Alterations in Alimentary and Hepatic Function


Chapter 7

Alterations in Alimentary and Hepatic Function



Bradford P. Smith, K. Gary Magdesian


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Diarrhea


K. Gary Magdesian • Bradford P. Smith


Diarrhea is an increase in the frequency, fluidity, or volume of feces. Diarrhea may be a sign of a primary gastrointestinal (GI) disease or a nonspecific response to sepsis, toxemia, or disease of another organ system.


Under normal circumstances a large volume of essentially isotonic fluid enters the proximal GI tract daily. Most of this fluid is resorbed, and only a small percentage is ultimately passed with the feces. The fluid comes from dietary intake and from endogenous secretions of the upper digestive tract. The total daily volume exchanged exceeds that of the animal’s total extracellular fluid volume. Normally absorption just exceeds secretion; therefore small changes in rate of absorption or secretion can result in diarrhea. In the horse most water resorption occurs in the cecum and large colon, and diarrhea in the horse (other than neonates) usually involves some abnormality in the lumen or wall of the large intestine.


Normal fecal color is tan, brown, or greenish, depending on diet. The adult horse normally produces 11 to 13 kg of fecal material per day (20 to 28 g/kg of body weight per day) while on a diet of grass hay and 3 lb of oats.1 Fecal output is as high as 20 kg/day in horses fed a mixture of alfalfa and orchard grass ad libitum.2 Horses with chronic watery diarrhea can produce up to 214 g/kg of body weight per day, 1 which is over 90 L of diarrhea in a 450-kg horse. Cattle normally produce 15 to 28 kg of feces per day with a water content of about 75% to 85% on a diet of grass hay.3 Fluidity of cattle feces can increase markedly in animals on lush green feed. Sheep and goat feces contain only 50% to 60% water.3 Fluid feces in the cow and unformed feces in the horse, goat, and sheep are nonspecific signs that often accompany sepsis or illness other than a primary gastrointestinal disease.


Animals with chronic diarrhea rarely develop severe dehydration because they compensate for increased fecal water losses by increasing water consumption by an equivalent amount. Normal water consumption in the horse on a hay diet in a mild ambient temperature environment is about 24 to 30 L/day, whereas cattle consume 30 to 60 L/day based on 10 kg of dry matter feed intake. Water and feed intake do not increase linearly with increasing body size, but by multiplying body weight in kilograms to the 0.75th power (BW Kg0.75) by a base factor (≈200 mL for water). Thus a 500-kg horse requires 21 L of water. The effect of temperature on water intake is dramatic and is not linear; as ambient temperatures rise close to 37° C (98° F), water intake per kilogram of dry matter increases much more rapidly than at lower temperatures. Exercise and loss through sweat, particularly in the horse, can dramatically increase salt and water requirements.



Mechanisms of Diarrhea (Box 7-1)


The following six major mechanisms produce diarrhea:




The common net result is an increase in fecal water.


Decreased surface area is mainly a result of villous blunting (atrophy) and/or microvillous damage in the small intestine, which lead to malabsorption. Both occur to some degree with most enteric diseases, and regeneration of surface area from crypt cells with healing is accompanied by a gradual decrease in the volume of diarrhea. Diseases in which this is a major mechanism include neonatal diseases such as rotavirus and coronavirus enteritis,4 cryptosporidiosis, acute inflammatory disease such as salmonellosis, and chronic diseases such as Johne’s disease and other granulomatous bowel diseases. The finding of villous atrophy is so nonspecific that it is not diagnostic in itself. It can also occur in advanced cases of secondary copper deficiency (molybdenosis) with diarrhea. Loss of villous epithelial cells can result in maldigestion because these cells produce important enzymes such as lactase. Many neonates with enteritis develop temporary lactose intolerance as a result, especially with rotaviral and clostridial infections. Damaged surface area occurs in such diseases as salmonellosis, where the mucosa of the large colon and cecum may be severely disrupted.


