FRANK J. MILNE STATE-OF-THE-ART LECTURE


centration can be administered intravenously to hy- perlipemic equines that are either hypoglycemic, normoglycemic, or have only mild hyperglycemia. Exogenous insulin therapy may be required if the horse/pony is hyperglycemic. Although hyperli- pemic equines may have an inherent decrease in insulin sensitivity, exogenous insulin can decrease hyperglycemia, inhibit lipolysis and improve cellu- lar energy balance. However, there are no con- trolled studies to provide evidence of efficacy of insulin in treating equine hyperlipemia, nor is there good information on the dose, route, and form of insulin to use although there are individual reports on the use of insulin.177,183 The easiest and gener- ally safest method of administering insulin might be to use 0.10–0.15 IU/kg of an intermediate or long- acting suspension administered subcutaneously ev- ery 12 or 24 hours, respectively. For severe hyperglycemia, a short-acting regular insulin will offer a quicker response and dosage can be quickly adjusted as needed with glucose monitoring. A starting dose for regular insulin that I have used is 0.05–0.1 IU/kg/h as a constant rate infusion (CRI) or intramuscularly every 4–8 hours. When insulin therapy is used, blood glucose and serum potassium must be closely monitored. Intravenous or oral flu- ids are also important in correcting prerenal azotemia, which might decrease LPL activity re- quired to hydrolyze circulating triglycerides. I would recommend oral or slow intravenous admin- istration of B-vitamins daily. Although l-carnitine supplementation is known to affect -oxidation and energy metabolism and it would be of interest (and I have used it in treatment of hyperlipemia) as a potential treatment for hyperlipemia/hepatic lipido- sis, the feeding of dietary l-carnitine supplementa- tion (2 g twice daily) had no effect on plasma FFAs and triglyceride concentrations in healthy ponies.196 Additional studies on l-carnitine in ponies with hyper- lipemia would be of interest. Heparin therapy is generally not recommended


given that LPL may already be maximally activated in equine hyperlipemia184 and, with severe fatty liver, PT and PTT are often prolonged.184,190 I think I made that mistake once of giving too much heparin to a pony with hyperlipemia as the pony developed a severe hemorrhagic crisis. The mortality rate from hyperlipemia and hepatic lipidosis reported in one case series is approximately 50% but the prognosis is variable, depending on the successful and prompt correction of the predisposing cause(s) and on the ability to supply adequate nu- tritional support (enteral or parenteral or both).183 Prognosis should not be based upon the level of triglycerides in the serum or upon liver enzyme el- evations. For example, one miniature horse mare with masseter myopathy (and no detectable sele- nium in her whole blood) had lipemia and a plasma triglyceride concentration of 1926 mg/dL. Follow- ing 2 days of enteral feeding, selenium treatment and intravenous fluids with dextrose, the horse had


88 2015  Vol. 61  AAEP PROCEEDINGS


a triglyceride concentration of 120 mg/dL, with marked improvement in liver function tests and clinical signs. The horse was able to eat on her own on day 4. Hyperlipemic horses with Cushing’s dis- ease that are receiving pergolide treatment in addi- tion to attention to general health care generally have a good prognosis. The prevention of hepatic lipidosis revolves


around identifying at-risk equines, especially preg- nant or lactating pony mares, obese or geriatric po- nies and donkeys, and miniature equines of all ages with diarrhea and other predisposing disorders. Donkeys that have any change in their social status, such as loss of a companion, should be considered at high risk for disease. Providing adequate caloric intake is important in late-pregnant and early-lac- tation mares. As a preventive, fat could be fed to increase caloric density and feeding fat to healthy ponies increases lipoprotein lipase and decreases circulating triglycerides.197 This would not be rec- ommended in at-risk equines that already have hy- perlipidemia. Performing routine body condition scoring and periodic sampling of at-risk equines for triglycerides and free fatty acids could be helpful in identifying metabolic abnormalities before the onset of clinical signs. Proper maintenance health care and husbandry are of utmost importance in at-risk equines. Testing for Cushing’s disease should be instituted in all older at-risk animals.


6. Vascular, Genetic and Miscellaneous Causes of Liver Failure


Hepatic disorders of vascular or genetic origin that result in severe central nervous system signs (he- patic encephalopathy or HE) include congenital por- tosystemic shunts (PSS), a suspected ammonia metabolism defect in Morgan weanlings198–200 and portal vein thrombosis. Additional miscellaneous causes of liver disease or failure include umbilical vein abscesses, liver lobe torsion, a congenital defi- ciency in bilirubin uridine diphosphate glucuronyl- transferase activity, and primary and secondary hepatic neoplasias.


Portosystemic Shunts


PSSs are not common in foals and, when present, are often not detected until the foal is 6 to 12 weeks of age.198,201–203 This relatively late clinical detec- tion could be because hindgut development in young foals is necessary to produce enough enteric ammo- nia to cause sufficient elevations in blood ammonia. We have also noticed that young calves with PSS do not generally exhibit clinical signs until they are ruminants.198,204 The diagnosis of PSS is made af- ter looking at the patient’s age, clinical signs of HE with marked elevation in blood ammonia and bile acids and normal serum hepatic enzymes. The signs of HE in foals with PSS are variable and in- clude lethargy, disorientation, compulsive circling, ptyalism, seizures, central blindness, walking through fences and so on. Blood ammonia can be


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