Intraluminal obstruction of the large colon Philip Johnson, Veterinary Health Center, University of Missouri Simple digesta (‘feed’) impaction of the ascending colon represents one of the 2 most common causes of colic. In these cases, obstruction results from lodgment of either normal digesta or abnormal digesta (for example: coarse forage, sand, fecoliths, enteroliths) in the lumen (contents of the colon are normally quite fluidic). Anything that results in dehydration of digesta (lack of water) can contribute risk. Specific locations along the ascending colon that are most commonly implicated (narrowing is part of the normal anatomy at these locations): Pelvic flexure Transverse colon Alternatively, colonic impaction may occur at an area of the colon that is narrowed by a disease process (scar/stenosis) [good example is right dorsal colitis – often, significant fibrosis occurs as a complication of the condition and leads to significant reduction of the luminal diameter]. However, MOST ascending colon impactions are ‘simple’ and result from coarse dietary fiber loading into the large intestine. Predisposing factors to colon impaction include: Coarse food (straw bedding, late-cutting fibrous hay) Consumption of bedding (e.g. straw, shavings) Insufficient access to water (ice in winter) Too much distance to water source for old horses affected with OA Mastication failure (bad teeth, painful teeth) Dehydration (all causes)(colonic water is an important reservoir for the whole body) Protracted inappropriate recumbency (neurological disease, lameness, musculoskeletal injury, etc) Insufficient exercise Abnormal nerve function/structure in the enteric nervous system – there is some evidence that some colicprone horses have an abnormally low number of enteric nerve plexus nerves Drugs that interfere with normal motility – NSAIDs are included in this regard (e.g. phenylbutazone) Debilitation and emaciation Obesity Other diseases (abdominal tumor) There is a need for sufficient intestinal force (peristalsis) to “push” digesta through points of normal (or abnormal) narrowing. There is an optimal viscosity for colonic digesta. Viscosity may be increased by reduced fluid content (insufficient water or dehydration) or an increase in particle size (inadequate mastication, food type). Any factor that results in delay or inhibition of normal motility may promote additional water resorption from the digesta and increase its physical bulk (and viscosity). Once lodged (‘stuck’), the surrounding gut muscle will struggle to try to move the impaction in an aboral direction – in so doing, it causes the fluid component of the offending bolus to be squeezed out and to cause the impaction to become even drier and harder! The first response of the colon to the presence of dry digesta is to increase motility in an attempt to promote movement of the “clog”. This increased activity (pushing against the clog) results in signs of pain. Some gas and fluid transit may continue (the obstruction is not always complete). Therefore, colonic tympany does not necessarily develop, especially in early cases. The affected horse may continue to pass some manure. Signs of systemic inflammation/endotoxemia are unlikely with simple (early) colonic impaction. Significant systemic dehydration is also unlikely (unless the impaction occurred as a result of dehydration). Other signs (aside from pain and reduced passage of manure) include hypophagia, muscle fasciculations, altered facial expression (grimacing - orbital (eye) tightening, tension above the eyes, and stiff, turned back ears), and sweating (sometimes). Passage of manure gradually decreases and fecal balls become rounded and hard, sometimes covered with yellow mucus (a feature of intestinal stasis).
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