Inflammation can be accompanied by increased mucous production and increases in size of membrane pores, through which tissue fluids and serum proteins leak into the lumen. This is associated with increased capillary and lymphatic hydraulic pressures. Both acute (salmonellosis) and chronic (Johne’s) inflammatory bowel diseases are protein-losing enteropathies. Low plasma protein concentrations, particularly low albumin, are often found (unless hypovolemia and hemoconcentration are present). Bowel inflammation often results in transudation and exudation of serum proteins, blood, and/or mucus, resulting in dysentery (bloody diarrhea). In addition to salmonellosis, dysentery may also commonly be seen with enterotoxemia caused by Clostridium perfringens, types A, B, or C; Clostridium difficile; Lawsonia intracellularis5; attaching effacing Escherichia coli; Campylobacter jejuni; coccidiosis; malignant catarrhal fever (MCF); arsenic toxicity; and oak toxicity. Inflammation results in malabsorption, maldigestion, osmotic effects, and, in acute disease, changes in intestinal motility. Because most water absorption in the horse occurs in the cecum and colon, inflammatory typhlitis and colitis are the major causes of diarrhea in the adult horse (Boxes 7-2 and 7-3). The neonatal foal commonly develops small intestinal enteritis.




Irritation of the bowel with a foreign body such as sand may result in either low-grade recurrent colic or diarrhea. Weight loss may also be evident with a large amount of sand. Sand accumulation in the large bowel of the horse may be suspected when there is evidence of a significant amount of sand in the feces or when sand can be auscultated with a stethoscope over the ventral abdomen. Irritation probably causes diarrhea through creation of an inflammatory response and altered motility.


Osmotic diarrhea results from any disease causing maldigestion and/or malabsorption. Any osmotically active solute can produce diarrhea in normal animals if given in quantities sufficient to surpass the intestinal capacity for digestion or absorption. Disaccharides are natural examples. Osmotic cathartics such as dioctyl sodium sulfo­succinate (DSS) hold water in the intestine and act as fecal softeners. Magnesium phosphates and sulfates and other divalent and trivalent cations and anions are poorly absorbed and thus are effective laxatives and cathartics.


Osmotic diarrhea can be associated with ingestion of osmotically active and poorly absorbed solutes, overloading of the intestine with carbohydrates or lipids beyond the amount that can be digested and absorbed, sudden dietary changes resulting in marked shifts in gut flora and resulting bacterial action on ingested substrate (e.g., grain overload), or bowel disease in which surface area is diminished or digestion interfered with in some manner. Lactase deficiency, secondary to rotavirus or C. difficile infections, may result in osmotic diarrhea in foals.6 This results in increased concentration of undigested and/or unabsorbed nutrients entering the lower bowel, increased bacterial fermentation, and an increase in the concentration of osmotically active particles. Unfavorable electrochemical gradients prevent resorption of water. Mucosal digestive enzyme levels are often decreased with any disease involving the small intestine, resulting in maldigestion. When osmotic diarrhea is suspected in mature animals, dietary modification to basic roughage should be tried as part of the nonspecific therapy. Sodium and potassium are normally present in roughly equal amounts in feces and (with small concentrations of ammonium) make up the vast majority of cations in the feces. Concentrations of sodium and potassium in feces and osmotically active nonelectrolytes influence fecal water. In general, osmotic diarrheas diminish when the animal is fasted. When the offending substance is reintroduced, diarrhea occurs.


Secretory diarrheas are most important in neonates4 (e.g., enteropathogenic E. coli), but many strains of Salmonella that are associated with colitis in large animals may also produce enterotoxins that stimulate secretion. Enterotoxins act by stimulating cyclic adenosine monophosphate (AMP) or other intracellular messengers to promote secretion of chloride, sodium, and other electrolytes into the gut lumen. Water is carried with these electrolytes and osmotically retained. The hallmark of secretory diarrheas is the large volume of feces produced.


Examples of secretory diarrheas are enterotoxigenic E. coli, many strains of Salmonella, and C. perfringens. Salmonella and other invasive microorganisms produce inflammation that may induce prostaglandin-mediated secretion as well. Secretion may occur with viral diarrhea by a different mechanism, as damaged mature (absorbing) villous cells are replaced by immature (secreting) crypt cells.7 An example of viral secretory enteritis is rotavirus.


