Abstract

Summary A 15-year-old trotter gelding was evaluated because of an acute onset of ataxia in all 4 limbs. There was no known history of trauma. The gelding showed grade 2/5 ataxia in all 4 limbs, which was localised after clinical neurological examination to the cervical vertebral spinal cord. Initial therapy consisted of oral anti-inflammatory doses of prednisolone and antimicrobial treatment with potentiated sulphonamides. The ataxia progressed to grade 3/5 at Day 10 of hospitalisation. Additionally, the horse was slightly depressed and showed spontaneous yawning during examination. Facial sensation was blunted. Blood chemistry revealed a marked elevation of liver specific enzymes and blood ammonia levels. Transcutaneous abdominal ultrasonography revealed hepatomegaly. Due to a guarded prognosis, the horse was subjected to euthanasia. At necropsy the left lateral liver lobe was markedly enlarged and showed a firm texture, whereas the cranial part and the right and quadratic liver lobe displayed a severe and diffuse atrophy. Histopathologically, the left lateral liver lobe revealed a moderate to severe cirrhosis with a severe, diffuse hepatocellular iron-accumulation. Increased numbers of Alzheimer type II astrocytes in the cerebral cortex and cerebral white matter vacuolisation were indicative for encephalopathy. These findings were interpreted as haemosiderosis and cirrhosis of the liver with consecutive hepatic encephalopathy. Aetiologically, haemosiderosis should be considered as a cause of liver cirrhosis with consecutive hepatic encephalopathy. Although hepatic encephalopathy in horses usually presents with predominating cerebral signs, it has to be taken into account as a differential diagnosis in cases of acute onset generalised ataxia.

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