Diseases of the Intestines

Chapter 69 Diseases of the Intestines



Robert G. Sherding, Susan E. Johnson



DIARRHEA


Diarrhea results from excessive fecal water content and is the most important clinical sign of intestinal disease in the dog and cat. It is characterized by an abnormal consistency and increase in frequency, fluidity, and volume of feces. The pathogenesis involves derangement of transmucosal water and solute fluxes caused by abnormal digestion, absorption, secretion, permeability, motility, or a combination of these.



Acute versus Chronic Diarrhea


For initial management of diarrhea, consider whether diarrhea is acute or chronic (based on history).



Acute Diarrhea


Acute diarrhea is characterized by sudden onset and short duration (3 weeks or less) of watery or watery-mucoid diarrhea. Diarrhea may be overtly bloody when associated with loss of mucosal integrity. Inappetence, lethargy, and vomiting are frequently associated signs; fever, abdominal pain, and significant dehydration suggest more serious intestinal disease.



• Preliminary diagnostic considerations for diarrhea in the dog and cat should include diet (indiscretion, intolerance, hypersensitivity), medication side effects, toxicity, intestinal parasites (helminths, protozoa), enteric viruses, enteropathogenic bacteria, and a variety of systemic or metabolic disturbances.

• Although there are exceptions, acute diarrhea associated with diet, parasites, and medications generally tends to be mild and self-limiting, whereas acute diarrhea that is severe and life-threatening occurs most frequently in young animals with infectious enteritis (e.g., parvoviral enteritis).

• Diagnostic evaluations in acute diarrhea need not be extensive. Because treatment is mainly supportive and nonspecific, many animals can be managed without determination of a definitive diagnosis. Nevertheless, it is important to identify parasites and enteropathogens that require specific treatments and to identify surgical diseases (e.g., foreign bodies and intussusception).

• Treatment of acute diarrhea is based on rehydration therapy and dietary modification. Symptomatic therapy with antidiarrheal agents may be considered. Nonspecific or mild acute diarrhea often is self-limiting in a day or two without treatment or with restricted food intake.


Chronic Diarrhea



• Diarrhea is categorized as chronic if it has been persistent (3-4 weeks or longer) or has a pattern of episodic recurrence. Chronicity generally excludes simple dietary indiscretion, intoxication, and viral enteritis as causes.



Key Point


Base management of chronic diarrhea on diagnosis rather than symptomatic treatment. Specific intervention or treatment usually is necessary, requiring a specific diagnosis or functional and histopathologic characterization.



• The first step in management is to classify the diarrhea as large or small bowel in origin, based on the history and physical examination. Diagnostic tests and procedures include routine hematologic and serum chemistry evaluations, tests of enteropancreatic function, fecal examinations, radiography, ultrasonography, and endoscopy. Biopsy of the small or large intestine may be necessary.


Small Bowel versus Large Bowel


The anatomic localization of the disease process to the small or large bowel is based on the patient’s defecation pattern and fecal characteristics (frequency, volume, consistency, color, odor, composition) (Table 69-1). This distinction is most useful in dogs for determining the direction of subsequent diagnostic evaluations. Diffuse diseases of the gastrointestinal (GI) tract may produce concurrent small and large bowel signs and, sometimes, gastric signs such as vomiting.


Table 69-1 SMALL BOWEL VERSUS LARGE BOWEL DIARRHEA























































Observation Small Intestine Large Intestine
Frequency of defecation Normal to slightly increased Very increased
Fecal output Large volumes Small volumes frequently
Urgency or tenesmus Absent Present
Dyschezia Absent Present with rectal disease
Mucus in feces Absent Present
Exudate (WBC) in feces Absent Present sometimes
Hematochezia (red blood) Rare Frequent
Melena (digested blood) Present sometimes Absent
Steatorrhea Present sometimes Absent
Flatulence and borborygmus Present sometimes Absent
Weight loss Present sometimes Rare
Vomiting Present sometimes in dogs; frequent in cats Occasional

WBC, white blood cells.



Small Bowel Diarrhea


Chronic small bowel diarrhea can be associated with maldigestion and malabsorption and is characterized by a high volume without urgency, tenesmus, or marked increase in frequency. Weight loss and decline in body condition (malnutrition) may occur.



• Because of unabsorbed nutrients that are degraded and fermented by intestinal bacteria, the feces are rancid and foul-smelling and the increased production of luminal gas by bacteria results in excessive flatulence and borborygmus.

• Steatorrhea (feces containing an excess of unabsorbed fat) can occur in maldigestive and malabsorptive small bowel diarrhea. In extreme cases, the feces may appear oily, greasy, and pale. Hair around the perineum may also have an oily texture from contact with fatty feces.

• Small bowel diarrhea is generally free of grossly visible mucus or blood. When there is bleeding from a lesion in the proximal GI tract, the blood pigment becomes dark black during transit (melena). In the absence of gastric bleeding, melena generally indicates small intestinal parasitism (e.g., hookworms), infection (viral, bacterial, fungal), ulceration (e.g., drug induced), severe inflammation, or neoplasia.


Large Bowel Diarrhea


Large bowel diarrhea is characterized by frequent urges to defecate (usually greater than 3 times normal frequency), with each defecation producing small quantities of feces that often contain excessive mucus and sometimes fresh red blood.



• Urgency resulting from irritability or inflammation of the distal colon causes frequent premature expulsions of small quantities of feces that would otherwise be insufficient to trigger the defecation reflex. Lapses in housetraining (“accidents”) may be caused by urgency and inability to control urges to defecate.

• Straining (tenesmus) may be noted as the patient remains in position for a prolonged time after defecation or makes repeated attempts to defecate within a few minutes. These attempts may produce little or no feces or sometimes just a few drops of mucus, exudate, and blood.

• Because many colonic diseases are associated with mucosal injury, inflammation, or ulceration, abnormal fecal constituents are frequently found in large bowel diarrhea, including (1) fresh red blood (hematochezia) that originates from sites of erosion or ulceration, (2) mucus that originates from the abundant goblet cells in the colon that respond to mucosal injury by an outpouring of mucus, and (3) exudate (leukocytes) that originates from the site of inflammation.



