Signalment:  
Gross Description:  
Histopathologic Description:
Morphologic Diagnosis:  
Chronic encephalopathy with laminar cortical necrosis; hydrocephalus ex vaccuo.
Cause: Potato chip binging, salt intoxication.
Condition:  
Contributor Comment:  
This is a unique lesion and becomes intriguing when you are told that little Wilber loved potato chips, and at Thanksgiving was waylaid by a bag of Lays. He survived the salt intoxication with deficits for 2 months. The gross images of his brain demonstrate injected cerebral vessels and cortex collapse. On cross section, the laminar necrosis is seen nicely. While the morphologic can be followed by a chain of descriptors, this is an encephalopathy. Calcification of neuropil necrosis is common, but the pattern of vessel calcification is interesting. The nests of Gitter cells with cholesterol clefts are reminiscent of lipogranulomas. The mononuclear cells are mostly macrophages like is seen in cases of chronic polioencephalopathy and many infarcts; therefore, encephalitis is probably not a valid morphologic. I am not aware of a similar case being described although a comment on similar chronic lesions is in texts.(5) One must wonder if seizures have a role in developing some of the cortical necrosis.
Salt poisoning of young pigs is well known in its acute form and occurs when high salt diets are given when inadequate water is available.(2,5) Upon the later consumption of water, the salt in the cortical tissues cannot be cleared before water enters to cause the laminar necrosis. Evidence of presumed previous eosinophil cuffing is nowhere to be seen at this time. It is thought that eosinophil cuffs are associated/induced by sodium excess in tissues but may not be seen and cuffs are not present several days after survival.(2,5) Laminar necrosis in cases of salt intoxication does not fluoresce (JFE).
Swine are considered the most sensitive species to salt intoxication.(3) Potato chips have been reported before in this disease in pigs and survivors with CNS deficits are reported.(2,4) It has been shown that diets high in salt lead to increased salt in the pig brain with the highest concentrations being in the cerebral and cerebellar hemispheres.(1,6)
JPC Diagnosis:  
1. Brain, cerebrum: Necrosis, cortical, laminar, with multifocal cholesterol clefts and spongiosis, Micro Pig, porcine.
2. Brain, cerebrum, arteries and veins: Mineralization, diffuse, moderate, with multifocal fibrinoid necrosis.
Conference Comment:  
For an acute case of salt toxicity in a pig, participants are urged to review conference 22, case #1 from the 2008-2009 WSC.
References:
2. Fountaine JH, Gashe DG, Oehme FW. Experimental salt poisoning (water deprivation syndrome) in swine. Vet Toxicol. 1975;17:5-8.
3. Heydarpour F, Derakhshandeh J, Fekri A, Heydarpour P. Salt poisoning blindness in wistar rat, rabbit, and pig. Toxicol & Environmental Chemistry. 2008;90:1035-42.
4. Holbrook TC, Barton MH. Neurologic dysfunction associated with hypernatremia and dietary indiscretion in Vietnamese pot bellied pigs. Cornell Vet. 1994;84:67-76.
5. Summers BA, Cummings JF, de Lahunta A. Veterinary Neuropathology. 1995;254-5.
6. Wells GAH, Lewis G, Hawkins SAC, Don PL. Evaluation of brain chloride determinations in the diagnosis of water deprivation salt intoxication in pigs. Vet Rec. 1984;114:631-635.