The clinical signs distinguishing small intestine disease from large intestine disease are shown elsewhere. There is a gigantic gamut of diseases and syndromes that may cause small intestinal distress resulting in either vomiting, diarrhea or both. These range from metabolic derangements that secondarily affect the health of the gastrointestinal tract to primary intestinal neoplasia, such as lymphosarcoma and adenocarcinoma. Some secondary diseases, such as pancreatitis, and hepatobiliary disease will be addressed on a separate page. Parvovirus enteritis has already been described. The scope of this page is not to address small bowel disease in a broad sense, but rather to focus on a few of the primary small intestinal problems that are often diagnosed in animals suffering with small bowel clinical signs.
Hemorrhagic gastroenteritis (HGE) is a disease of small breed dogs with no known cause. Hypothesized etiologies include reactions bacterial or other, unknown toxins; however at the moment, the disease is considered idiopathic (no known cause).
Generally, signs appear suddenly (peracute or acute) most commonly with animals experiencing severe, profuse, maloderous, bloody diarrhea and vomiting. If untreated, death occurs early. If treated promptly, animals recover, usually quickly (1-2 days).
The diagnosis is usually straight-forward. Typical breed, coupled with the typical onset of clinical signs, and blood laboratory data indicative of profound hemoconcentration (meaning that the percentage of blood volume assigned to red blood cells (also referred to as the "packed cell volume"-PCV or "hematocrit" -Hct) is greater than normal; ordinarily, red cells occupy from about 37% to 50% or so of the volume of blood but in cases of HGE, this percentage increases to 70% or or sometimes 80% or greater). Some of the increase in the PCV is no doubt attributable to contraction of the spleen during severe stress (the spleen sequesters extra red blood cells) but importantly in this instance, the profuse diarrhea and vomiting results in considerable dehydration...a net loss of fluid, relative to red blood cells; the PCV thus increases. Because there is also gastrointestinal loss of serum protein, (serum protein is a driving force for vascular fluid homeostasis...maintaining adeqate fluid balance), there is little means for the body to facilitate fluid recovery or retension.
As hypovolemic shock and concurrent electrolyte and system acid-base imbalances are the hallmarks of the disease and the most imminent threats to survival, immediate restoration of fluid volumes and corrections of metabolic derangements are the goals of treatment. Rapid intravenous infusion of fluids and electrolytes, frequent monitoring of PCV, electrolytes and if appropriate, blood gases follows. If the animal is painful, analgesics are provided. If vomiting/nausea are persistent, antiemetics are administered. For hypothermic animals, warmth is provided. Some veterinarians may include antibiotics in the treatment regimen, though there is no evidence the disease results from infection. Nevertheless, there is compromise of the entire gastrointestinal tract with potential for translocation of bacteria or bacterial toxins into the blood, thus justifying the inclusion of antibiotics. Additionally, antibiotics are indicated if the animal is febrile or if there is a low or high white blood cell count.
Within a day or two, animals are typically back to normal. Interestingly, affected animals are rarely if ever afflicted again!
The small intestine contains a stable but mixed population of bacteria in normal health. The size and relative composition of this population is influenced by several factors: the molecular and physical interactions of the various bacterial species, the source and composition of ingesta/digesta, the host animal's immune system status and the steady, normal movement of ingesta from one end (stomach) to the other (the rectum...and beyond). The latter gastrointestinal motility mechanism is a critical component in maintaining a constant balance and size of the bacterial ecosystem. Perturbations in this mechanism, manifest as vomiting and/or diarrhea will significantly upset the relationships and numbers of respective bacterial subpopulations. Additionally, diseases that are associated with altered secretions of gastric (stomach) acid, diseases that affect the integrity of the intestinal mucosa (villi-lined layer of the small intestine), other conditions affecting the natural secretion of digestive enzymes (pancreatic or hepatic diseases for example) may, likewise, alter the natural flora, favoring the proliferation of one or more bacterial subpopulations over others. The most common bacterial species present are Escherichia coli, Clostridium species, and various cocci (enterococci species).