Decreased intestinal transit time, associated with increased peristalsis and/or decreased segmentation, appears to occur in many bowel diseases because of bowel irritation. Peritonitis is a major cause of bowel inflammation and should always be explored as a contributing cause of diarrhea, especially when fecal output volume is scant. Abnormal motor patterns have been demonstrated to occur with many infectious diarrheas and may be a bowel response to irritation and/or increased intraluminal volume. Elimination of gut contents thus appears to be a normal gut defense mechanism against infection and should not be pharmacologically alleviated in acute infectious diarrheas. Primary motility disorders of animals are not well recognized; diarrhea associated with nervous or excited animals may be the best example of this type. In general, fecal volume associated with motility disorders is not great.


Increased hydraulic or hydrostatic pressure, from the blood to the intestinal lumen, also decreases net fluid absorption. These can result from decreased oncotic pressure (hypoalbuminemia), increased capillary hydrostatic pressure (heart failure or portal hypertension as with liver disease), or decreased lymphatic drainage associated with inflamed or blocked lymph vessels or nodes (lymphosarcoma). These mechanisms are most commonly associated with chronic diarrhea, but acute inflammation can also result in diarrhea associated with this mechanism.


Two or more of these mechanisms are probably at work in most diarrheal diseases. Therapy of diarrhea is therefore nonspecific and supportive, except when the actual causative agent can be identified and is treatable. Diagnosis of a specific causative agent is most important when diarrhea is caused by an infectious agent, so that appropriate therapeutic steps can be taken before chronicity develops, spread of disease can be prevented, and an accurate prognosis can be made.


In mature horses, small intestinal diseases such as granulomatous bowel disease or duodenitis/proximal jejunitis (anterior enteritis) may not be associated with diarrhea and diseases of the stomach almost never cause diarrhea. Most significant diarrheal disease in adult horses involves the large colon because this is the principal site of water absorption. The exception to this is the neonatal foal, in which primarily small intestinal diseases such as rotavirus infection and cryptosporidiosis may cause severe diarrhea.


The frequency of defecation is usually increased when diarrhea is present, and defecation frequency is highest when the colon or rectum is irritated. When these areas are involved, tenesmus (straining) may result. Tenesmus can also occur with hepatic failure in ruminants and in horses and ruminants with rectal tears or strictures, vaginitis, retained placenta, dystocia, intussusception, urolithiasis, perirectal abscesses, rabies, and diseases involving the nervous system when there is retention of feces or urine. Severe rectal irritation can lead to straining and rectal prolapse.


In ruminants, abnormalities such as grain overload (toxic indigestion) resulting in ruminal osmotic changes can produce diarrhea, as can changes in abomasal pH such as occur with type II ostertagiasis. Diarrhea in ruminants is frequently caused by forestomach problems (Boxes 7-4 and 7-5). The colon and remainder of the distal bowel are involved in diseases such as salmonellosis. Gram-negative infections and resulting endotoxemia, found in conditions such as coliform mastitis and septic metritis, are relatively common causes of nonspecific diarrhea. Foals with septicemia also commonly develop non­specific diarrhea associated with SIRS. Diarrhea may be (1) a manifestation of a primary disease (bovine viral diarrhea [BVD]; Johne’s disease; C. difficile, salmonellosis); (2) one of the signs of a generalized disease (MCF, uremia); or (3) secondary to toxemia (coliform mastitis, septic metritis, septicemia, salmonellosis).



Box 7-4


Causes of Diarrhea in Ruminants (Except Neonates; see Chapter 20 for Neonates)






* Rinderpest was a cause of diarrhea in ruminants until 2011, when it was eradicated worldwide.




Nonspecific Fluid Therapy for Diarrhea


Dehydration, electrolyte losses, and acid-base abnormalities can occur rapidly when diarrhea is present. Treatment to correct these problems is an important component of nonspecific therapy in animals with diarrhea. Often the cause of diarrhea remains undetermined, yet correction of hypovolemia, dehydration, and acid-base and electrolyte abnormalities can result in a return to normal systemic function, particularly if the diarrhea is acute and severe. Fluids and electrolytes can be given orally or parenterally. Oral fluids can be given rapidly and inexpensively but only if dysmotility is not present. Oral fluids should be isotonic or hypotonic. The degree of dehydration should be estimated as a percentage of body weight. Mild dehydration is usually considered less than 5%; moderate, 5% to 8%; and severe, over 8%. Thus a severely dehydrated 450-kg patient with an estimated 10% dehydration (weakness, cold extremities, sunken eyes, decreased urine output, decreased elastic skin rebound, weak pulse, rapid heart rate) may require up to 45 L of fluids over time. Boluses of 10 to 20 mL/kg of isotonic crystalloid can be administered until signs of shock abate or plateau.


