Etiology
The etiology of these different disorders is bacterial proliferation
in the small intestinal lumen secondary to either anatomic or functional
stasis or to a communication between the relatively sterile
small intestine and the colon with its high levels of aerobic and
anaerobic bacteria. Several examples of anatomic stasis have been
identified: (1) one or more diverticula (both duodenal and jejunal)
( Fig. 294-3 C ); (2) fistulas and strictures related to Crohn’s disease
( Fig. 294-3 D ); (3) a proximal duodenal afferent loop following a
subtotal gastrectomy and gastrojejunostomy; (4) a bypass of the
intestine, e.g., jejunoileal bypass for obesity; and (5) dilation at the
site of a previous intestinal anastomosis. These anatomic derangements
are often associated with the presence of a segment (or
segments) of intestine out of continuity of propagated peristalsis,
resulting in stasis and bacterial proliferation. Bacterial overgrowth
syndromes can also occur in the absence of an anatomic blind loop
when functional stasis is present. Impaired peristalsis and bacterial
overgrowth in the absence of a blind loop occur in scleroderma,
where motility abnormalities exist in both the esophagus and small
intestine (Chap. 323). Functional stasis and bacterial overgrowth
can also occur in association with diabetes mellitus and in the small
intestine when a direct connection exists between the small and
large intestine, including an ileocolonic resection, or occasionally
following an enterocolic anastomosis that permits entry of bacteria
into the small intestine as a result of bypassing the ileocecal valve.