Long-standing diarrhea and weight loss are the most common complaints in affected animals. Diarrhea tends to be of the small intestinal type, that is watery, maloderous, and of lighter or darker than normal color. Owners may complain that there is frequent flatulence. Some animals are reluctant to eat while others may demonstrate a ravenous appetite. Some of these clinical signs may be related to an underlying disorder (such as pancreatic insufficieny or a partial intestinal obstruction).
Diagnosis is extremely difficult without actually culturing small intestinal content, obtained surgically or endoscopically. However, strong presumptive diagnosis can be obtained via measuring serum vitamin B12 and folate levels. The rationale for obtaining these values is summarized in Table 1 and Table 2.
Interpretation of Results
|B12 (Cobalamin)||1. Requires intrinsic factor from the pancreas to be absorbed.
2. Absorbed only in the distal portion of the intestine (the ileum)
|1. Decreased serum levels with ANY diseases of the ileum (affecting absorption receptors)
2. Decreased serum levels with bacterial overgrowth (bacteria bind the instrinsic factor as well as binding/trapping B12 itself)
3. Decreased serum levels with exocrine pancreatic insufficiency (aka EPI; no intrinsic factor)
|Folate||1. Absorption depends on a intestinal deconjugase enzyme found in the upper small intestine only that releases folate from its conjugated form with glutamate
2. Is also synthesized by bacteria present in the small intestine
|1. Decreased with severe upper small intestine disease (decreased absorption)
2. Increased with excess dietary supplementation (therefore, should test fasted serum sample only)
3.Increased with small intestine bacterial overgrowth (increased bacterial synthesis)
4. Increased with exocrine pancreatic insufficiency (which results in small intestine bacterial overgrowth)
5. Artifactually increased by hemolysis of red blood cells (not truly increased but falsely increased)
|Decreased||Increased||SIBO with or without distal small intestine disease or EPI|
|Normal||Increased||Proximal (before-ileum) SIBO or folate supplementation|
|Decreased||Normal||Distal (ileum) disease with or without SIBO|
|Normal||Decreased||Severe proximal (before ileum) small intestinal disease|
|Decreased||Decreased||Generalized small intestinal disease with or without SIBO|
Regardless of the underlying cause...there are many possibilities...judicious use of antibiotics is warranted. Usually, antibiotics with a fairly wide spectrum of antibacterial activity are chosen. Metronidazole, tylosin, and/or one of the penicillins, (amoxicillin/clavulate, or straight amoxicillin) are good first choices. Ideally, determining and resolving the underlying problem is desirable. If full resolution is not obtained and the underlying problem is not identified and resolved, or if the problem is recurring, a pulse or intermittent antibiotics regimen for the long-term management of SIBO may be necessary
Dietary indiscretion is also referred to as "garbage can intoxication", or "garbage can toxicosis". Affected animals usually present with a recent history of eating garbage or other decaying organic matter. Clinical signs usually result from the ingestion of bacterial toxins, or...as some have hypothesized...from "osmotic overload" (non-digestible substances are ingested which draw fluid into the intestinal lumen).
Usually, victims present with vomiting and/or diarrhea and often the abdomen is painful. In most instances, routine laboratory test values are unremarkable.
This is usually based upon the history of acute onset along with a verified or suspected ingestion of decayed or other noxious substance(s). Elimination of other causes of acute enteritis via physical exam and other diagnostics, including blood and urine laboratory values, fecal flotation and cytology and, in an occasional instance in which a physical obstruction is suspected, imaging (e.g. radiographs) is, in some cases, necessary.
Treatment care is generally supportive only. Food and sometimes water are withheld for 12 - 24 hours to give the injured gastrointestinal tissues an opportunity to heal. Fluids with balanced electrolytes are provided to maintain normal hydration and to correct potential electrolyte imbalance(s). Drugs for nausea or vomiting may be included as well as anti-inflammatory/antibiotics if a bacterial component is suspected. When vomiting is not a significant component of the problem, a bismuth/salicylate (e.g. PeptoBisol®) may be beneficial for its antibacterial and anti-inflammatory properties. If improvement is noted in the first 24 hours, food is offered...usually something highly digestable, such as boiled, skinned and diced chicken, boiled white (precooked) rice and, occasionally, a low fat cottage cheese. Animals in which a history of vomiting was noted may do better when newly introduced, highly digestable foods are blenderized to a semi-liquid to liquid consistency; the more liquid-like the diet, the less likely the animal is to vomit after feeding. As improvement is clinical signs is seen, the normal diet is gradually re-introduced...over several days, each day increasing the percentage of the normal diet provided.