Key Point


Abnormal fecal constituents such as fresh red blood, mucus, and leukocytes are localizing signs indicative of colonic disease.



• Blood may coat the feces, streaks of blood may be mixed within the feces, or drops of blood may be passed at the end of defecation.

• Excessive mucus may give the feces a glistening or jelly-like appearance.

• Exudates are detected by the positive identification of fecal leukocytes using cytology stains.


• Because the principal function of the colon is absorption of water and electrolytes rather than digestion and absorption of nutrients, nutrient malabsorption and steatorrhea are absent in large bowel diarrhea. Thus, dramatic weight loss and wasting are unlikely if the animal is eating, and the daily fecal output (volume or weight of feces) usually is only minimally increased.

• Vomiting is a clinical sign in about 30% of patients with colitis.


DIAGNOSTIC APPROACH FOR DIARRHEA


Initial evaluations are aimed at diagnosis of dietary, parasitic, and infectious causes of diarrhea. This should include fecal examinations, therapeutic deworming trials (fenbendazole, 50 mg/kg PO daily for 3 days), and a 4-week dietary trial using a highly digestible commercial or homemade GI diet, either alone (for small bowel diarrhea) or with psyllium added as a fiber source (for dogs with large bowel diarrhea). If diarrhea persists and the cause is not apparent, additional diagnostic evaluations may include a complete blood count (CBC), serum chemistry profile, urinalysis, additional fecal exams for infectious agents (cytology, toxin assay, and cultures), abdominal imaging (radiography and ultrasonography), and enteropancreatic function tests. Finally, endoscopic examination and biopsy may be indicated.



History


The history is especially helpful for localizing the disease process to the small or large bowel. It also may indicate underlying non-intestinal causes of diarrhea (e.g., renal failure, liver disease, hypoadrenocorticism, or feline hyperthyroidism) and identify important predisposing factors such as breed, diet, environmental factors, current medications, and exposure to parasites, infectious agents, and toxins. The following historical aspects of the diarrhea may be diagnostically useful:



• Mode of onset (abrupt versus gradual)

• Duration (acute versus chronic)

• Clinical course (intermittent, continuous, or progressive)

• Fecal characteristics (small bowel versus large bowel; see previous section)

• Correlation with diet (food intolerances and dietary indiscretions)

• Correlation with medication usage (drug side effects)

• Correlation with stressful events (psychogenic, anxiety, or “irritability” factors)

• Response to previous treatments (prescribed diets, antibiotics, corticosteroids, or fenbendazole)

• Association with other signs (weight loss, vomiting, or polyuria-polydipsia)



Key Point


Consider extraintestinal causes of diarrhea, such as diseases of the pancreas (exocrine pancreatic insufficiency, pancreatitis), liver, kidneys (azotemia), endocrine system (e.g., hypoadrenocorticism and hyperthyroidism), cardiovascular system, and central nervous system (CNS).



Physical Examination


A complete physical examination may reveal important clues about the severity, nature, and cause of diarrhea (Table 69-2), although in many patients the findings are nonspecific.


Table 69-2 PHYSICAL FINDINGS IN INTESTINAL DISEASE































































Physical Finding Potential Clinical Associations
General Physical Examination
Dehydration Diarrheal fluid loss
Depression/weakness Electrolyte imbalance, severe debilitation
Emaciation/malnutrition Chronic malabsorption, protein-losing enteropathy
Dull unthrifty haircoat Malabsorption of fatty acids, protein, and vitamins
Fever Infection, transmural inflammation, neoplasia
Edema, ascites, pleural effusion Protein-losing enteropathy
Pallor (anemia) Gastrointestinal blood loss, anemia of chronic inflammation
Intestinal Palpation
Masses Foreign body, neoplasia, granuloma
Thickened loops Infiltration (inflammation, lymphoma)
“Sausage loop” Intussusception
Aggregated loops Linear intestinal foreign body, peritoneal adhesions
Pain Inflammation, obstruction, ischemia, peritonitis
Gas or fluid distention Obstruction, ileus, diarrhea
Mesenteric lymphadenopathy Inflammation, infection, neoplasia
Rectal Palpation
Masses Polyp, granuloma, neoplasia
Circumferential narrowing Stricture, spasm, neoplasia
Coarse mucosal texture Colitis, neoplasia


• Identify physical findings that may indicate underlying systemic disease that could be a cause or consequence of diarrhea.

• Identify abnormalities on abdominal palpation of the intestinal loops and digital palpation of the rectum.

• Inspect the fecal material obtained on the palpation glove for abrasive particles (such as bone chips), blood, and mucus. If indicated, examine the fecal material microscopically for parasites, microorganisms, and inflammatory cells or submit for culture.


Routine Laboratory Tests



• Evaluate a CBC for leukocyte responses and anemia that may be associated with intestinal disease (Table 69-3).

• Perform a serum biochemical profile and urinalysis to identify metabolic or systemic disorders that could cause or result from diarrhea (see Table 69-3).

• Measure serum thyroxin (T4) concentration in all cats over 5 years of age with diarrhea or weight loss to exclude hyperthyroidism as a cause (see Chapter 31).