The optimal means of determining electrolyte status is to analyze a plasma or serum sample before initiating fluid therapy. Electrolyte requirements can be estimated; with diarrhea, mixed water and electrolyte losses occur, so sodium-containing fluids are usually required to replace lost sodium and improve blood volume (see also Critical Care and Fluid Therapy, Chapter 44). Unless the acid-base status can be measured, the safest sodium-containing fluids are balanced polyionic fluids such as PlasmaLyte A, PlasmaLyte 148, or lactated Ringer solution. Normal saline is a satisfactory alternative in most cases, but the relatively high concentration of chloride ions in saline can aggravate a preexisting metabolic acidosis through raising chloride concentration, producing a hyperchloremic metabolic acidosis (HCMA). In calves with severe metabolic acidosis, use of fluids containing sodium bicarbonate is indicated. In horses, it is best not to include large quantities of sodium bicarbonate in fluids unless there is good evidence that a severe strong ion metabolic acidosis exists (such as hyperchloremia). Flow rates for administering isotonic intravenous fluids should be monitored, with close attention to perfusion parameters, in order to avoid fluid overload, pulmonary edema, and excessive diuresis. When the patient is shocky, flow rates close to 20 mL/kg/h or faster may be required for administration of isotonic crystalloid fluids, but in general rates below 10 mL/kg/h are desirable, especially once hypovolemic shock has been addressed. Hypertonic saline (7% NaCl) may be given rapidly intravenously at a dose of 4 to 5 mL/kg. When a colloid fluid is required to combat low plasma protein concentrations, hetastarch or plasma can be used. Hetastarch is available as 6% hetastarch in a balanced electrolyte or normal saline solution. A dose of 10 mL/kg should not be exceeded for hetastarch because of development of dose-dependent coagulopathies. The use of hetastarch in human critical care has recently been questioned. A meta-analysis has suggested an increase in renal disease and mortality in patients treated with hetastarch.7a How this applies to large animals is unknown, but creatinine should be monitored closely. See Neonatal Diarrhea, Chapters 17 (neonatal foals) and 20 (neonatal ruminants); Fluid and Electrolyte Balance, Chapter 22; and Fluid Therapy, Chapter 44 for more details on fluids and acid-base balance.



Approach to Diagnosis of Diarrhea in the Horse (for Neonates, see Chapter 17)



1. Take history. Especially note change in diet, deworming program, housing and management, and whether diarrhea is acute or chronic. Note appetite, whether animal is drinking an adequate volume of water, and whether salt is available. Note whether it is a single or multiple case, if there are concurrent diseases, or if other medications or exposure to toxins is involved. Most antimicrobials have been associated with diarrhea in horses at times, but especially lincomycin, tetracyclines, and erythromycin. Antimicrobials should be discontinued if diarrhea develops during administration. Most pathogenic bacterial and protozoal agents rely on altered intestinal microflora to proliferate in the gut and cause diarrhea. Note whether nonsteroidal antiinflammatory agents were used before the development of diarrhea. Many causes of diarrhea can be eliminated from consideration on the basis of history. Find out about housing and whether animals have access to pasture or natural water sources or are stall confined. For example, Potomac horse fever would be considered in horses with access to water sources in endemic areas.


2. Perform physical examination. Take vital signs (these are often normal in chronic cases). Perform rectal examination unless an infectious contagious agent is suspected, especially if diarrhea is scant in volume. Note body condition score (see Chapter 9). Systemic signs of toxemia, SIRS, hypovolemia, and dehydration often accompany acute colitis, salmonellosis, equine monocytic ehrlichiosis (Potomac horse fever), clostridiosis, and many other acute diseases.


