Hepatic encephalopathy refers to the nervous disease that follows severe liver damage. The liver has a large reserve capacity meaning that loss of three-quarters of liver capacity generally must occur before signs of liver dysfunction appear. As liver function reduces following extensive liver damage, toxic metabolites including ammonia that are normally detoxified by the liver, will accumulate in blood and tissues. Accumulation of ammonia and other toxins may then reach levels that cause deterioration of brain function.
Liver injury may occur in animals ingesting toxic plants that contain pyrrolizidine alkaloids such as heliotrope (Heliotropeum europeum) and Paterson's curse (Echium plantagineum), or fungal infected lupin stubbles that produce phomopsin. The liver damage may be exacerbated if in the export process, animals consume feed (pasture, hay or pellets) contaminated with hepatotoxic plants, or drink from water sources containing blue-green algae.
Affected animals are unthrifty, dull, appear to be blind, stagger, and exhibit head pressing before becoming comatose and dying.
At necropsy the liver may be swollen and pale or misshapen and nodular. Laboratory determination of the toxin may be assisted by histological examination of sections of liver submitted in buffered formalin.
Polioencephalomalacia is the main differential diagnosis.
There is no effective treatment. Regeneration of liver can occur but only after a long delay. Severely affected animals should be humanely euthanased.
Source animals from areas where toxic plants are controlled. Avoid further exposure to hepatotoxins in the export process.