Table 69-3 LABORATORY FINDINGS IN INTESTINAL DISEASE



































































Abnormal Laboratory Findings Clinical Associations
Hematologic Findings
Eosinophilia Parasitism, eosinophilic enteritis, hypoadrenocorticism, mast cell tumor
Neutrophilia Bowel inflammation, necrosis, or neoplasia
Neutropenia or “toxic” neutrophils Parvovirus, FeLV, FIV, endotoxemia, or overwhelming sepsis (e.g., leakage peritonitis)
Monocytosis Chronic or granulomatous inflammation (e.g., mycosis)
Lymphopenia Loss of lymphocytes associated with intestinal lymphangiectasia
Anemia GI blood loss, depressed erythropoiesis (chronic inflammation, neoplasia, malnutrition)
Elevated PCV Hemoconcentration from GI fluid loss
RBC microcytosis Iron deficiency (chronic GI blood loss), portosystemic shunt
RBC macrocytosis RBC regeneration, feline hyperthyroidism, FeLV, nutritional deficiencies (rare)
Serum Biochemical Findings
Panhypoproteinemia Protein-losing enteropathy
Hyperglobulinemia Chronic immune stimulation, basenji enteropathy
Azotemia Dehydration (prerenal), primary renal failure
Hypokalemia GI loss of fluid and electrolytes, anorexia
Hyperkalemia/hyponatremia Hypoadrenocorticism, trichuriasis (rare)
Hypocalcemia Hypoalbuminemia, lymphangiectasia, pancreatitis
Hypocholesterolemia Lymphangiectasia, liver disease
Elevated liver enzymes or bile acids Liver disease
Elevated amylase/lipase Pancreatitis, enteritis, or azotemia
Elevated thyroxine (T4) Feline hyperthyroidism

FeLV, feline leukemia virus; FIV, feline immunodeficiency virus; GI, gastrointestinal; PCV, packed cell volume; RBC, red blood cell.



Fecal Examinations


Fecal examinations are an important aspect of the diagnostic approach to diarrhea and should involve visual inspection (for blood, mucus, and foreign matter), parasite evaluation, and microscopic examinations. Specialized evaluations can include quantitative fecal collection and fat analysis, chemical determinations, cultures, toxin assays, virology, and nuclear scans, but these are used only in selective cases.




Key Point


Examination of feces for parasites should be part of the minimum database for all animals with diarrhea.



• In cases of chronic unresponsive diarrhea, expand the database to include microscopic examination of stained fecal smears for fat, starch, and leukocytes.

• If circumstances suggest infection, perform fecal culture for specific enteropathogenic bacteria (Salmonella, Campylobacter) or toxin assay for enterotoxigenic Clostridium perfringens.

• Diagnostic methods for intestinal parasites and infectious agents are listed in Table 69-4.

Table 69-4 DIAGNOSIS OF INTESTINAL PATHOGENS OF DOGS AND CATS


















































































































Pathogen Method of Diagnosis
Helminths
Ascarids (Toxocara, Toxascaris leonina) Routine fecal flotation for ova
Hookworms (Ancylostoma) Routine fecal flotation for ova
Whipworms (Trichuris vulpis) Routine fecal flotation for ova; fenbendazole trial
Tapeworms (Taenia, Dipylidium caninum) Fecal proglottids or flotation for ova
Strongyloides Fecal sediment or Baermann test for larvae
Others (flukes) Fecal zinc sulfate centrifugation-flotation for ova
Protozoa
Coccidia (Isospora) Fecal flotation for oocysts
Cryptosporidium spp. Microplate ELISA, direct immunofluorescence, PCR, Sheather’s flotation
Giardia Fecal zinc sulfate centrifugation-flotation for cysts; fecal ELISA or IFA; duodenal wash for trophozoites; fenbendazole trial
Tritrichomonas foetus Fecal wet smear for trophozoites; InPouch TF culture; PCR
Entamoeba histolytica Fecal wet smear for trophozoites
Balantidium coli Fecal wet smear for trophozoites
Viruses
Canine parvovirus Fecal ELISA (SNAP-Parvo Test) for viral antigen (see Chapter 14)
Feline panleukopenia virus Signs, leucopenia (see Chapter 14)
Canine coronavirus Fecal EM, virus culture, PCR (see Chapter 14)
Feline enteric coronavirus and FIP Signs, serology, fecal EM, PCR, biopsies (see Chapter 10)
Rotaviruses Fecal EM, virus culture, PCR (see Chapter 14)
Astrovirus Fecal EM, PCR (see Chapter 14)
Canine distemper virus Signs (see Chapter 13)
Retroviruses (FeLV, FIV) FeLV antigen test (ELISA, IFA); FIV antibody test (see Chapters 8, 9)
Rickettsia
Salmon poisoning (Neorickettsia helminthoeca) Operculated trematode eggs in feces; rickettsia in lymph node cytology (see Chapter 17)
Bacteria
Salmonella Fecal culture
Campylobacter jejuni Fecal microscopy and culture
Yersinia enterocolitica, Y. pseudotuberculosis Fecal culture
Bacillus piliformis (Tyzzer’s disease) Biopsy (gut, liver) for filamentous bacteria; mouse inoculation
Mycobacterium spp. Acid-fast bacteria in cytology/biopsy; culture, PCR (see Chapter 19)
Clostridium perfringens, C. difficile ELISA-based fecal enterotoxin assays; PCR
Enteropathogenic Escherichia coli (?) Fecal culture and toxin assays
Fungi
Histoplasma capsulatum Fungi in biopsies/cytologies; serology (see Chapter 20)
Pythium, Zygomycetes Pythium ELISA; poorly septate hyphae in biopsies (Chapters 20, 40)
Others (Candida albicans, Aspergillus, etc.) Yeast or hyphae in biopsies; fungal culture (see Chapters 20, 40)
Algae (Prototheca) Unicellular algae in cytology or biopsy; fecal culture (Sabouraud’s)

ELISA, enzyme-linked immunosorbent assay; EM, electron microscopy; FeLV, feline leukemia virus; FIP, feline infectious peritonitis; FIV, feline immunodefi-ciency virus; IFA, immunofluorescent antibody; PCR, polymerase chain reaction test; Rx, therapeutic response.



Fecal Examination for Parasites


Fecal examination for parasites can include fecal flotation, zinc sulfate centrifugation-flotation, direct wet smears, and immunoassays. Examine fresh feces within 1 hour of collection. Alternatively, refrigerate feces within 1 hour and examine within 3 days, or preserve feces in formalin for later examination.



• Use routine fecal flotation to identify nematode ova and coccidian oocysts other than Cryptosporidium.

