Intraluminal Obstructions of the Large Colon

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).

Left untreated, an obstruction may eventually become complete and result in tympany (with distention of the abdomen). Pressure at the site of impaction may lead to necrosis of the adherent mucosa that could cause endotoxemia. Protracted anorexia may lead to significant dehydration (worsening the situation in the colon). Unrecognized or untreated, colonic displacement may occur (especially right displacement). Similarly, unrecognized or untreated, colonic rupture is a possibility.

Physical examination findings: Lethargy, hypophagia, and pain (initially intermittent) Reduced borborygmi (percussion may elicit local tympany) Reduced passage of manure (becoming drier) Dehydration and darkening membranes (endotoxemia) – in the later stages, if unresolved. Abdominal distention (‘bloat’) – in the later stages, if unresolved. NG reflux – usually negative

Per rectum abdominal palpation: Impaction can often (but not always) be detected Quantity of manure in rectal lumen is decreased (or absent) Manure may be small in quantity (+ hard and covered with mucus) It is not always possible to detect colonic impaction on palpation

Abdominocentesis: PF is usually normal Increased protein concentration and evidence of inflammation may be present in advanced (protracted) cases.

Routine labs: PCV and plasma total solids may increase as a result of dehydration (and pain, in the case of PCV). Mature leukocytosis (mature neutrophilia) occurs because of stress. Might see degenerative changes and leucopenia in advanced cases if there is disruption of the mucosal lining Elevated blood lactate concentration may be detected if there is bodily dehydration.

Treatment: • NPO (if the horse is not inappetent, small meals might help promote GI motility)(failure to provide any food leads to diminishment of motility). Important to NOT feed horse much until the obstruction has been relieved (especially following administration of analgesics) – otherwise the obstruction simply gets bigger! • Analgesia – as needed. The two most commonly used drugs include flunixin meglumine (Banamine™) and xylazine hydrochloride (Rompun™). Other analgesic drugs may be employed sometimes. • Laxative/stool softening strategies. • Walking or light exercise during treatment.

Recommend enteral fluid therapy to restore hydration, stimulate peristalsis (gastro-colic reflex) and promote rehydration of impacted colonic digesta. Recommend employment of an enteral electrolyte solution [49 g of sodium chloride; 37.8 g of sodium bicarbonate; 7.4 g of Lite Salt™; 10 liters of water]. Can run the enteral fluid therapy as a CRI [5 – 10 ml/kg/h for 2 h, then increase rate to 10 - 15 ml/kg/h]. Check to make sure that no more than 1-2 liters can be retrieved from the stomach via the NG tube at 30 minutes following stopping CRI. If there is >2 l, stop flow and reduce the rate.

Consider IV fluid therapy More expensive. Not as ‘effective’ as the enteral method for rehydrating impacted digesta. Restores hydration and promotes hydration of the colonic digesta (does NOT stimulate peristalsis directly but promotes colonic perfusion).

Must use IV route (or per rectum route) whenever reflux is present (but reflux is not typical for a simple colon impaction). If necessary for systemic circulatory therapy, fluids can also be administered per rectum (that method will not directly rehydrate colon impaction, however).

Surgical treatment is not usually required. Surgical treatment should be considered for refractory cases, in the face of developing tympany, and in those cases in which structural failure may be occurring (follow up PF). Consider surgical treatment when the conservative approach has not resolved the problem within 48 h. Surgical intervention may also be considered for extremely large-sized impactions (thus staving off the risk of GIT rupture).

Observe carefully for resolution – usually requires 24-48 h: Signs of improvement include increasing borborygmi, softening of impaction (based on results of palpation), increased passage of manure (passing softer manure), comfortable facial expression, and reduced/absent signs of pain (especially when pain relieving medication effect has diminished). If needed for dehydration/hypovolemia, positive results of fluid therapy may include improvement in mucous membranes, strength of peripheral arterial pulses, urination, and resolution of hyperlactatemia.

Feeding the patient? It is important to NOT allow the patient to eat too much during management of colic. Holding the patient NPO for a while is a common treatment, allowing time for fluids and stool softeners to relieve the impaction. Treatment with analgesic drugs (such as Banamine™) will relieve pain and the patient’s appetite usually returns. However, if the patient is allowed to eat under the influence of Banamine™, new ingesta may ADD to the size of the obstruction and further pain will resume when the effect of Banamine™ wears off. Also, the size of the impaction will be much bigger! Following a period of NPO during the early stages of an impaction treatment, some small quantities of food may be allowed. Such small feedings may be helpful by stimulating colonic peristalsis (gastro-colic reflex). We usually allow the patients to graze a little grass for a few bites or they may be offered a small volume (handful) of grain/Senior ration. Alternatively, a hay net is sometimes ‘hung’ on the outside of the bars of the stall – it serves to remind the patient about food, stimulate appetite and allow a small amount of ingestion through the stall bars. Some people like to spread a few handfuls of hay on the stall bedding and let the horse ‘work’ to find and eat it.

Prognosis for ascending colon impaction: Favorable. Note that recurrence is possible, even likely, in an individual patient (idiosyncratic predisposition). Some contend that there exists an initial predisposition associated with either damage to the gut (idiopathic) or an idiosyncratic abnormality in the enteric nerve plexuses. Others suggest that the presence of one impaction that resolved may cause some damage to the enteric nerve plexuses that serves to increase the risk for recurrence. It is important to identify risk factors and, through client education, and to do one’s best to eliminate those risk factors. Commonly encountered risk factors (listed above) include insufficient water access (ice in winter), dental issues, rough/coarse forage, change of forage source, insufficient exercise, drug treatments for osteoarthritis/laminitis (phenylbutazone), protracted recumbency (neurological comorbidity), geosediment, parasites, etc.

OTHER If a case of colonic impaction does not appear to be responding to conservative treatment, consider other causes of colonic (intra-luminal) obstruction or causes of extra-luminal colonic obstruction (such as displacements, volvulus, etc). Other underlying causes of colonic (intra-luminal) obstruction include: geosediment (sand), foreign body, enterolith, fecolith, etc.

Consider:

Simple colonic impaction is a common (frequent) cause of colic. Other less common causes of large intestinal colic (example = non-strangulating displacement) often ARISSE as a complication of a primary colonic impaction.

Some preventive strategies to discuss with owner based on local circumstances: Assurance of access to water. Make sure water is available in winter (ice). Provision of a greater number of water sources (especially for older horses if affected with OA). Adding salt to the daily food intake (~2 tablespoons, daily) and providing salt blocks. Soaking the hay (feeding it before it becomes moldy). Provide ‘sweet tea’ as water source option. Promote exercise and self-motivated mobility (reduce times of confinement). Routine dental prophylaxis. Careful attention to GIT helminth parasitism. Client education and strategies to offset known risks associated with sand/geosediment, enterolith formation, diet changes, NSAID treatments, etc. Use of complete pelleted food sources instead of long stem hay (reduced fiber load). Role of probiotics (yeast?)? A change in food type/source or hay batch within the antecedent two weeks is very commonly identified when presented with colic. An abundance of our patients have developed some degree of obesity – improved client awareness regarding cause and effect may lead to reduced colic risk associated with lipoma development.