3. Examine feces. Perform gross inspection; note whether blood or fibrin is present (see list of causes of dysentery).


a. Gram stain of feces. A predominance of gram-positive rods may indicate an anaerobic overgrowth such as occurs with C. difficile infections, although this is not highly sensitive or specific. Perform microscopic examination for ova and protozoa, especially for chronic cases.


b. Perform multiple cultures for Salmonella, C. difficile,8 and C. perfringens if onset is acute, if animal is febrile, or if feces contain fibrin and mucus. A commercial polymerase chain reaction (PCR) test can be used as an aid to evaluate for the presence of salmonellosis.9 Cultures for C. difficile should be performed on selective media (cycloserine-cefoxitin-fructose agar). Recently Brachyspira pilosicoli has been isolated from the feces of weanlings with chronic diarrhea.10 This warrants further investigation as a cause of diarrhea and failure to thrive in young horses. Fecal PCR and serology for L. intracellularis should be performed on young horses with hypoproteinemia, unthriftiness, and variable diarrhea.


c. An evaluation for C. difficile and C. perfringens toxins (with fecal enzyme-linked immunosorbent assays [ELISAs] or a stool cytotoxin assay for C. difficile) should be made if the diarrhea is temporally associated with antibiotic administration. Several ELISA kits are available for identification of toxins A (enterotoxin) and B (cytotoxin) of C. difficile in feces. A stool cytotoxin cell culture is available for toxin B.11,12 Toxin B cell culture testing is considered the gold standard.13


d. Isolates of C. perfringens should be examined for the ability to produce alpha, beta, epsilon, and beta 2–toxins because certain strains may be associated with gastrointestinal disease.14,15 Type C C. perfringens isolates have been associated with the most severe disease in horses and foals. Gene sequences for these toxins are found by PCR once the isolates are cultured. In addition, a commercial fecal ELISA is now available for detection of alpha-toxin, beta-toxin, and epsilon-toxin in feces directly at the California Animal Health and Food Safety Laboratory (San Bernardino). This allows diagnosis of C. perfringens, types A (alpha toxin) and C (alpha and beta toxins).


e. Fecal occult blood (if positive, see list of causes of melena and blood in feces).


f. Fecal osmolality, sodium, and potassium concentrations (optional). Electrolyte concentration in feces is roughly twice the sodium plus potassium. When this value is much lower than the measured osmolality of the feces, the difference is an osmolar gap caused by osmotically active nonelectrolytes, and osmotic diarrhea is confirmed.


g. Check for sand by placing some feces in a bucket of water, mixing thoroughly, and decanting the water. If a radiographic unit with the appropriate power capability is available, abdominal radiographs should be taken to detect the presence and amount of sand. Ultrasound of the ventral abdomen can be used to diagnose the presence of sand, although this requires considerable expertise.


h. A PCR test for feces is available at University of Minnesota Diagnostic Laboratory at www.vdl.umn.edu and the University of California Molecular Laboratory at www.vetmed.ucdavis.edu/vme/taqmanservice/ (see Chapter 29 for complete list) for detection of L. intracellularis, organisms in weanlings and yearlings with diarrhea, weight loss, general malaise, and hypoalbuminemia.16 Also see serum test described later.


i. Rhodococcus equi can cause diarrhea in 3-week to 6-month-old foals. Diagnostic tests include cultures of transtracheal aspirates, abdominal fluid cytology and culture, abdominal ultrasonography, and ruling out other etiologies of diarrhea. Fecal PCR techniques are also available.17


j. If all other cultures are negative and an infectious cause of diarrhea is suspected, the feces should be cultured for Aeromonas species and C. perfringens (see earlier).18,19


4. Obtain blood for the following database:


a. Complete blood count (CBC; includes fibrinogen and plasma protein concentrations). Increased fibrinogen concentration indicates inflammation. Decreased protein concentrations indicate protein-losing enteropathy. Thrombocytopenia may indicate a coagulopathy. Neutropenia with or without a toxic, left shift (immature neutrophilia) is often present with infectious and inflammatory causes of acute colitis, indicating SIRS. Increases in packed cell volume (PCV) and red cell mass are often present, indicating hemoconcentration and/or splenic contraction in horses.


b. Acid-base analysis should be performed if the condition is acute and the horse is dehydrated or toxic. Although acid-base values are not useful diagnostically in terms of specific etiology, they allow for initiation of proper acid base and electrolyte supportive therapy.


