Page 204 - WSAVA2017
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An Urban Experience
WSVA7-0512
GLOBAL NUTRITION
PROTEIN-LOSING ENTEROPATHY: CAN DIETARY MANAGEMENT HELP?
L. Weeth1
1Veterinary Cancer Group -Los Angeles, Clinical Nutrition, Culver City, USA
PROTEIN-LOSING ENTEROPATHY: CAN DIETARY MANAGEMENT HELP?
Frederic Gaschen, Dr.med.vet., Dr.habil., DACVIM (SAIM), DECVIM-CA Louisiana State University, Baton Rouge, LA USA, fgaschen@lsu.edu
Lisa Weeth, DVM, MRCVS, DACVN
Weeth Nutrition Services, Los Angeles, weethnutrition@gmail.com
OVERVIEW
Chronic intestinal protein loss is a sign of failure of digestive function that may result from severe acute or chronic inflammatory lesions or from a disruption of chyle absorption and intestinal lymph flow. While the exact mechanisms leading to intestinal protein loss have not been elucidated in the dog, the three basic mechanisms defined for humans with protein-losing enteropathy
(PLE) likely also apply to canine PLE. It is frequently associated with severe chronic idiopathic inflammatory enteropathies such as inflammatory bowel disease (IBD) or with idiopathic intestinal lymphangiectasia in specific breeds. Protein loss may result from: 1) erosive or ulcerative mucosal lesions causing secondary exudation of proteins; 2) lymphatic dysfunction causing leakage of protein-rich lymph into the intestinal lumen; 3) mucosal changes disturbing the mucosal barrier, causing abnormal permeability and protein leakage into the lumen; or 4) a combination of all three of the previously listed conditions.
This presentation will focus on chronic intestinal disorders associated with intestinal protein loss in dogs and the dietary and medical treatments for this condition.
DIAGNOSTIC APPROACH
Dogs with PLE often present with typical clinical signs of chronic intermittent small intestinal diarrhea with possible vomiting. In severe cases, hyporexia/anorexia and malnutrition with evidence of malabsorption and weight loss may be observed. However, significant intestinal protein loss and hypoalbuminemia may also occur without obvious diarrheic episodes. In the presence of severe hypoalbuminemia (serum albumin < 20 g/l, often ≤ 15 g/l) the main complaint may relate to significantly decreased oncotic pressure (cavitary effusion, subcutaneous edema).
The first diagnostic challenge consists in establishing the origin of the protein loss by ruling out other processes such as protein-losing nephropathy or liver failure. Generally, PLE is associated with panhypoproteinemia due to non-selective intestinal protein loss, but exceptions may occur. Other common abnormalities
of dogs with PLE include hypocholesterolemia, hypocalcemia (total and free/ionized), hypomagnesemia, lymphopenia, and hypocobalaminemia.
Once the GI tract has been confirmed as the site of protein loss, further work-up should include abdominal ultrasound, a technique with acceptable sensitivity that often helps assessing severity and anatomic distribution of intestinal lesions. Hyperechogenic mucosal striations are frequently observed in dogs with PLE, and appear to be quite specific.
Diagnosing the cause of PLE requires histopathologic analysis of intestinal biopsies. However, dogs with severe hypoalbuminemia are often poor anesthetic candidates, and it is sometimes preferable to avoid taking excessive risks and postpone endoscopy or surgery. Additionally, many dogs with PLE have bicavitary effusion, and thoracic radiographs are recommended as a screening tool for
the presence of thoracic effusion, as it may represent an additional anesthetic risk. Synthetic colloids such as 6% hetastarch solutions are very useful in order to acutely increase oncotic pressure in critical cases (1 ml/kg/h or 25 mg/kg/day). Transfusions with human albumin have been recommended in the recent past for partial restoration
of serum albumin concentration and minimizing the risks of general anesthesia, but are unfortunately associated with immune-mediated vasculitis in approximately 10% of recipients (5% human albumin at 2 ml/kg/h during 10 h/ day, total daily volume of 20 ml/kg/day).
CAUSES OF PLE
Diseases frequently associated with PLE include intestinal lymphangiectasia, IBD, and chronic enteropathies with significant mucosal architectural lesions. Moreover, alimentary lymphoma and fungal infections (histoplasmosis) may also cause PLE.
Intestinal lymphangiectasia (IL): Primary idiopathic
IL: breeds such as Yorkshire terriers, Chinese Shar-Peis, Maltese terriers, Norwegian Lundehunds, and Rottweilers are predisposed. The pathogenesis of primary IL is still poorly understood. It results from obstruction to the flow of lymph in the intestinal wall, and has been associated with granulomas obstructing lymph vessels located in
in the deep layers of the intestinal wall. Secondary IL is commonly associated with significant intestinal mucosal inflammation (e.g. IBD) and neoplasia (alimentary lymphoma) that increase tissue pressure and prevent lymph flow in the lamina propria.
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 42ND WORLD SMALL ANIMAL VETERINARY ASSOCIATION CONGRESS AND FECAVA 23RD EUROCONGRESS
  





































































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