Fulminant small bowel enteritis: A rare complication of Clostridium difficile-associated disease

To the Editor: A 54-year-old male was admitted to a community hospital with a 3-month history of diarrhea up to 8 times a day associated with bloody bowel motions and weight loss of 6 kg. He had no past medical history or family history of note. A clinical diagnosis of colitis was made and the patient underwent a limited colonoscopy which demonstrated continuous mucosal inflammation and ulceration that was most marked in the rectum. The clinical and endoscopic findings were suggestive of acute ulcerative colitis (UC), which was subsequently supported by histopathology. The patient was managed with bowel rest and intravenous steroids. However, he developed toxic megacolon on day 4 of his admission and underwent a total colectomy with end ileostomy. On the third postoperative day the patient developed a pyrexia of 39°C, a septic screen was performed, and the central venous line (CVP) was changed with the tip culturing methicillin-resistant Staphylococcus aureus (MRSA). Intravenous gentamycin was commenced and discontinued after 5 days, with the patient remaining afebrile and stable. On the tenth postoperative day the patient became tachycardic (pulse 110/min), diaphoretic (temperature of 39.4°C), hypotensive (diastolic of 60 mm Hg), and with a high volume nasogastric aspirates noted (2000 mL). A diagnosis of septic shock was considered although the etiology was unclear. The patient was resuscitated with intravenous fluids and transferred to the regional surgical unit for Intensive Care Unit monitoring and management. A computed tomography (CT) of the abdomen showed a marked inflammatory process with bowel wall thickening along the entire small bowel with possible intramural air, raising the suggestion of ischemic bowel (Fig. 1). CT demonstrating marked small bowel dilatation (a) and intramural air (b). However, on clinical assessment the patient elicited no signs of peritonism, his vitals were stable, he was not acidotic (pH 7.40), urine output was adequate, and his blood pressure was being maintained without inotropic support. Furthermore, his ileostomy appeared healthy and well perfused, although a high volume (2500 mL in the previous 18 hours), malodorous output was noted. A sample of the stoma output was sent for microbiological analysis. Given that the patient was not exhibiting evidence of peritonitis with normal vital signs, a conservative policy of fluid resuscitation was pursued with plans for exploratory laparotomy if he disimproved. Ileostomy output sent for microbiology assessment was positive for Clostridium difficile toxin A and B utilizing culture and enzyme immunoassays (EIA). Intravenous vancomycin, metronidazole, and rifampicin via a nasogastric tube were commenced in conjunction with bowel rest and total parenteral nutrition. The ileostomy output reduced markedly within 2 days and the patient's clinical condition improved. Follow-up culture of the ileostomy output was negative for C. difficile toxins. The patient was discharged in good health on full oral diet 12 days following transfer. Review of histopathology relating to the resected colon and subsequent endoscopic assessment of the retained rectum confirmed the initial diagnosis of UC, rather than a primary diagnosis of pseudomembranous colitis. Clostridium difficile is the leading cause of nosocomial diarrhea associated with antibiotic therapy and is almost always limited to the colonic mucosa.1 Small bowel enteritis secondary to C. difficile is exceedingly rare, with only 21 previous cases cited in the literature.2,3 Of this cohort, 18 patients had a surgical procedure at some timepoint prior to the development of C. difficile enteritis, while the remaining 3 patients had no surgical procedure prior to the infection. The time span between surgery and the development of enteritis ranged from 4 days to 31 years. Antibiotic therapy predisposed to the development of C. difficile enteritis in 20 of the cases. A majority of the patients (n = 11) had a history of inflammatory bowel disease (IBD), with 8 having UC similar to our patient and the remaining 3 patients having a history of Crohn's disease. The etiology of small bowel enteritis remains unclear. C. difficile has been successfully isolated from the small bowel in both autopsy specimens and from jejunal aspirate of patients with chronic diarrhea, suggesting that the small bowel may act as a reservoir for C. difficile.4 This would suggest that C. difficile could become pathogenic in the small bowel following a disruption in the small bowel flora in the setting of antibiotic therapy. This would be supported by the observation that the majority of cases reported occurred within 90 days of surgery with attendant disruption of bowel function. The prevalence of C. difficile-associated disease (CDAD) in patients with IBD is increasing. Issa et al5 examined the impact of CDAD in a cohort of patients with IBD. They found that more than half of the patients with a positive culture for C. difficile were admitted and 20% required a colectomy. They reported that maintenance immunomodulator use and colonic involvement were independent risk factors for C. difficile infection in patients with IBD. The rising incidence of C. difficile in patients with IBD coupled with the use of increasingly potent immunomodulatory therapies means that clinicians must have a high index of suspicion in the setting of profuse diarrhea in a patient with a history of IBD who has been on immunomodulators and undergone surgical intervention. Prompt microbiological input and targeted antibiotic therapy can lead to successful clinical resolution of a condition which, while rare, has a high reported mortality rate of 60%–83%.2