5. Test serum for the following:


a. Electrolyte (Na, K, Cl, Mg, Ca, HCO3) concentrations.


b. Serum creatinine and blood urea nitrogen (BUN) concentrations—prerenal azotemia is common as a result of dehydration; check again after rehydration. Acute renal failure is also common. Serum chemistries should be evaluated for liver and other organ disease.


c. Albumin and globulin concentrations; hypoalbuminemia is seen with chronic protein-losing enteropathies such as inflammatory bowel disease (e.g., granulomatous enteritis), phenylbutazone toxicity (right dorsal colitis), and acute colitis conditions (such as salmonellosis).


d. Specific immunoglobulin (Ig) A, IgM, and IgG concentrations; immunodeficient individuals may have chronic diarrhea. Specific immunoglobulin concentrations may be altered with lymphoma or multiple myeloma. Elevated globulins may indicate the presence of chronic disease.


e. PCR for Neorickettsia risticii (Potomac horse fever) in whole blood and feces samples. Paired sera for Neorickettsia risticii titer following acute diarrhea with fever can also be performed.


f. Clotting times (prothrombin time [PT] and partial thromboplastin time [PTT] or activated clotting time [ACT]) should be monitored as indicators of coagulopathies such as disseminated intravascular coagulation (DIC) in horses with acute typhlocolitis. Antithrombin III levels can be monitored for the risk of thromboses, particularly in horses with hypoproteinemia.


6. Perform abdominocentesis, especially if signs of colic are present. Evaluate cytology, protein, and fibrinogen values in chronic cases to rule out peritonitis, tumors, and mesenteric abscess.


7. Perform function and absorption tests in chronic diarrhea cases, especially when weight loss is present.


a. Oral glucose or xylose small intestine absorption tests (see Chapter 32) for chronic cases, particularly if a high index of suspicion of malabsorption exists because of hypoalbuminemia. If tests indicate malabsorption, either biopsy the gut (duodenum through duodenoscopy or rectum) or assess the response to treatment following larvicidal anthelmintic treatment.


b. Perform liver function tests such as measurement of serum bile acid concentrations if liver involvement is suspected as a result of increased liver enzyme concentrations and/or hypoalbuminemia. Liver enzymes are increased in many cases of enterocolitis and in these cases do not necessarily indicate primary liver disease (see Chapter 33). Secondary liver disease may occur secondary to endotoxemia or altered hemodynamics, as well as cholangiohepatitis.


8. Examine tissue.


a. Rectal or intestinal (duodenal) biopsy for microscopic examination and fluorescent antibody for immune-mediated diseases (also culture for Salmonella). Rectal histopathology is particularly useful in horses with hypoalbuminemia or weight loss.20


b. Detection of C. perfringens beta 2–toxin from types A or C by immunohistochemistry of gut mucosa is diagnostic on biopsy or postmortem specimens.21


c. Liver biopsy if indication of significant or persistent liver disease, especially in chronic cases.


9. Toxicology.


a. Blood lead, liver lead, and liver arsenic concentrations can be measured if toxicity is suspected.22


b. High-pressure liquid chromatography or gas chroma­tography-mass spectrometry can be used to detect cantharidin (blister beetle toxin) in urine or gastrointestinal contents.23


c. Urine, serum, and gastrointestinal contents can be evalu­ated for the presence of oleandrin toxins using thin-layer chromatography. Oleander toxicity should be suspected in animals with diarrhea, colic, arrhythmias, and renal disease.24


10. Evaluate response to treatment with undiagnosed chronic diarrhea.


a. Alter diet to simple grass hay. Alternatively, a complete pelleted diet can be tried, especially if right dorsal colitis or maldigestion/malabsorption is suspected. Psyllium mucilloid (4 oz), and 1 to 2 cups of corn oil can be added to the daily diets of horses with right dorsal colitis.25,26


b. Stop nonsteroidal drugs such as phenylbutazone if toxicity is a possible cause.


c. If no protozoa are seen in fecal samples, attempt transfaunation with fecal (or colon or cecum if available) contents from a healthy animal.


d. Attempt to classify by rectal biopsy; many changes are nonspecific.