• In warm, humid regions (e.g., southern United States) endemic for Strongyloides species, perform a direct wet smear, sedimentation, or Baermann procedure to identify larvae in the feces.

• For Giardia, use zinc sulfate centrifugation-flotation to identify cysts or an immunoassay to identify fecal antigen. Reliable fecal immunoassays are the point-of-care SNAP Giardia Test Kit (IDEXX), the microplate enzyme-linked immunosorbent assay (ELISA) (Remel), or an immunofluorescent antibody (IFA) test at a commercial lab. Evidence suggests the rapid ELISA test for human Giardia is not reliable in animals.

• Use a direct saline smear of fresh feces to detect motile trophozoites of protozoan parasites, including Giardia, Tritrichomonas, Entamoeba histolytica, and Balantidium coli. This is an insensitive method for diagnosis of Giardia. The distinguishing characteristics of each of these protozoa are discussed under “Protozoan Parasites.”

• For diagnosis of Tritrichomonas foetus infection in cats, fecal culture using InPouch-TF and fecal polymerase chain reaction (PCR) assay are more sensitive than direct fecal smear microscopy.

• For Cryptosporidium parvum, a very small coccidian, use fecal antigen immunoassay (microplate ELISA or IFA), Sheather’s sugar flotation for oocysts, or modified acid-fast staining. Evidence suggests the rapid ELISA test for human Cryptosporidium is not reliable in animals.

• Diagnosis of occult parasite infections (e.g., Giardia and most nematodes including whipworms) can be based on response to a therapeutic trial using fenbendazole (50 mg/kg PO q24h for 3-5 days).



Key Point


Intestinal parasitism can resemble many other small and large bowel disorders. Common examples are hookworms, whipworms, and Giardia.



Fecal Examination for Infectious Agents


The diagnosis of infectious diarrhea often depends on the detection of the offending viral, bacterial, or fungal organisms in the feces. Details of diagnosis of these various enteric infections are found in the respective sections of this chapter.



Viruses


Viral diarrhea is generally acute and is confirmed by detection of viral antigen in the feces (ELISA, PCR, etc.) or virus particles by electron microscopy (see Chapter 14).



Bacteria


The common enteropathogenic bacteria in dogs and cats are listed in Table 69-4.



• Specific enteropathogenic bacteria, such as Salmonella and Campylobacter, can be isolated from fresh feces using appropriate culture media. Cultures are particularly indicated when examination of fecal cytology preparations reveals the presence of numerous fecal leukocytes or Campylobacter-like bacteria or when there is an outbreak of diarrhea in groups of animals housed together.

• For diagnosis of Clostridium perfringens and Clostridium difficile enterotoxigenic diarrhea, use validated fecal ELISA (Techlab, Blacksburg, VA) and PCR assays to detect clostridial enterotoxins. The finding of numerous large gram-positive sporulating rods with a “safety pin” appearance in stained fecal smears is not a reliable indicator of toxin-producing C. perfringens. Non-toxigenic C. perfringens is part of the normal intestinal flora in dogs and cats; thus, cultures are not useful.


Fungi and Prototheca


The diagnosis of fungal (Histoplasma, Aspergillus, Pythium, Candida) and protothecal infections is usually based on identification of the organisms in feces or more often in rectal scrapings (Histoplasma), tissue aspirates, or intestinal biopsies (see Chapters 20 and 40).



• Serodiagnostic tests for presumptive diagnosis of histoplasmosis and pythiosis also are available.

• Affected tissues can be cultured for systemic fungi and Prototheca (a rare cause of colitis), but culture growth takes weeks and the isolation rate is low.


Fecal Examination Using Special Stains


Feces can be examined microscopically for abnormal constituents using Sudan, Lugol iodine, Gram, and various other cytologic stains. In each test, one to two drops of fresh feces are stained on a microscope slide and examined. In general, these procedures are relatively insensitive and nonspecific and are affected by many factors, including diet.



Sudan and Iodine Stain


Fecal staining with Sudan for undigested fat and Lugol iodine for undigested starch may suggest exocrine pancreatic insufficiency (maldigestion); however, these evaluations are too insensitive, nonspecific, and diet dependent to be recommended. These procedures have been replaced by more reliable diagnostic tests for exocrine pancreatic insufficiency (see Chapter 73).



Cytology Stain


Routine cytology staining (e.g., new methylene blue, Wright, and Diff-Quik stains) identifies fecal leukocytes that are markers of exudative inflammatory colonic disease. Cytology may occasionally identify neoplastic cells or Histoplasma or Prototheca organisms. It is advisable to follow up with patients that are positive for fecal leukocytes with colonoscopy and fecal cultures for invasive bacteria such as Campylobacter and Salmonella.



Gram Stain


With gram staining, the experienced observer may identify large numbers of C. perfringens or Campylobacter-like spiral bacteria; however, microscopy is much less reliable than toxin assays for Clostridium and culture for Campylobacter.



Tests for Fecal Occult Blood


These include a simple, in-office qualitative screening test (Hemoccult test) and a more accurate, semiquantitative send-out test (HemoQuant, SmithKline). These tests are sensitive for detecting even very small amounts of GI hemorrhage. Because of this sensitivity, it is recommended that the owner exclude meat from the animal’s diet for at least 3 days prior to testing to avoid false-positive results.



• The presence of fecal occult blood signifies a bleeding lesion of the GI tract, which suggests an ulcerative, inflammatory, or neoplastic condition, or a hemostatic abnormality.

• The fecal occult blood test is also indicated to document GI bleeding as a cause of blood loss anemia.


Quantitative Fecal Fat Analysis


This can be used as an intestinal function test to confirm steatorrhea, but it is rarely used because it is cumbersome and impractical to perform and does not differentiate pancreatic maldigestion from intestinal malabsorption. Feces must be collected for a 24- to 72-hour period while the animal is confined and fed a standard diet. The feces are weighed and sent to a commercial laboratory for analysis. Normally, less than 10% of ingested fat is excreted in the feces, or less than 0.3 g/kg/day in dogs and less than 0.4 g/kg/day in cats.



