Diseases Of Large Intestine

Radhika VaidyaMVSc. Scholar IVRIDiseases Of Large Intestine In Animals

Breed predisposition Terriers: protein loosing enteropathy and nephropathy ( IBD and food allergy)Irish Setters: gluten sensitive enteropathyBasenjis: immunoproliferative enteropathyBoxers and French bulldogs: histiocytic ulcerative colitis

Colitis in Small AnimalsInflammation of the colon reduces the amount of water and electrolytes absorbed and changes colonic motility by suppressing the normal colonic contractions that mix and knead and by stimulating giant migrating contractions (i.e, more powerful contractions that rapidly propel intestinal contents)

Approximately one-third of dogs with a history of chronic diarrhea have colitis.Chronic colitis is defined as inflammation of the colon that is present for 2 wkColitis has been classified into four forms: Lymphocytic-plasmacytic,Eosinophilic Neutrophilic Granulomatous.

Disruptions to normal colonic function lead to changes in both absorption and motility; clinically, this often manifests as large-bowel diarrhea.4

Lymphocytic-plasmacyticcolitisMost common form in both dogs and cats (middle-aged animals)

Association between colitis and perianal fistula, especially in german shepherds

There is an increased number of lymphocytes and plasmocytes in the lamina propria

Eosinophilic colitisIncreased number of eosinophils in the lamina propriaAnimals tend to be younger It is more difficult to treatInfectious agents, parasites, and food allergies may be inciting factors, but none has been provedCBC may reveal eosinophilia

Granulomatous colitisRare, breed-specific inflammatory bowel disease of young boxer dogsSegmental, thickened, partially obstructed segment of bowel (ileum and colon most commonly)Presence of macrophages and other inflammatory cells within the lamina propria

Current treatment recommendations for GC require antimicrobials effective againstE coliand that penetrate intracellularly, such as enrofloxacin

DD: inflammation secondary to fungal disease, intestinal parasites, feline infectious peritonitis, and foreign material.

Etiology and PathophysiologyAcute or chronicBacterial, parasitic, fungal, traumatic, uremic, and allergic causesInflammation may be the result of a defect in mucosal immunoregulation.After initial mucosal injury, submucosal lymphocytes and macrophages become exposed to luminal antigens and subsequently trigger inflammation Exaggerated reaction to dietary or bacterial factors within the lumen of the bowel, genetic predisposition, psychological pathology affecting the neurologic or vascular supply to the colon, or sequelae of previous infectious or parasitic disease have also been implicated.

In acute colitis, there is mucosal infiltration with neutrophils and epithelial disruption and ulceration

Chronic colitis is most often characterized by mucosal infiltration of plasma cells and lymphocytes, fibrosis, and sometimes ulceration

The inflamed bowel is more sensitive to stretch, and contents entering the colon stimulate strong migrating muscular contractions, an urge to defecate, and abdominal discomfort.

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Clinical FindingsLarge-bowel diarrhea, characterized by mucus, hematochezia, tenesmus, and occasionally pain when defecating

There is often an increased urgency and frequency of defecation, with decreased fecal volume per bowel movement

Initially, the clinical signs may be sporadic, but progression usually occurs.

DiagnosisFecal smears forgiardia, trichuris, and fungal elementsCulture for bacteria (campylobacter,salmonella,clostridium)Rectal cytology- inflammatory cells, neoplastic cells, and certain infectious agents (eg,h capsulatum)Colonoscopy is indicated to visually inspect the mucosal surface of the colon and to obtain biopsy specimens

Treatment and ControlFood should be withheld for an initial 2448 hr in animals with acute colitis in an effort to rest the bowel

Because shedding of ova by whipworms is intermittent, therapeutic deworming (eg, fenbendazole 50 mg/kg/day, for 3 days, repeated in 3 wk and again in 3 mo if there is a positive response

Supplementing the diet with fiber (16 tsp of psyllium hydrophilic mucilloid or 14 tbsp of coarse wheat bran/feeding)

Dietary fiber reduces free fecal water, prolongs luminal transit time (increasing the opportunity to absorb water), absorbs toxins, increases fecal bulk and stretches the colonic smooth muscle, and improves contractility. However, the addition of fiber alone rarely results in complete resolution of clinical signs of large-intestinal diarrhea in dogs, and beneficial effects may take as long as 6 wk to become evident. Over time, the fiber dose can be reduced or eliminated in some dogs and a standard dog food substituted without causing a return of the diarrhea.12

Novel protein dietsThe protein source used should be one to which the animal has not previously been exposed

In one study, clinical signs associated with lymphocytic-plasmacytic colitis resolved in all dogs within ~2 wk after feeding a low-residue, digestible, hypoallergenic diet (1 part low-fat cottage cheese and 2 parts boiled white rice)

Thereafter, most dogs were maintained without recurrence of clinical signs on commercially available prescription diets they had not been previously fed.

