Peer-reviewed veterinary case report
Calf with ataxia caused by congenital liver shunt
By Marçal, Valéria Café et al.·Published in Journal of veterinary science·2008·Institute of Animal Pathology·View original on PubMed →
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Original publication title: Hepatic encephalomyelopathy in a calf with congenital portosystemic shunt (CPSS).
- Species:
- cattle
Plain-English summary
A 4-month-old female Holstein calf was brought in for symptoms like weakness, unsteady movements, and poor growth. The vet found that the calf had significant coordination issues and a decreased response to stimuli. Unfortunately, a postmortem examination revealed that the calf had a congenital portosystemic shunt, which is a liver condition that can lead to brain problems. This condition caused the calf's neurological symptoms, but no major organ changes were visible. Sadly, the calf did not survive due to the severity of the liver issues.
People also search for: calf weakness and ataxia · congenital portosystemic shunt in calves · calf liver disease symptoms
Abstract
A 4-month-old female Holstein Friesian calf was referred to the Veterinary Teaching Hospital, University of Berne, Switzerland for evaluation of ataxia, weakness, apathy and stunted growth. Clinical examination revealed generalized ataxia, propioceptive deficits, decreased menace response and sensibility. Postmortem examination did not reveal macroscopic changes of major organs. Histologically, the brain and the spinal cord lesions were characterized by polymicrocavitation, preferentially affecting the white matter fibers at the junction of grey and white matter and by the presence of Alzheimer type II cells. The liver revealed lesions consistent with a congenital portosystemic shunt, characterized by increased numbers of arteriolar profiles and hypoplasia to absence of portal veins. The pathological investigations along with the animal history and clinical signs indicated a hepatic encephalomyelopathy due to a congenital portosystemic shunt.
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Search related cases →Original publication on PubMed: https://pubmed.ncbi.nlm.nih.gov/18296896/