Fecal Proteolytic Activity


Fecal proteolytic activity can be assayed as an indicator of pancreatic secretion of proteases (trypsin) for the diagnosis of exocrine pancreatic insufficiency (EPI). The serum trypsin-like immunoreactivity (TLI) assay is more accurate and is now preferred for the diagnosis of exocrine pancreatic insufficiency in both dogs and cats (see Chapter 73).



Tests for Fecal Protein Loss


See under “Tests for Protein-Losing Enteropathy.”



Enteropancreatic Function Tests


The following tests are designed to evaluate digestive and absorptive functions.



Tests for Exocrine Pancreatic Insufficiency


Tests for exocrine pancreatic insufficiency (pancreatic maldigestion), such as serum trypsin-like immunoreactivity and fecal assays for proteolytic activity, are described in Chapter 73.



Serum Folate and Cobalamin Assays


Serum concentrations of folate and cobalamin (vitamin B12) are indicative exocrine pancreatic function (cobalamin), intestinal absorptive function, and the status of the intestinal bacterial flora.



Serum Folate


Folate, a water-soluble B vitamin, is plentiful in most commercial pet foods, and serum concentration depends primarily on the absorptive function of the proximal small intestine.



• Serum folate (normal, dog: 6.5-11.5μg/L; cat: 9.7-21.6μg/L) may be decreased in enteropathies that impair absorption in the proximal small intestine or in diffuse small intestinal disease. Widespread malignancy and sulfasalazine treatment also may decrease serum folate.

• Serum folate may be increased with overproliferation of the normal intestinal flora because many species of bacteria synthesize folic acid.

• Serum folate also may be increased by high dietary intake of folic acid, low intestinal pH, exocrine pancreatic insufficiency (32% of cases), and artifactually by hemolysis or heating of the blood specimen.


Serum Cobalamin


Cobalamin, a water-soluble B vitamin, is plentiful in most commercial pet foods, and serum concentration depends on the secretion of pancreatic intrinsic factor necessary for normal cobalamin absorption and on the absorptive function of the ileum.



• Serum cobalamin (normal, dog: 249-733 ng/L; cat: 290-1500 ng/L) is frequently decreased in exocrine pancreatic insufficiency (deficiency of intrinsic factor) and in enteropathies that impair absorption in the distal small intestine, including diffuse small intestinal disease. It also is decreased in presumed small intestinal bacterial overgrowth.

• Because cobalamin has a shorter half-life in cats, cats with chronic intestinal disease are particularly susceptible to developing cobalamin deficiency.

• Prolonged exposure of the blood specimen to bright light may artifactually decrease cobalamin.

• An isolated hereditary defect in cobalamin absorption has been recognized in some dog breeds (giant schnauzer, Border collie, Shar-Pei).



Key Point


In small intestinal bacterial overgrowth, serum folate may be increased due to synthesis of folate by the proliferated bacteria, whereas cobalamin may be decreased because bacteria can utilize or bind the vitamin, making it unavailable for absorption.



Breath Hydrogen Test


This assesses monosaccharide or disaccharide malabsorption or bacterial overgrowth, based on the principle that intestinal bacteria ferment intraluminal carbohydrate and produce hydrogen gas, some of which is absorbed into the blood and excreted by the lungs. This test is impractical for routine clinical use and is affected by diet, gastric emptying, intestinal transit, and the status of the intestinal flora.



Five-Sugar Absorption Tests for Intestinal Permeability


These oral sugar absorption tests are variations on the other carbohydrate absorption tests. A mixture of sugars is used as a noninvasive molecular probe of mucosal permeability and injury based on urine recovery (in a 6-hour urine sample) after oral administration. These sugar probes measure passive diffusion. Lactulose, cellobiose, and raffinose are probes of the large pores of the paracellular pathway, and urine recovery increases with mucosal epithelial damage. Mannitol and rhamnose are probes of the numerous small pores of the transcellular pathway, and urine recovery decreases with loss of mucosal absorptive surface area (such as villous atrophy). An increase in the lactulose-to-rhamnose ratio is typical of intestinal disease with mucosal damage and increased permeability.


One variation on this procedure involves giving a mixture of lactulose, rhamnose, xylose, methylglucose, and sucrose, and the ratios are determined in 6-hour urine for lactose-to-rhamnose (permeability test), xylose-to-methylglucose (absorption test), and sucrose-to-methylglucose (mucosal digestion test).


In addition to reflecting absorptive function and permeability, results are also affected by gastric emptying, intestinal dilution and transit, systemic distribution, metabolism, and renal clearance. Results have not shown good correlation with clinical disease activity and histologic findings.



Unreliable Absorption Tests


In general, the reliability of oral absorption tests is affected by gastric emptying time, intestinal dilution and transit time, digestion and absorption, systemic distribution, metabolism, and renal excretion. Because of inconsistent results, the following absorption tests are not considered clinically useful in dogs and cats:



• Absorption of glucose substrates (glucose, lactose, starch)—Affected by insulin, etc.

• Xylose absorption—For detection of brush border monosaccharide malabsorption

• Quantitative fecal fat analysis—For detection of fat malabsorption (steatorrhea)

• Oral triglyceride absorption

• Vitamin A absorption

• Bentiromide para-aminobenzoic acid (BT-PABA) absorption


Tests for Protein-Losing Enteropathy


Excessive GI loss of plasma proteins can be documented using fecal assays that quantitate the intestinal loss of specific serum proteins, such as alpha-1-proteinase inhibitor, or an IV dose of 51 chromium-labeled albumin, a radiopharmaceutical.



• Alpha-1-proteinase inhibitor is a serum protein similar in molecular size to albumin. The intestinal loss of alpha-1-proteinase inhibitor in protein-losing enteropathy parallels the loss of albumin, except that it is not digested and is excreted intact in the feces. Thus, using a canine-specific assay, alpha-1-proteinase inhibitor can be measured in the feces as a marker for intestinal protein loss in dogs. This test is useful for evaluation of dogs with unexplained hypoproteinemia and for early detection of affected dogs in high-risk breeds, such as the soft-coated wheaten terrier.

