A 25 year old Warmblood stallion presented to the Cornell University Hospital for Animals for acute onset of signs of hepatic failure. No exposure to toxic plants could be confirmed, however a Norway maple was present in the stallion's enclosure. The only clinical sign noted by the animal's caretaker had been sudden onset of anorexia, although upon further questioning, it became apparent that the stallion had displayed skin lesions typical of photosensitization over the course of the previous year. The only abnormality noted on physical examination by the referring veterinarian was icterus, which prompted the referring veterinarian to submit samples for CBC, chemistry, and serum bile acids, and refer the stallion for further evaluation of liver disease. While in the hospital, the stallion initially had elevated hepatocellular leakage enzymes, which declined over the course of his hospitalization, even as clinical signs of hepatic encephalopathy worsened and hepatic function tests deteriorated. Hepatic needle biopsy showed evidence of a toxicosis, but was not definitively diagnostic. On the fifth day of hospitalization the stallion was euthanized due to unremitting signs of colic. Necropsy was performed, revealing hepatic megalocytosis, chronic mixed inflammation, eosinophilic cytoplasmic inclusion bodies, profound loss of hepatic architecture with bridging fibrosis, and biliary hyperplasia. A definitive diagnosis was never reached, but a toxic or viral insult was suspected. Norway maple leaves from the stallion's pasture were frozen to be used in a feeding trial should additional cases of hepatopathy surface with a history of exposure to this plant.