The role of parasites in the manifestation of gastointestinal disease has been described elsewhere on this website; please see those pages for more information
Food allergies and intolerance are a significant cause of gastrointestinal and dermatological problems in dogs and in cats. The problems associated with allergies to food come under a more generalized discussion of a broader syndrome known as Inflammatory Bowel Disease (IBD), a topic mentioned elsewhere on this website. The latter is characterized by the infiltrates of one or more types of inflammatory cells in one or more layers of the small or large intestine. The thickened and inflamed portions of the affected intestinal segments results in vomiting, diarrhea (one or both of these...though some animals show neither sign), weight loss and in severe cases, ill-thriftyness that can be life threatening. Among the many proposed causes of IBD (a very large topic unto itself) are allergies to one or more component of food. In cats the syndrome is often associated with a concurrently inflamed liver and pancreas (see more about pancreatitis and hepatitis elsewhere on this website). This peculiar association of IBD with pancreatitis and hepatitis in cats is loosely referred to as "triaditis". It is believed that this relationship derives from the close anatomical association of the common bile duct (from the liver/gall bladder), the pancreatic duct and the intestine into which these ducts empty. Food allergy often manifests with complaints of pruritis (itchy skin), and sometimes skin signs are not accompanied by gastrointestinal abnormalities!
The ubiquitous signs associated with gastrointestinal distress (vomiting and/or diarrhea) and/or pruritis are present, sometimes for months or longer. These may be chronic or may flare up acutely and intermittently. In some cats, diarrhea is not observed unless there is a concurrent environmental stressor. Weight loss is common; appetite may be decreased (due to abdominal discomfort?) or increased from normal. Pruritis is usually not seasonal, though if an animal is concurrently allergic to seasonal allergens (e.g. pollens, flea saliva), there may be a seasonal exacerbation of skin problems, confounding the diagnosis of concurrent food allergy.
Clearly, there is a huge list of potential diseases and syndromes that may present with any of the aforementioned clinical signs, a few of which are covered on this and other pages on this website. And complicating this is the fact that IBD may be idiopathic (i.e. without any proven cause). Diagnosis requires systematic elimination of the most common problems initially. Some of the differential diagnoses that are considered are listed as follows:
Differential Diagnosis of Disorders Resembling or Causing Inflammatory Bowel Disease*
|Intestinal Neoplasia (Lymphoma, Adenocarcinoma|
|Exocrine Pancreatic Insufficiency|
|Parasites (especially Giardia, Cryptosporidia)|
|Bacterial Endotoxicosis (Clostridia spp)|
|Fungal Infection (Histoplasmosis)|
|Secondary Intestinal Obstructions|
|*Modified from Handbook of Small Animal Gastroenterology, Todd R. Tams, WB Saunders, 1996|
The above mentioned diseases, except food allergies, are diagnosed via laboratory testing and/or tissue biopsy of gastrointestinal tract.
Food allergies are diagnosed via dietary elimination trials (click on the "Allergies" link on that page). Basically, a complete dietary history is obtained and a novel protein diet without potential allergens or poorly digestable ingredients is fed, exclusively for 8-10 weeks. No treats, crumbs or other food is allowed; strict compliance to this regimen is required and the animal's skin and gastrointestinal signs are evaluated at the end of the test period. If these are improved, it is likely that the animal has a food allergy. Ingredients in earlier diets are then re-introduced, one at a time, for one or more weeks and the recurrence of undesirable skin or gastrointestinal symptoms indicates an allergy to the recently added nutrient. In some instances clinical signs are due to multiple allergies, so it may be unrealistic to expect complete remission even with a successful result while on the novel protein diet.
Some veterinary testing laboratories are offering serum testing for food allergies, much like serum testing is now done for atopic dermatitis (click on the "Allergies" link on that page). However, there is no evidence that the results of serum testing for food allergies is a valid method for diagnosis, and this author recommends not using these tests...it is likely a waste of time and money.
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