(1) Mononuclear cell infiltrate (lymphocytic or granu­lomatous enteritis): Administer 0.04-0.06 mg/kg dexamethasone per day, tapering down to 0.02 mg/kg in 1 week; if response is favorable, continue with 1-1.5 mg/kg prednisolone PO per day, taper over 2 months.
Eosinophilic infiltrate: Administer larvicidal anthel­mintic dose of fenbendazole plus corticosteroids as earlier.


e. Transfusion with plasma (1 to 2 mL/kg) in young horses 2 to 12 months of age that may need some additional proteins, antithrombin, or immunoglobulin. Synthetic colloids such as hetastarch can be used in animals with reduced colloid osmotic pressure (hypoalbuminemia); check especially if edema is present. Hetastarch has been used at 10 mL/kg, and this dose should not be exceeded daily because of risks of dose-dependent coagulopathies.27


f. Horses with Potomac horse fever often respond favorably to systemic treatment with tetracycline.


g. Metronidazole (15 mg/kg PO q 8 h) can be used empirically, especially if an anaerobic overgrowth is suspected, or when the diarrhea is secondary to antibiotic use.28



Approach to Diagnosis of Diarrhea in Ruminants (for Neonates, see Chapter 20)



1. Take history. Especially note diet, appetite, previous deworming and vaccinations, and whether it is an individual or herd problem. In animals younger than 1 year of age, Coccidia, Ostertagia, or other helminths should be strongly considered. Determine if onset is acute or chronic. If chronic, first consider diseases such as parasitism, Johne’s disease, copper deficiency (molybdenosis), selenium deficiency, liver failure, and other diseases of individual cows such as bovine leukosis virus (BLV), amyloidosis, heart failure, or uremia.


2. Perform physical examination. Especially note weight loss, fever, systemic signs, rumen activity, and oral lesions. Perform rectal examination. In most acute-onset diseases, vital signs are abnormal and systemic involvement or oral lesions (especially with BVD) may be obvious.


3. Examine feces.


a. Gross inspection


b. Microscopic examination for ova and parasites


c. Culture for Salmonella if animal is febrile or feces appear inflammatory (fibrin or mucus)


d. Check for fecal occult blood


e. Culture of Mycobacterium avium subsp. paratuberculosis, if weight loss is a problem (especially if a herd problem in animals older than 2 years of age)


4. Take rectal scrapings of mucous if weight loss and chronic diarrhea are present.


a. Make thin smear on glass slide for acid-fast staining for M. avium subsp. paratuberculosis. Examine under oil immersion lens.


5. Obtain blood for the following:


a. Plasma proteins


b. Fibrinogen


c. In acute cases, electrolytes and acid-base status


d. If a herd problem, copper and selenium status


6. Test serum for the following:


a. BUN


b. Liver enzymes (γ-glutamyltransferase [GGT] and sorbitol dehydrogenase [SDH])


c. Albumin and globulin values


d. Agar gel immunodiffusion (AGID) for BLV (single animals); request gp51 and p24 antibody status


e. If Johne’s disease is suspected, perform ELISA test


7. Perform paracentesis. Paracentesis rules out gross peritonitis, but many false-negatives are possible as a result of focal or fibrinous peritonitis.


8. Perform urinalysis for protein to rule out consideration of amyloidosis or other multisystemic immune-mediated disease. Because ruminants normally have a urine pH of 8 or higher, most dipstick tests will give a trace or a 1+ positive reading for urine protein even when the animal’s urine is normal.


9. Examine tissue. Perform rectal, intestinal, or mesenteric lymph node biopsy for acid-fast stain for Johne’s disease, for culture for Salmonella, and for presence of lymphosarcoma.


10. Perform feed analysis (herd problem only); check copper, molybdenum, and selenium levels.


a. Toxins suspected (e.g., mercury, arsenic)


11. Tap abomasum for increased pH; rule out type II ostertagiasis.


12. Perform necropsy (herd problem only).


a. Pick severely affected individual to examine thoroughly.


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Aug 11, 2016 | Posted by in INTERNAL MEDICINE | Comments Off on Alterations in Alimentary and Hepatic Function

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