These complications may be reduced by performing a hemostasis profile to assess the risk of hemorrhage and by using ultrasonography
to guide needle placement. Although subclinical coagulopathy has been reported frequently in horses with liver disease, clinically
significant or fatal hemorrhage after a liver biopsy are rare.
The wide variety of clinical signs with hepatic disease, coupled with the fact that the majority of the hepatic parenchyma
must be affected before function is lost, make the clinical distinction between acute and chronic liver disease challenging.
The onset of signs may be sudden, even with chronic disease. A history of progressive weight loss or "failure to thrive" may
Although no single blood test is specific for distinguishing acute from chronic hepatic disease, the presence of hyperglobulinemia
and/or hypoalbuminemia may suggest chronicity. Histopathologically, the hallmark evidence of chronicity is the presence
of fibrosis. For the purpose of discussion of specific hepatic disorders, diseases have been classified as either acute or
chronic, based on the known etiology of the disease and by the frequency of occurrence (Table 1). For this discussion, a brief
review of the most common differential diagnoses follows.
Table 1: Differential list for liver disease in horses
Although it remains one of the most common causes of acute hepatic failure in horses, the exact cause of Theiler's disease
remains unclear. The onset of clinical signs of hepatic failure is acute, often rapidly progressing over several days. Most
horses are anorectic and icteric; hepatic encephalopathy is reported in the majority of cases. The disease typically occurs
Frequently, horses with Theiler's disease have received an equine-origin biological four to 10 weeks prior to the onset of
hepatic failure; hence the name "serum-associated hepatitis."
Some reports suggest that lactating broodmares given tetanus antitoxin after parturition are particularly prone to Theiler's
Recent inoculation with an equine-origin biological, coupled with an abrupt onset of clinical signs and laboratory evidence
of hepatic insufficiency, are strongly suggestive of Theiler's disease. No single laboratory test is diagnostic; however,
disproportionately increased SDH activity is supportive evidence of acute hepatic necrosis.
The histopathologic findings of widespread centrilobular-to-midzonal hepatocellular necrosis with hemorrhage offer the strongest
diagnostic evidence of Theiler's disease.
Hyperlipidemia and hepatic lipidosis
Ponies, miniature horses and donkeys are most susceptible to hyperlipemia. Fat mobilization from adipose stores usually is
first triggered by a stress, inability to maintain energy homeostasis or a negative energy balance, as may occur during late
gestation, lactation, starvation or secondary to anorexia induced by some other primary disease, such as entero colitis, endotoxemia,
parasitism, pituitary adenoma, azotemia and neonatal septicemia.
If fat mobilization exceeds the liver's ability to use it as an energy source or the liver's ability to repackage the fat
and return it to the periphery, hepatic lipidosis ensues, disrupting normal hepatic function.
The onset of clinical signs of hyper lipemia often is acute and includes icterus, anorexia, weakness, severe depression, ataxia,
muscular weakness, recumbency, diarrhea, mild colic, fever and dependent edema. In severe cases, clinical signs of hepatic
failure may prevail, and sudden death due to hepatic rupture may occur.