Page 176 - WSAVA2017
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An Urban Experience
S. Unterer1
1Clinic of Small Animal Medicine, Centre for Clinical Veterinary Medicine, Munich, Germany
Clinic of Small Animal Medicine, Centre for Clinical Veterinary Medicine, LMU Munich
Protein losing enteropathy (PLE) is defined as an excessive loss of serum proteins into the gastrointestinal (GI) tract, resulting in hypoproteinemia. Protein loss
into the GI tract reflects always a significant damage, destruction, or structural change of the gastrointestinal wall and can be caused by any GI disease if it is severe enough. PLE is suspected in any patient with clinical signs related to GI tract and with hypoalbuminemia.
It is important to keep in mind that PLE is not always associated with obvious GI signs (e. g. dogs with PLE can be presented because of abdominal effusion due to hypoalbuminemia), and that hypoalbuminemia in a dog with GI signs is not always due to GI loss. Therefore,
in any patient with significant hypalbuminemia (<2 gm/ dl; reference range 2.5 – 4.4 gm/dl), following tests should be performed: a urinary dipstick test in order to rule out protein loss in the urinary tract, serum bile acids to rule out liver dysfunction, and diagnostic imaging.
In case fluid is present in body cavities, it is necessary
to determine protein concentration in order to rule out albumin loss. Rarely, albumin concentration can be low due to exudative skin disease or as a compensation due to extensive hyperglobulinemia. GI protein loss can be documented directly by measuring α1-proteinase inhibitor concentration in dog fecal samples, however this test is currently available only in the USA.
Once albumin loss is localized to the GI tract, sensitive tests to detect intestinal parasites (e. g. roundworms, especially hookworms and acute Giardia sp. infection in young dogs) should be performed. Additionally, basal cortisol levels should be determined, since hypoadrenocorticism can mimic primary intestinal disease causing PLE. After intestinal parasitism and Addison’s disease have been ruled out, intestinal biopsy should be performed as the ultimate means
for diagnosing inflammatory bowel disease, intestinal lymphangiectasia, intestinal lymphoma, crypt lesions, and fungal granuloma.
Abdominal imaging is an important tool for making a decision on how to biopsy the GI tract (via laparotomy or via endoscopy). After ruling out metastatic or multifocal lesions, surgical removal is indicated in focal GI disorders (such as localised neoplastic infiltration, intussusception, fungal granuloma, and foreign body). If enlarged
lymph nodes are detected, they should be aspirated. Additionally, abdominal ultrasonographic examination
is useful for detecting hyperechoic mucosal striations, which are suggestive of PLE, and for guiding the biopsies. Administration of medium chain triglyceride oil, cream or corn oil orally 2 to 4 hours before ultrasound or endoscopy can improve the detection of enlarged lymph vessels in the intestinal mucosa. If a diffuse infiltrative intestinal disease is suspected, endoscopic biopsies should be performed. Endoscopy allows visualizing mucosal lesions and minimizes the risk of bacterial infections compared to possible suture line leakage in surgical biopsy cases.
Before performing an expensive diagnostic work up, the owners should be informed about the risks and prognosis. PLE carries a guarded prognosis, due to complications during and after invasive procedures. Vitamin D (cholecalciferol) can be used as a prognostic marker, since hypovitaminosis D in PLE dogs has been associated with poor outcome.
In patients with low albumin levels (< 1.5 gm/dl),
low oncotic pressure in the blood vessels can lead
to effusions in body cavities, edema and low blood pressure. Synthetic colloid support, amino acid
solutions and plasma (primarily in small dogs) should
be given before anaesthesia to minimize the risks of anaesthetic complications. The effect of osmotic fluids
is of a short duration and can cause side effects (e. g. thrombocytopathia). Human albumin should be restricted only to critical cases, since severe and sometimes fatal adverse reactions were observed in dogs with PLE. In some patients, hypocalcemia due to PLE can cause clinical signs (e.g. weakness, increased muscle activity) and has to be addressed by supplementation of calcium and possibly vitamin D.
Treatment of patients with PLE is focused on the primary disease causing the protein loss. Non-specific treatment in all cases includes nutritional support, prevention of thromboembolism and supplementation of deficient vitamins. The goal of nutritional support is to provide high-energy support by restricting the fat content to 10% of fat in dogs with lymphangiectasia. In severely affected cases, total parenteral nutrition can be beneficial at least initially. In cases of intestinal inflammation suggestive
of food allergy, a low fat hypoallergenic diet should be introduced and clinical improvement assessed after several weeks.

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