• Normal fecal excretion of the alpha-1-proteinase inhibitor is <5.7μg/g feces in dogs and <1.6μg/g feces in cats. The assay requires submission of three fresh fecal specimens to the Gastrointestinal Laboratory, Department of Small Animal Medicine and Surgery, College of Veterinary Medicine, Texas A&M University, College Station, TX 77843-4474 (website: http://www.cvm.tamu.edu/gilab).


Tests for Bacterial Overgrowth


Direct evidence of small intestinal bacterial overgrowth is conventionally based on quantitative cultures of small intestinal juice; however, because of extensive overlap in the bacterial counts found in normal and diarrheic dogs and cats, the diagnostic criteria for small intestinal bacterial overgrowth in animal patients is uncertain. Indirect evidence of small intestinal bacterial overgrowth is indicated by the following:



• Increased serum folate and decreased serum cobalamin, reflecting increased bacterial metabolic activity

• Abnormal hydrogen breath test results, reflecting increased bacterial fermentation activity

• Increased serum unconjugated bile acids, reflecting increased bacterial deconjugation activity

• Idiopathic chronic small bowel diarrhea that is antibiotic responsive


Tests for Intestinal Motility


Tests for clinically assessing intestinal motility have limited clinical usefulness except for identifying obstruction to flow. These include intestinal transit time of barium, barium-impregnated spheres, or radiopharmaceuticals. The hydrogen breath indirectly reflects transit time of the proximal GI tract.



Radiography and Ultrasonography



Plain Abdominal Radiography


Plain radiography is indicated for detection of intestinal masses or abnormal gas-fluid patterns, especially when mechanical or obstructive disorders are suspected (e.g., intestinal mass, foreign body, or intussusception).



Gastrointestinal Barium Contrast Radiography


Upper GI barium radiography is indicated when other evaluations fail to determine the cause of small bowel diarrhea or when intestinal obstruction is suspected (see Chapter 4). This may help detect obstructive lesions, neoplastic masses, and inflammatory lesions that cause an irregular mucosal pattern or distortion of the bowel wall. In most cases, however, diarrhea involves microscopic and functional changes in the bowel that are not detected by barium radiography.



Barium Enema Contrast Radiography


Barium enema radiography is indicated in selected cases of large bowel diarrhea for evaluating the colon and cecum for intussusceptions, neoplasms, polyps, strictures, inflammatory lesions, and colonic displacement or malformation. Colonoscopy is generally preferred over barium enema for evaluating the colon because it yields more definitive diagnostic information.



Abdominal Ultrasonography


Ultrasonography is indicated for assessing intestinal wall thickness and layering, for defining intestinal and other abdominal masses, and for evaluating other abdominal organs—e.g., lymph nodes, spleen, pancreas, liver, biliary tract, kidneys, adrenals, and prostate (see Chapter 4).



Endoscopy




Key Point


Endoscopic examination with mucosal biopsy is required for definitive diagnosis or accurate characterization of the disease in many cases of chronic intractable diarrhea in which non-intestinal, dietary, parasitic, and infectious causes have been excluded.



Gastrointestinal Endoscopy


Duodenoscopy with a flexible fiberoptic endoscope can be performed in the anesthetized animal for visual examination of the upper GI tract, including duodenum; for duodenal aspiration (for quantitative bacterial culture or detection of Giardia trophozoites); and for directed forceps biopsy of the intestinal mucosa (see Chapter 67 for a description of endoscopic equipment and discussion of gastroscopy).



• The normal duodenal mucosa appears pale pink with a uniformly granular villus pattern.

• Biliary and pancreatic duct papillae and Peyer lymphoid patches are normally seen.

• The mucosa is non-friable and should be free of excessive granularity, hemorrhages, erosions, ulcers, thickened folds, masses, or strictures. Villous lymphatics (lacteals) should not be prominent in the fasted animal.

• The lumen is easily and uniformly distensible with air.


Colonoscopy


Colonoscopy allows direct visualization of the lumen of the colon, sampling of luminal content for culture and exfoliative cytology, and directed forceps biopsy of the ileocolic mucosa.



• Suitable rigid colonoscopes are relatively inexpensive and easy to use. Because colonic diseases are often diffuse, examination and biopsy of the descending colon with a rigid instrument is sufficient for diagnosis in many patients.

• When lesions are located predominantly in the ascending or transverse colon, areas inaccessible with a rigid colonoscope, use a flexible fiberoptic or video colonoscope. A flexible colonoscope can be navigated through the ileocolic sphincter for examination and biopsy of the ileum in some animals.

• The normal colonic mucosa appears pale pink through the colonoscope and reflects light uniformly. It is non-friable, thin enough that the submucosal vessels are visible, and free of erosions, ulcers, thickened folds, masses, or strictures.


Intestinal Biopsy


The least invasive and, in many cases, preferred method for procurement of intestinal biopsies is endoscopy. If endoscopy is not available, or if endoscopic biopsies are inconclusive, consider full-thickness intestinal biopsy by laparotomy (see Chapter 70).



• Obtain multiple biopsies along the length of the gut even if no lesions are visible by gross inspection, which is often the case.

• Biopsy mesenteric lymph nodes and evaluate other abdominal organs, especially the pancreas, liver, and colon.

• Duodenal aspirates or duodenal mucosal impression smears may be examined for Giardia trophozoites or cultured quantitatively for aerobic and anaerobic bacterial overgrowth.


Therapeutic Trials


In some cases, the response to a dietary modification or therapeutic drug trial is used as an empirical diagnostic approach, when supported by adequate clinical information. Common therapeutic trials are given in the sections that follow.



