Abstract
A 21-year-old healthy female EMT presented with 10 days of watery diarrhea and 3 days of abdominal pain and fever. She denied any recent antibiotic use or travel. Physical exam was notable for a diffusely tender abdomen without rebound or guarding. Labs were significant for: Hb 10.1, WBC 13.2, Na 125, Cr 0.5, ALS/AST 117/227, and CK 45K. Initial CT showed diffuse mural thickening of the large bowel without evidence of pneumatosis or obstruction. She was started on ciprofloxacin and metronidazole until the stool sample resulted positive for C. difficile at which point she was started on Vancomycin PO & PR and metronidazole IV. Over the next week the patient's fever resolved and her WBC, ALT/AST, CK began to normalize but her diarrhea and distention persisted. Serial Abdominal x-rays showed continued colonic distention. Patient had also developed notable anasarca. Repeat CT at day 7 showed pneumatosis and air fluid levels concerning for toxic megacolon. Patient was then transferred to our center for fecal transplant evaluation however shortly after arrival she noted abruptly increased abdominal pain with a markedly tender and distended abdomen. Urgent CT showed free intraperitoneal air. She was taken to the OR and underwent a colectomy with end ileostomy. Colon pathology was consistent with fulminant colitis, without signs of underlying IBD. She was eventually discharged from the hospital and is planned for an ileostomy reversal after 6 months. Our patient appeared to develop protein-losing enteropathy with anasarca, and toxic megacolon with perforation, an uncommon but potentially lethal complication of C. difficile colitis. It is very unusual to see such a dramatic, severe C. difficile infection in a young, healthy patient. Our patient's prolonged watery diarrhea, elevated AST/ALT and CK, suggest a co-existing viral gastroenteritis which may have put her at increased risk. There is some data that suggest that C. difficile infection with concomitant viral infection leads to a higher C. difficile bacterial burden through an unknown mechanism. We hypothesize that concomitant viral gastroenteritis potentially disrupts colonic flora and promotes C. difficile overgrowth. The recently introduced multiplex molecular assays for GI pathogens may aid in identifying GI co-infections in non-nosocomial C. difficile patients and may help elucidate possible mechanisms for the higher C. difficile burden.1571_A Figure 1. CT demonstrating distended colon1571_B Figure 2. CT demonstrating perforation of colon1571_C Figure 3. Colon pathology performed after resection with Colonic mucosa, ulcerated (central area of photo) with surrounding acute and chronic inflammation including prominent lymphoid aggregates (greater on left side of the image).
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