# FulminantClostridiumdifficile Enteritis after Proctocolectomy and Ileal Pouch-Anal Anastamosis

Authors: Elena Boland; Jon S. Thompson
Journal: Gastroenterology Research and Practice
 (2008)

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## Abstract

Clostridium difficile (C. difficile) infection of the small bowel is very rare. The disease course is more severe than that of C. difficile colitis, and the mortality is high. We present a case of C. difficile enteritis in a patient with with ileal pouch-anal anastamosis (IPAA), and review previous case reports in order to better characterize this unusual condition.


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## Body

## 1. Introduction

C. difficile infection is  associated with antibiotic-induced pseudomembranous  colitis. This
infection   is usually thought to be restricted to the colon. Isolated small
bowel C. difficile enteritis is rare and can manifest in the absence of
a colon.C. difficile has been shown to colonize
small bowel mucosa in about 3% of the population, which then serves as a
reservoir for infection [1].
Most carriers are  asymptomatic. Altered intestinal anatomy
and  antibiotic use have been implicated in triggering symptomatic infection. Fecal
flora in the small bowel of patients who had undergone a colectomy is altered
to resemble that of the colon. Morphological changes (colonic-type metaplasia
with partial villous atrophy) which occur in the mucosa of an ileal pouch
secondary to altered fecal flow may predispose to infection [2]. These
factors may increase small bowel colonization by C. difficile.
Alteration of fecal flora by antibiotic can trigger symptomatic infection.The clinical
presentation ofC. difficile colitis is typically mild, occasionally progressing to fulminant colitis. The
disease course is more fulminant when small bowel is affected, with reported
mortality ranging from 60–83% [3].
We report a case of fulminant
C. difficile enteritis in a patient with ileal pouch-anal anastamosis (IPAA), and review
previous reports of this unusual condition.


## 2. Report of A Case

A 42-year-old man underwent
proctocolectomy with IPAA and ileostomy for medically refractory ulcerative
colitis (UC). The patient returned for ileostomy takedown six months later. His
hospital course was complicated by a urinary tract infection, which was treated
with ciprofloxacin. The patient was discharged tolerating a regular diet with
good bowel function. The patient returned 10 days later complaining of a three-day
history of nausea, diarrhea, and abdominal pain. Patient was febrile (38.3°C),
tachycardic (138), with elevated white blood cell count (17.000), creatinine
(2.5), and platelet count (1450). CT scan of the abdomen showed dilated small
bowel with fluid and air to the ileoanal anastomosis. Blood, urine, and stool
cultures were sent, and empiric intravenous piperacillin/ tazobactam and vancomycin were
started. However, the patient became progressively more septic and required
vasopressors for blood pressure support. Unexpectedly, C. difficile enzyme immunoassay (EIA) came back positive for toxins
A
and B, and the patient started on oral vancomycin and metronidazole. Flexible endoscopy
was performed and revealed copious amounts of mucus with adherent
pseudomembranes throughout the pouch and distal small bowel (Figure 1). Over
the next few days, the patient remained in critical condition, but then slowly
stabilized. Vasopressors were weaned; WBC and creatinine came down to normal limits. Within 7
days of  admission, patient was restarted on a diet and was ultimately
discharged after a 12-day hospitalization. At one year follow up, the patient
still occasionally has frequent bowel movements, but his stool cultures have
remained negative for C. difficile toxins.Flexible endoscopy of pelvic pouch
demonstrating copious amounts of mucus with adherent pseudomembranes throughout
the pouch and distal small bowel, consistent withC. difficile infection.
(a)(b)(c)(d)