Diet Modification



• Commercial GI diet for optimal digestability

• Novel protein diet—For dietary hypersensitivity or food allergy

• Fiber supplemented diet—For fiber-responsive large bowel diarrhea (dogs)


Fenbendazole



• For helminths (especially whipworms)

• For Giardia


Metronidazole



• For Giardia

• For enteropathogenic bacteria (especially Clostridium)

• To suppress flora in bacterial overgrowth

• To treat idiopathic inflammatory bowel disease (via flora effects or immune modulation)


NONSPECIFIC TREATMENT OF DIARRHEA


Dietary, supportive, and symptomatic therapy often is beneficial in diarrhea, especially acute diarrhea. In severe acute diarrhea, fluid and electrolyte therapy can be lifesaving.



Dietary Management



Acute Diarrhea



• The initial goal is to physiologically “rest” the GI tract by restricting food intake for at least 24 hours.

• When resuming feeding, give bland, low-fat foods in small amounts at frequent intervals. Various commercial diets are available that have been specially formulated for animals with GI disease. Recipes for appropriate homemade diets are available as well. Examples of appropriate foods include boiled rice combined with turkey, boiled skinless chicken, yogurt, or low-fat cottage cheese as protein sources.

• Examples of commercial “intestinal diets” appropriate for nonspecific therapy of diarrhea include Eukanuba Low Residue (Iams), Prescription Diet i/d (Hill’s), Low Fat (Waltham), and EN Formula (Purina). Other highly digestible diets can also be used.

• When the diarrhea has been resolved for 48 hours, gradually reintroduce the animal’s regular diet.


Chronic Diarrhea


Divide daily food intake into three or four feedings, and use (1) commercial diets designed for GI disease with high digestibility and mild fat restriction (for all types of diarrhea); (2) novel protein diets (for dietary hypersensitivity and inflammatory bowel disease); or (3) fiber-enriched diets (for canine large bowel diarrhea).



Fluid Therapy



• In severe, acute diarrhea, such as occurs with parvoviral enteritis, fluid and electrolyte replacement is essential for management of intestinal fluid loss that may lead to serious dehydration, shock, and death (see Chapter 5).

• Parenteral methods of fluid therapy are preferred in most cases; however, over-the-counter oral glucose-electrolyte solutions (Pedialyte) are available for counterbalancing intestinal fluid losses in cases of mild diarrhea.


Antidiarrheal Drugs


Symptomatic treatment is based on drugs that modify motility, fluid secretion, and absorption or on drugs that act locally within the lumen as protectants or adsorbents.



• In most cases, these drugs are reserved for short-term use, usually for periods of 5 days or less. Some commonly used antidiarrheal drugs and their dosages are listed in Table 69-5.

• The purposes of antidiarrheal drugs are to provide short term relief from diarrhea, to provide relief from bowel discomfort (“crampiness”), and to control intestinal fluid losses.


Table 69-5 DRUGS USED FOR SYMPTOMATIC TREATMENT OF DIARRHEA

image


Opiate and Opioid Narcotic Analgesics




Key Point


Opioid drugs such as loperamide are the most effective all-purpose antidiarrheal agents (see Table 69-5).



• Examples include loperamide (Imodium A-D), diphenoxylate (Lomotil), paregoric, morphine, and codeine.

• Opioids delay gastric emptying and slow bowel transit by stimulating non-propulsive contractions while decreasing propulsive motility (peristalsis), thereby allowing more contact time for absorption. This promotes fluid and electrolyte absorption.

• Opioids inhibit intestinal fluid loss through modification of mucosal fluid and electrolyte transport.

• Opioids increase anal tone and reduce the discomfort (i.e., crampiness) associated with acute diarrhea.

• Side effects are bloating, cramping, constipation, vomiting, and CNS depression. Use is not recommended with invasive bacterial enteritis.


Anticholinergic Drugs



• Examples include aminopentamide (Centrine), dicyclomine, and propantheline.

• They cause a generalized suppression of all gut motility, including beneficial non-propulsive motility, that may lead to unwanted ileus. The atropine-like antispasmodic action may be beneficial for controlling the urgency and discomfort of anorectal disease in some cases.

• They inhibit intestinal fluid loss, presumably through an antisecretory effect.

• Side effects are GI paralysis (ileus), worsening of diarrhea, constipation, tachycardia, xerostomia, urinary retention, ocular effects, and CNS stimulation.


Protectants and Adsorbents



• Examples include kaolin-pectin (Kaopectate), bismuth (Pepto-Bismol), aluminum and magnesium salts, activated charcoal, cholestyramine, and barium.

• These oral agents remain in the lumen, and they are proposed to adsorb or bind harmful bacteria and bacterial toxins and to provide a protective coating on inflamed mucosal surfaces.

• The efficacy of these drugs is controversial. There is little evidence that they diminish intestinal fluid losses. Large doses are often required, and they are difficult for owners to administer.


Anti-inflammatory Therapy


Non-infectious inflammatory bowel diseases are often treated with corticosteroids or nonsteroidal anti-inflammatory agents (NSAIDs).



Corticosteroids



• Examples include prednisone, prednisolone, dexamethasone, and budesonide.

• Corticosteroids have anti-inflammatory, antisecretory, and mucosal-stimulating properties. The primary indication is for inflammatory bowel disease.


Nonsteroidal Anti-inflammatory Drugs



• Bismuth subsalicylate (Pepto-Bismol) has a mild mucosal anti-inflammatory action in the lumen of the proximal GI tract. Efficacy for small animal diarrhea is infrequent.

• Preparations of 5-aminosalicylic acid (5-ASA) (mesalamine) are poorly absorbed in the proximal GI tract so that they reach the colon where colonic bacteria release the active drug to produce a mucosal anti-inflammatory action for treatment of chronic colitis. Examples include sulfasalazine (Azulfidine), olsalazine (Dipentum), encapsulated mesalamine (Asacol), polymer-coated mesalamine (Pentasa), and mesalamine enema (Rowasa).

• Avoid systemic nonsteroidal anti-inflammatory drugs (e.g., flunixin meglumine, ibuprofen, and aspirin) in dogs and cats with GI disease, or use them cautiously because they cause GI ulceration.