Metronidazole is considered one of the primary pharmacologic agents in chronic colitis Tylosin is useful in chronic enteropathies because it interferes with bacterial adhesion to the mucosaClinical signs resolve more rapidly when anti-inflammatory medication is given, along with the change in dietSulfasalazine, prednisone or prednisolone, and azathioprine are used most commonlySulfasalazine @12.5 mg/kg, qid for 14 days, then 12.5 mg/kg, bid for 28 daysPrednisone should be started at 2 mg/kg/day, PO; for 2 wk after clinical signs resolve, the dosage should be reduced by 25% every 24 wk, which can usually maintain remission.

However,E coliandSalmonellaare resistant to tylosin.14

Budesonide is a nonhalogenated glucocorticoid used in treatment of crohn's disease in peopleSignificant first-pass metabolism in the liver; theoretically, this should reduce the adverse effects often seen with traditional glucocorticoids, because little of the active drug is systemically availableIn one study of 10 healthy dogs, the pituitary-adrenocortical axis was suppressed, but no other adverse effects were seen

Loperamide (0.10.2 mg/kg, bid-qid) stimulates segmental activity and slows passage of fecal contents

Fructooligosaccharides (FOSs)Enhance colonic micro flora and assist in the prevention and treatment of colonic diseaseThese complex carbohydrates are not digested in the small intestine. FOSs promote the growth of beneficial bacteria and inhibit growth of potentially harmful bacteriaSCFAs (acetate, propionate, butyrate) are an important energy source essential for maintenance of normal mucosal health

PrognosisShort-term prognosis for chronic colitis is good Long term prognosis for complete resolution without relapses appears poorStricture formation and extensive fibrosis warrant a more guarded prognosis

Colic in horses

Colonic Motility PatternsNormograde peristalsis in the left ventral colon moves ingesta toward the left dorsal colonMuscles in the left ventral colon contract in a retrograde fashionThese contractions appear to originate from a pacemaker region in the pelvic flexure. It has been hypothesized that this pacemaker senses either the size or the consistency of the feed particles in the ingesta and then initiates the appropriate motility pattern

If the ingesta has been digested sufficiently, it is moved in a normograde direction; if additional digestion is necessary, the ingesta is moved in a retrograde direction to retain it in the ventral colon. This theory has been proposed to help account for the common clinical occurrence of obstruction at or near the pelvic flexure.

Etiology Wall of the intestine is stretched excessively by either gas, fluid, or ingesta. This stimulates the stretch-sensitive nerve endings located within the intestinal wall, and pain impulses are transmitted to the brain. Pain develops due to excessive tension on the mesentery, as might occur with an intestinal displacement Ischemia develops, most often as a result of incarceration or severe twisting of the intestine Inflammation develops and may involve either the entire intestinal wall (enteritis) or the covering of the intestine (peritonitis)

Clinical FindingsPawing repeatedly with a front foot Looking back at the flank regionCurling the upper lip and arching the neckRepeatedly raising a rear leg or kicking at the abdomenLying down Rolling from side to sideSweatingStretching out as if to urinateStraining to defecateDistention of the abdomenDecreased number of bowel movements.

Diagnosis Excessive gas in the intestinal lumen (flatulent colic), Simple obstruction of the intestinal lumen, obstruction of both the intestinal lumen and the blood supply to the intestine (strangulating obstruction) Interruption of the blood supply to the intestine alone (nonstrangulating infarction)Inflammation of the intestine (enteritis)Inflammation of the lining of the abdominal cavity (peritonitis)erosion of the intestinal lining (ulceration), unexplained colic.

History: deworming history, changes in feed or water supplyPhysical examination: An important aspect of the physical examination is the response to passing a nasogastric tubeAbdominal percussionRectal palpationPeritoneal fluid examinationUSG

. Because horses can neither regurgitate nor vomit, adynamic ileus, obstructions involving the small intestine, or distention of the stomach with gas or fluid may result in gastric rupture. Passing a stomach tube may, therefore, save the horse's life and assist in diagnosis of these conditions. If fluid reflux occurs, the volume and color of the fluid should be noted. In healthy horses, it is common to retrieve 65% even shortly after the onset of clinical signs

The leukogram ranges from normal to neutropenia with a degenerative left shift

Metabolic acidosis and electrolyte disorders

Disease onset is often closely associated with stress, eg, surgery or transport

Colitis-X is the term reserved for those cases in which no definitive diagnosis can be made and the horse dies