{"title":"Neurologic dysfunction associated with hypernatremia and dietary indiscretion in Vietnamese pot bellied pigs.","authors":"T C Holbrook, M H Barton","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>Neurologic disease associated with hypernatremia in 2 young Vietnamese potbellied pigs is discussed. Both pigs had recent dietary changes likely associated with excessive salt intake. Case 1 was changed from a commercial mini pig ration to a commercial cat food diet containing up to 1.5% salt 3-4 days before the onset of clinical signs. Case 2 was being maintained on a commercial mini pig ration, however the owner often fed the pig potato chips as treats since its purchase 3 weeks previously. There was no history of water deprivation in either pig. Clinical signs in case 1 included facial-motor seizures, sialorrhea, generalized seizures, tenesmus, disorientation, circling, head pressing, and blindness. Case 2 was disoriented, ataxic, underweight, and appeared blind. Both pigs fully recovered with medical therapy. The rationale for fluid and ancillary therapy are discussed in light of the pathophysiology of salt toxicosis in commercial swine.</p>","PeriodicalId":22466,"journal":{"name":"The Cornell veterinarian","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"The Cornell veterinarian","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Neurologic disease associated with hypernatremia in 2 young Vietnamese potbellied pigs is discussed. Both pigs had recent dietary changes likely associated with excessive salt intake. Case 1 was changed from a commercial mini pig ration to a commercial cat food diet containing up to 1.5% salt 3-4 days before the onset of clinical signs. Case 2 was being maintained on a commercial mini pig ration, however the owner often fed the pig potato chips as treats since its purchase 3 weeks previously. There was no history of water deprivation in either pig. Clinical signs in case 1 included facial-motor seizures, sialorrhea, generalized seizures, tenesmus, disorientation, circling, head pressing, and blindness. Case 2 was disoriented, ataxic, underweight, and appeared blind. Both pigs fully recovered with medical therapy. The rationale for fluid and ancillary therapy are discussed in light of the pathophysiology of salt toxicosis in commercial swine.