: Phlegmonous enteritis is a rare and often fatal infective inflammatory disease of the intestines, with diffuse neutrophilic infiltration of the submucosal layer. It is frequently diagnosed at autopsy due to the difficult nature of making this diagnosis. Only about 200 cases have been reported in the literature. The average age at diagnosis is 68 years old. Etiologies of phlegmonous enteritis include sepsis and mucosal injury. Known risk factors for disruption of the mucosal barrier and phlegmonous enteritis are alcohol abuse, liver disease, or an immunocompromised state, which our patient lacked. We hypothesized that H. pylori infection may have been an inciting event for our patient. Very few cases have been reported in healthy patients, and almost none have been reported in young adults making this patient a unique case. Kim et al.’s review of cases reported from 1973 to 2003 demonstrated an overall mortality rate of 42% for 36 cases, with a 20% mortality rate for patients undergoing surgical resection vs. 50% with medical therapy alone. Due to the high mortality rate with medical therapy, gastrectomy was initially considered. However, given that he improved with antibiotics and reports in the literature of several cases of successful treatment with medical therapy alone, we elected to discharge the patient with close follow-up and without surgical resection.

Conclusions: Early diagnosis and treatment are essential to prevent morbidity and mortality from phlegmonous enteritis. While uncommon, hospitalists should recognize this lethal and difficult to diagnose entity and consider it in patients presenting with severe upper GI symptoms that are unexplained or fail to improve with conservative therapy. Early endoscopic evaluation, biopsy, and close pathology review were essential in making this diagnosis for our patient.