Liver disease in the horse: clinical signs and diagnostic aids

Liver disease in the horse: clinical signs and diagnostic aids

May 01, 2007

The clinical signs of hepatic insufficiency in horses are highly variable, nonspecific and depend on the extent and duration of hepatic disease.

Their onset often is abrupt, because typically at least 75 percent of the liver mass must be affected before the signs become apparent, regardless of the cause of hepatic disease.

The most common clinical signs are weight loss, hepatic encephalopathy, icterus and colic. Less common signs are hepatogenic photosensitization, diarrhea, bilateral laryngeal paralysis, hemorrhage and fever. Rarely reported clinical signs of hepatic insufficiency in horses are ascites, dependent abdominal edema, endotoxic shock and hemolysis.

Significant weight loss and failure to thrive are most consistently present during chronic hepatic insufficiency. However, chronic liver disease may be present without apparent weight loss. Weight loss is due to anorexia and the loss of normal hepatocellular metabolic activities.

Hepatic encephalopathy (HE) is a complex clinical syndrome characterized by abnormal mental status that accompanies severe hepatic insufficiency of any etiology.

Behavioral manifestations

The earliest phase of HE manifests as subtle behavioral changes. As it progresses, there may be signs of depression, head-pressing, circling, mild ataxia, aimless walking, persistent yawning and other inappropriate behavior (Photo 1). In advanced cases, somnolence develops and obtunded behavior ensues. At this stage horses often show aggressive or violent behavior interspersed with the periods of stupor. Occasionally seizures occur during the later stages of HE, but in general they are atypical.

The severity of encephalopathy corresponds to the degree of hepatic dysfunction; however, neither of these parameters correlates with type or reversibility of the underlying hepatic disease.

The diagnosis of HE is based on the presence of signs of cerebral dysfunction, with physical examination and laboratory findings compatible with liver disease. Other possible causes for the neurologic signs should be excluded, because there are no specific features of HE that enable this syndrome to be definitively distinguished from other encephalopathies.


Icterus, or jaundice, is caused by hyperbilirubinemia and is most apparent in nonpigmented skin, mucous membranes and the sclerae. When hepatocellular disease or obstruction to bile flow is present, icterus develops as a consequence of impaired conjugation of bilirubin and impeded excretion of conjugated bilirubin into the biliary tract, respectively.

Photo 1: This horse is demonstrating signs of hepatic encephalopathy. Note the pattern in the bedding from circling. This gelding frequently retained hay in his mouth, though he did not chew. Finally, note the wounds at the fetlocks; they were self-inflicted from maniacal chewing.
The presence of icterus is not specific to liver disease. About 10 percent of healthy horses have slightly yellow sclerae and horses that are anorexic for any reason will develop icterus. Intense icterus also develops subsequent to hemolysis.

Finally, certain drugs (steroids, heparin) can impede bilirubin uptake and conjugation by hepatocytes, despite an otherwise normally functioning liver.

Abdominal pain or colic may be a result of acute hepatic swelling or pressure from obstruction of bile flow. Signs of colic and liver disease also may be caused by alterations in intestinal motility. Interestingly, many horses with liver disease and signs of colic have clinically significant gastric impactions.

Light sensitivity

Photo 2: This mare has hepatic photosensitization characterized by erythema and necrosis involving only the white blaze on her face.
Hepatic photosensitization refers to abnormally heightened reactivity of the skin to ultraviolet sunlight, owing to the increased blood concentration of the photodynamic agent phylloerythrin. Phylloerythrin normally is formed in the gastrointestinal tract as a result of bacterial degradation of chlorophyll. It is then absorbed into the general circulation, conjugated and excreted by the liver. During hepatic insufficiency, the blood concentrations of phylloerythrin are increased. Ultraviolet light is absorbed most efficiently in unpigmented areas; thus the lesions of photosensitization are restricted to white skin which first appears erythematous and edematous. Pruritus, pain, vesiculation, ulceration, necrosis and sloughing may ensue (Photo 2).