Veterinary Medicine - October 2007 - (Page 648)

Toxicology Brief PEER-REVIEWED by the liver. It is involved in fatty acid transportation and mitochondrial function. A study of chronic aflatoxicosis in quail found enhanced antioxidant effects with L-carnitine supplementation.39 L-carnitine helps mobilize fatty acids in cats with hepatic lipidosis, but it is unknown whether it has similar activity in dogs with aflatoxicosis.40 The recommended dosage in cats is 50 to 100 mg/kg given orally once a day for two to four weeks.41 • Others. Other nutraceuticals that may be beneficial in aflatoxininduced liver disease include zinc, ursodeoxycholic acid (contraindicated in patients with biliary obstrucconsist of isotonic crystalloids supplemented with electrolytes and dextrose as needed. Monitor the patient’s acid-base status and electrolyte and blood glucose concentrations regularly, and adjust fluids accordingly. If hypernatremia is present, one-third to one-half strength saline solution is recommended.43 state in patients with aflatoxicosis. Treatment with vitamin K1 has been shown to improve, though not resolve, the coagulation abnormalities. Vitamin K should be given at a dose of 1 to 5 mg/kg either subcutaneously or orally, although subcutaneous administration is preferred because of decreased gastrointestinal absorption of oral vitamin K.44,45 Another reason for increased bleeding tendencies in patients with aflatoxicosis is enteric hemorrhage incited by portal hypertension. Histologic examination of tissue samples from dogs with aflatoxicosis reveals hepatic outflow occlusion and portal fibrosis, and the gastrointestinal tract shows resultant mucosal congestion, edema, and hemorrhage. Dogs with aflatoxicosis may exhibit hematochezia, melena, and hematemesis.4,13,15,17 Blood loss from the gastrointestinal tract and hemorrhagic effusions into the abdomen can lead to anemia.16,18 Packed red blood cells, bovine hemoglobin glutamer-200 (Oxyglobin—Biopure), or whole blood may be administered to increase oxygenation and blood volume, but these products will not decrease the portal hypertension.43,46 Finally, DIC has been reported in several cases of canine aflatoxicosis.18 The inciting cause of DIC in cases of acute hepatitis or liver failure is thought to be tissue procoagulants released into circulation from damaged hepatocytes.45 The combination of increased consumption of coagulation factors from DIC and reduced synthesis and activation of coagulation factors in aflatoxicosis may lead to severe hemorrhage. Fresh whole blood or fresh frozen plasma would be indicated in these cases, but unfortunately, patients with hemorrhagic signs have extremely poor prognoses.18 Control of hemorrhage An immediate and life-threatening concern in dogs with aflatoxicosis is an increased bleeding tendency resulting from hepatocellular damage and decreased synthesis of coagulation factors, which creates a hypocoagulable state. Constant-rate infusions of fresh frozen plasma may be indicated to supplement coagulation factors. If Hypovolemia and hypoperfusion from hemorrhage, reduced colloidal osmotic pressure, peritoneal effusions, and vomiting or diarrhea are common in liver failure. tion), phosphatidylcholine, and vitamins C and A.37,42 the patient is moderately to severely anemic, fresh whole blood is preferred.4,13,43 In addition to decreased production of coagulation factors, a vitamin K deficiency may contribute to the coagulation deficiencies seen with aflatoxicosis. On histologic examination of liver samples from dogs with aflatoxicosis, bile canaliculi are sometimes plugged with casts. Biliary obstruction interferes with the bile-salt facilitated absorption of lipid-soluble vitamin K. Moreover, aflatoxin is a coumarin-like derivative and may have a direct inhibitory effect on vitamin K activity.4 Vitamin K is an essential cofactor in the activation of coagulation factors II, VII, IX, and X, as well as anticoagulant proteins C and S. Thus, a vitamin K deficiency may contribute to the hypocoagulable Fluid support Patients with liver failure often require fluid therapy to treat dehydration from fluid loss, correct electrolyte and acidbase imbalances, lower serum ammonia concentrations, and reduce the risk of DIC. Hypovolemia and hypoperfusion are common in liver failure; contributing factors include hemorrhage from coagulation abnormalities, reduced colloidal osmotic pressure, peritoneal effusions, and water loss from vomiting or diarrhea. Initial resuscitation with colloids may be advisable (e.g. dextran-70, hetastarch, or fresh frozen plasma). Continuing fluid therapy in patients with acute liver failure may Antibiotics Because of a compromised gastrointestinal barrier in acute liver disease, patients with aflatoxicosis have an increased risk 648 October 2007 VETERINARY MEDICINE

Table of Contents Feed for the Digital Edition of Veterinary Medicine - October 2007

Veterinary Medicine - October 2007 Contents Leading Off The Veterinary Medicine Interview: Dr. Kevin Fitzgerald Toxicology Brief Idea Exchange Animal Sheltering in the United States: Yesterday, Today, and Tomorrow The Euthanasia Problem Offer Basic Behavior Counseling for Every Pet at Every Visit Promote and Perform Early Spaying and Neutering Assist Owners in Selecting the Best Pets for their Lifestyles Champion Animal Welfare in Your Community CE Form Product Review Advertiser Index Marketplace/Classifieds Mind Over Miller

Veterinary Medicine - October 2007

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