Toxic megacolon secondary to Clostridium difficile
colitis.
Important points regarding the history
of patients with this condition include:
Toxic megacolon is defined as a severe attack of colitis involving
the large bowel and accompanied by total or segmental dilatation of the colon.
Two features must be present: systemic toxicity and dilatation of the large
bowel. Although most commonly a complication of inflammatory bowel disease,
toxic megacolon may also complicate infectious colitis, as well as ischemic
colitis, diverticulitis, volvulus, and obstructive colon cancer (Visual1).
Clostridium difficile colitis (symptomatic) occurs in about 1% of all
patients admitted to hospital. The most common presentation is low grade fever,
abdominal pain, and watery diarrhea, occuring after 5 days of hospitalization,
usually after the administration of antibiotics. A few of these patients may
develop severe colitis with toxic megacolon (9). This is what happened to
our patient. Why some patients develop severe disease and others have mild
or asymptomatic infection is related to host factors and not to strain differences.
Rubin et al. identified the following factors as predisposing to severe C.
difficile colitis: malignancy, COPD, renal failure, clindamycin use, and
antiperistaltic drugs. The asymptomatic carrier state is related to serum
antibodies to the toxin. These anti-toxin antibodies prevent disease but not
colonization or infection.
Important points regarding the physical
examination in patients with this condition include:
As in our patient, the usual findings of toxic megacolon are
abdominal distension, tenderness, fever, tachycardia and postural hypotension.
The patient may also have altered consciousness. In patients with known C.
difficile colitis, these features are associated with a worse outcome.
Localized tenderness and rebound tenderness may suggest impending perforation;
generalized tenderness with guarding and rebound tenderness strongly indicates
a free perforation. Percussion of the right upper quadrant demonstrating loss
of hepatic dullness may be the first clinical evidence of a perforation complicating
toxic megacolon. The most widely used criteria for the clinical diagnosis
of toxic megacolon were proposed by Jalan et al. (Visual2).
Important points regarding the laboratory
tests in patients with this condition include:
As in our patient, the laboratory can provide evidence of
the etiology of the colitis and evidence of the severity of the systemic response.
All patients who present with severe colitis with systemic toxicity should
have stools examined by culture (salmonella, shigella, campylobacter), microscopy
(ameba), and C. difficile toxin. A leukocytosis with a left shift is
usually present unless there is a disordered immune response (AIDS, immune
supression). Electrolyte disturbances are very common and multifactorial.
Metabolic alkalosis secondary to volume depletion and potassium loss is associated
with a poor prognosis.
The abdominal flat plate showed a diffusely air filled colon,
with air in the recto-sigmoid (small arrows), transverse (medium arrow) and
cecum (large arrow). Although the recto-sigmoid bowel wall appeared thickened,
no frank thumbprinting could be seen. The largest colonic diameter in our
patient's xray is about 6 cm. The abdominal x-ray is a crucial study in diagnosing
and managing toxic megacolon. The most prominent feature is colonic dilatation.
The upper limit of normal for the width of the transverse colon is 6cm. Many
patient's have more dramatic radiographic findings than were demonstrated
in our paient, such as more widely dilated colon and complete absence of haustal
folds. Dilatation of the colon in and of itself may be a nonspecific finding.
Thus, even though a maximum colonic diameter signifies megacolon, the overall
clinical condition of the patient is more important in diagnosis of toxic
megacolon than the absolute width of the dilated segment. There is little
need for ultrasonography and CT in the diagnosis and management of toxic megacolon.
A recent study showed that bowel distension on abdominal radiograph
was a very important prognostic feature in severe ulcerative colitis (8).
The endoscopy demonstrated the
following features:
The short look into our patient's rectum did not alter the
management much. It rapidly confirmed the diagnosis of pseudomembranous colitis.
An endoscopic examination provides more useful diagnostic information in patients
who are presenting for the first time with colitis and in whom it may be of
some help in differential diagnosis (i.e. infectious colitis versus inflammatory
bowel disease). If performed, the scope should not be passed above 20 cm,
nor should air be insufflated. A full colonoscopy is extremely risky and should
generally be avoided.
The pathology slides showed the
following important diagnostic features:
The pathology is presented primarily for teaching purposes.
The unique lesion of C. difficile colitis (resembling a volcanic eruption)
provides a striking contrast to the mucosal inflammation and crypt abscesses
seen in bacterial colitis or inflammatory bowel disease.
Other important teaching points about this condition include
the following:
The goals of treatment of toxic megacolon are to reduce the
severity of colitis, to restore normal colonic motility, and to decrease the
likelihood of perforation. The bowel should be completely rested, and a nasogastric
tube should be placed to decompress the gastrointestinal tract. All antimotility
agents, narcotics, and anticholinergics should be discontinued. The offending
antibiotic needs to be stopped and intravenous metronidazole or oral vancomycin
should be started to treat the Clostridium difficile. Present et al.
reported successful colonic decompression by changing body position ("rolling")
in 19 of 19 patients with toxic megacolon secondary to inflammatory bowel
disease. In this study, the patients were rolled to the prone position for
10-15 minutes every 2-3 hours, in addition to the usual intensive medical
regimen. There is scant data on endoscopic colonic decompression of toxic
megacolon. Banez et al. reported on one patient with ulcerative colitis and
toxic megacolon who was successfully decompressed by colonoscopy and left
with an indwellling colonic tube. Subtotal colectomy is reserved for patients
who do not respond within 48-72 hours, or who show evidence of perforation.
Trudel et al. reviewed patients with toxic megacolon due to C. difficile
seen between 1968 and 1992. The overall mortality was 31-35%, including 42%
for surgically and 18% for medically treated patients.