Antibiotic Therapy


Do not use antibiotics routinely as empirical therapy in cases of uncomplicated diarrhea of undetermined cause because of the adverse effects of antibiotics on the normal intestinal flora and the risk of promoting resistant strains of bacteria.



• Use well-chosen antibiotics when specific bacterial enteropathogens, such as Salmonella, Campylobacter, or enterotoxigenic C. perfringens, are suspected.

• Antibiotics are appropriate in conditions associated with severe mucosal damage and a high risk of secondary sepsis or endotoxemia, such as parvoviral enteritis and hemorrhagic gastroenteritis (HGE). Thus, indications for antibacterial therapy in animals with acute GI disease include bloody diarrhea, fever, leukocytosis, leukopenia, fecal leukocytes, and shock.

• Metronidazole is an antibiotic frequently used in animals with diarrhea. Its potential indications are as follows:
• To treat Giardia (and various other protozoa)

• To treat certain enteropathogenic bacteria, such as Clostridium species

• To suppress overabundant enteric flora in small intestinal bacterial overgrowth

• To modify normal enteric flora that may play a role in chronic inflammatory bowel disease

• To immunomodulate in chronic inflammatory bowel disease


Fenbendazole-Responsive Diarrhea


Fenbendazole (50 mg/kg PO q24h for 3 days) is highly effective for treating common intestinal nematode and Giardia infections.



Cobalamin Therapy


Cobalamin (vitamin B12) is vital for many cellular processes, and it is frequently depleted in patients with chronic small intestinal disease or exocrine pancreatic insufficiency. Cobalamin deficiency can impair intestinal mucosal regeneration and cause villous atrophy and malabsorption, exacerbating diarrhea and contributing to anorexia and depression in patients with chronic GI disease.



• Treat with parenteral cobalamin (1000μg/ml) when serum levels are decreased, especially if <200 ng/L. Give injections weekly for at least 6 weeks, then every other week for 6 weeks, and then monthly.

• For cats and small dogs: Give 250μg SC, weekly

• For medium dogs: Give 500μg SC, weekly

• For large dogs: Give up to 1000μg SC, weekly


DIETARY DIARRHEA



Etiology



• Diarrhea as a result of indiscriminant eating and chewing behavior is particularly common in dogs. Dietary indiscretions include overeating, ingestion of spoiled garbage or decomposing carrion, and ingestion of abrasive or indigestible foreign material (e.g., bones, stones, hair, plants, wood, cloth, carpeting, foil, or plastic) that can traumatize the GI mucosa.

• Diarrhea may result from an abrupt change in diet. Any change in the composition of the diet should be made in gradual increments over a period of several days to allow adaptation.

• Animals may be intolerant of certain foods, such as lactose ingested as milk, fatty foods, spicy foods, and food additives found in certain commercial diets. Food hypersensitivity to specific protein sources is implicated as a cause of inflammatory bowel disease in dogs and cats.

• Fiber-responsive diarrhea is sometimes seen in dogs.


Diagnosis


Dietary causes of diarrhea usually are identified by careful history-taking and the response to a restricted diet.



• Carefully question the owner about all aspects of diet and environment, including recent changes in type and brand of food, all supplemental feeding practices using “people foods,” patterns of chewing behavior involving non-food items (including toys, plants, and haircoat), likelihood of garbage ingestion, and potential for unobserved indiscretions in free-roaming animals.

• Examine the feces for abrasive particles.


Treatment


Dietary diarrhea is self-limiting with feeding of a restricted diet, elimination of identifiable offending substances from the diet, and prevention of indiscriminant eating or chewing behavior. Management of dietary hypersensitivity is discussed under “Chronic Inflammatory Bowel Disease” later in this chapter.



DRUG- AND TOXIN-INDUCED DIARRHEA



Etiology



• Diarrhea is a frequent adverse side effect of many medications, including nonsteroidal anti-inflammatory agents (e.g., aspirin, ibuprofen, indomethacin, phenylbutazone, and flunixin meglumine), digitalis and other cardiac drugs, dithiazanine (Dizan), magnesium-containing compounds, lactulose (for hepatic encephalopathy), some anthelmintics, most anticancer drugs, and many antibacterial drugs (partly from adverse effects on the flora).

• Dexamethasone has been associated with hemorrhagic gastroenterocolitis characterized by erosion, ulceration, necrosis, and sometimes fatal colonic perforation, especially in dogs treated for intervertebral disc disease.

• Many exogenous toxins cause diarrhea, including biologic toxins such as the enterotoxins that cause staphylococcal and clostridial food poisoning and various diarrheogenic chemical poisons, such as heavy metals (lead, arsenic, thallium), insecticides (organophosphate dips, flea treatments), lawn and garden products (insecticides, herbicides, fungicides), and some houseplants.

• Free-roaming animals may drink from stagnant or runoff water polluted or potentially contaminated with toxic industrial, petroleum, or agricultural chemicals.


Diagnosis


Suspect drug- and toxin-induced diarrhea on the basis of history of exposure (or opportunity for exposure), clinical signs, and exclusion of other causes of diarrhea.



• Many medications and most toxins that cause diarrhea also cause vomiting.

• Some toxicities are associated with various extraintestinal signs (e.g., neurologic manifestations of lead and organophosphate toxicity).


Treatment



• Drug-induced diarrhea usually resolves after discontinuation of the offending medication or a reduction in its dosage.

• Toxin-induced diarrhea resolves with symptomatic antidiarrheal therapy, prevention of further exposure to the toxin, and gradual elimination of the substance from the body. However, if the exact toxin is known, consult other sources of information for additional specific treatments and antidotes.

Related posts:

  1. Feline Infectious Peritonitis (Feline Coronavirus)
  2. Borreliosis (Lyme Disease)
  3. Immune-Mediated Dermatoses
  4. Otitis Media and Otitis Interna

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Aug 27, 2016 | Posted by in SMALL ANIMAL | Comments Off on Diseases of the Intestines

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