## 3. Discussion

PubMed literature search forC. difficile enteritis was performed  and revealed 26 cases from 1980–2008 (Table 1)
[3–22].
There was significant age variability, with a range of 18 to 83 years of age
(mean 50.3). Sixteen of the 26 patients had inflammatory bowel disease (IBD), thirteen
patients had ulcerative colitis, and three had Crohn’s disease. Ten patients
had total colectomies and six underwent IPAA. All but three patients had
altered intestinal anatomy. Twenty four patients had recent hospitalization
and/or operation as well as recent antibiotic use. Thirteen patients were
septic and required ICU admission. In all 26 cases, the stool assays were positive
for C. difficile toxin. Diagnosis of small bowel involvement was made
based on biopsy,
pathology, or autopsy results. Only seven patients were evaluated endoscopically.
Four underwent flexible sigmoidoscopy, and three of those had pseudomembranes.
Of the patients with IPAA, only two were examined endoscopically and no
pseudomembranes were visualized. One patient had an esophagogastroduodenoscopy
(EGD) which demonstrated pseudomembranes in the duodenum. Treatment in all but two
patients included metronidazole or vancomycin, or a combination of both. Two
patients were resistant to metronidazole. Fourteen of the 26 underwent operative
intervention. Mortality rate was 35%.Table 1
Previously
reported cases of small bowelC. difficile.
AuthorAgeIBDIntestinal operationRecent hospitalization/operationRecent AbxICU/SepsisOREndoscopyTreatmentDeathNotes1LaMont and Trnka [4] 198023Crohn'sPartial colectomyNoNoNoNoEGD—pseudomembranes in
duodenumVancomycinNo2Shortland et al. [5] 198370NoIleal conduitYesYes—NoSigmoidoscopy—pseudomembranesVancomycinYes3Testore et al. [6] 198469NoAPRYesYesYesNo——Yes4Miller et al. [7] 198918No—YesYesYesYesFlexible sigmoidoscopy—inflammation; no pseudomembranesStreptomycinNo2 jejunal perforations5Kuntz et al. [8] 199353UCTACYesYesYesYes—Vancomycin, flagylYesIntramural gas on CT6Tsutaoka et al. [9] 199466NoRt hemicolectomy + APRYesYesYesYes—Vancomycin, flagylYes7Yee et al. [10] 199671NoTACYesYesYesYes—FlagylYes8Kralovich
et al. [11] 199765NoJejunal-ileal bypassYesYesYesYesFlexible sigmoidoscopy—pseudomembranesVancomycin, flagylYes9Vesoulis
et al. [12] 200056Crohn'sTPCYesYesYesYes—FlagylNo10Freiler
et al. [13] 200126UCTACYesYesNoNo—FlagylNo11Jacobs et al. [14] 200183——YesYes—Yes——No12Tjandra
et al. [15] 200160NoSigmoid colectomyYesYesYesYesFlexible sigmoidoscopy—pseudomembranesVancomycin, flagylYes13Mann et al. [16] 200335UCIPAANoNoNoNoFlexible endoscopy—inflammed, ulcerated mucosaVancomycin; resistant to flagylNoChronic pouchitis14Hayetian et al. [17] 200680NoLARYesYesYesYes—FlagylYesIleal perforation15Hayetian et al. [17] 200683NoNoneYesYesYesYes—Vancomycin, flagylNoIleal perforation16Kim et al. [18] 200765Crohn'sTPCYesYesYesNo—FlagylYes17Lundeen et al. [3]
(6 patients) 2007Mean 35.3UC (6 patients)3 IPAA3 TAC6/66/61/61/6—Vancomycin, flagylNo18Wood et al. [19] 200848UCIPAAYesYesYesYesFlexible endoscopy—normal pouchFlagylNo19Follmar et al. [20] 200849UCIPAAYesYesNoYes—Vancomycin, resistant to
flagylNoOr–mesh removal20Fleming et al. [21] 200854UCTACYesYes?No—Flagyl, vancomycin, rifampinNo21Yafi et al. [22] 200821UCTACYesYes?Yes—VancomycinNoPelvic abscessTotal50.316/2623/2624/2624/2613/2614/267/2621/269/26Our patient was
similar to the previously reported cases ofC. difficile enteritis in that he had a history of IBD, recent surgery,
and antibiotic use. He required ICU admission secondary to sepsis, but he did
not require operative intervention. Unlike any of the previously reported
cases, our patient’s pouch endoscopy revealed pseudomembranes, facilitating
timely intervention and his ultimate recovery.C. difficile enteritis appears to have a
fulminant course, with high risk of sepsis, need for operation, and mortality.
It is unclear why the disease course is more severe than in colitis. Increased
small bowel permeability is one potential explanation. Delay in diagnosis and
treatment may play a role as well.The clinical presentation
can be similar for both enteritis and colitis. Symptoms include diarrhea,
dehydration, and increased ileostomy output. Unlike colitis, enteritis more
commonly presents with systemic manifestations such as fever, hypotension,
leukocytosis and thrombocytosis [3], and occasionally with peritonitis
or bowel perforation [7, 17].C. difficile enteritis may be difficult to
differentiate from other inflammatory processes, and requires high degree of
suspicion to make the diagnosis.
C. difficile has also been implicated as a cause of chronic pouchitis in patients with IPAA [16],
and should be suspected in this setting. Given the higher risk that IBD
patients may have for developing
C. difficile enteritis, it is important to be able to differentiate it from an exacerbation
of IBD. Diagnosis is made by identifying
C. difficile toxin
A or B in the stool. Similarly, endoscopy should be utilized in patients with
suspected small bowel involvement even with history of prior colectomy. This
may facilitate differentiation between Crohn’s enteritis, pouchitis, and
C. difficile enteritis.As with our
patient, most cases will respond to treatment with metronidazole or vancomycin.
However, more virulent and resistant strains have been reported [23].
Some patients will need emergent surgical resection of any perforated or
gangrenous bowel if they fail to respond to medical treatment.C. difficile enteritis is emerging with increased
frequency and can have devastating results. Patients with IBD and prior
colectomy are at increased risk. Prompt identification of the organism via
stool culture and endoscopy may result in more favorable outcomes.



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