Today's case was of a 70-year-old man with a history of possible inflammatory bowel disease who
presented with a two-week history of bloody diarrhea, abdominal pain and
tenesmus. The patient was admitted to
internal medicine for workup.
We spoke about a lot
of valuable points:
The differential diagnosis
of bloody diarrhea depends very heavily on whether the process is acute or chronic. Acute bloody diarrhea
has only three things on the differential diagnosis: infection, infection, and
infection. Chronic bloody diarrhea has a
few more diagnostic possibilities:
· Infection – this can be with bacterial
organisms that cause invasive disease (e.g. Salmonella,
Shigella, E. coli, Campylobacter, Yersinia, and sometimes C. difficile), rarely with viral
organisms in an immunocompetent host, but CMV is certainly seen, occasionally
with fungal or parasitic organisms like E.
histolytica.
· Inflammatory causes – this would include Crohn
disease or Ulcerative colitis. Do not discount these as diagnostic
possibilities in an older individual as there is a bimodal peak in the
incidence of IBD with the second peak occurring in the 6th and 7th
decades.
· Vascular causes – Ischemic colitis can occur as
a result of global hypoperfusion as in the case of shock or selective
vasopressors that can induce gut ischemia, embolic or atherothrombotic
phenomena are also possible.
Microvascular causes as a result of vasculitides can also cause bloody
diarrhea.
· Drug-related – Certainly diarrhea can occur as
a result of laxative overuse, but also bloody diarrhea can be the result of
sympathomimetic drugs like amphetamines.
Antiplatelet and anticoagulant agents can certainly predispose to mucosal
bleeding as well.
· In our TGH population, it’s important to
remember Graft-versus-host disease as well as radiation-induced colitis.
· A myriad of other causes can lead to lower-GI
bleeding including hemorrhoids, colonic angiodysplasia, microscopic colitis,
and diverticular disease.
We spoke about some of
the extraintestinal manifestations of inflammatory bowel disease such as:
· Fevers and constitutional symptoms
· Iritis/Uveitis
· Arthritis (of which there is an oligoarticular
variant related to disease activity, and a polyarticular variant not related to
disease activity)
· Skin manifestations: Erythema nodosum and
pyoderma gangrenosum
· Anemia
· Primary sclerosing cholangitis (UC only)
· Apthous ulcers (Crohn only)
· Sequele of chronic inflammatory processes: Deep-vein
thrombosis, AA amyloidosis
· Colon cancer (risk is much greater with UC)
· Fistulization (risk much greater with Crohn)
We also spoke about
differentiating factors between the two inflammatory bowel diseases:
· Crohn disease can involve any portion of the GI
tract from mouth to anus, and typically spares the rectum whereas UC is limited
to the rectum and colon
· Crohn disease can have “skip lesions” where
portions of discontinuous GI tract are affected whereas UC tends to start in
the rectum and continue proximally until normal mucosa is reached
· Crohn disease causes transmural granulomatous
inflammation and fistulization whereas UC causes mucosal inflammation.
· The pathologic and endoscopic appearances of
the colonic lesions can be quite different
Ultimately, treatment
of these patients will be done in consultation with a specialist in IBD. The treatment differs quite greatly between
the two entities, and immunomodulatory medication such as TNF-alpha inhibitors
are becoming more popular choices. The
general rule when someone presents to the emergency department with something
compatible with an IBD flare would be to first ensure stability by giving
resuscitation fluid and treating overt consequences of hypovolemia. Then, infection and major consequences such
as toxic megacolon are ruled out, as
these are life threatening emergencies.
If an infectious etiology isn’t identified quickly, then the chances are
that the patient requires immunomodulatory therapy usually with steroids,
followed by a maintenance agent. In UC,
the severity of the flare tends to dictate the therapy – milder flares are
treated with 5-ASA preparations, whereas more serious flares require oral or
parenteral glucocorticoids.
Further Reading:
Greenstein, A. J.,
Janowitz, H. D., & Sachar, D. B. (1976). The extra-intestinal complications
of Crohn's disease and ulcerative colitis: a study of 700 patients. Medicine,
55(5), 401-412.
Podolsky, D. K.
(1991). Inflammatory bowel disease. New England Journal of Medicine, 325(13),
928-937.
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