Page 143 - Small Animal Clinical Nutrition 5th Edition

144 Small Animal Clinical Nutrition

contain selenium. Selenium had been added to a bottle of vitamin E intended for use in calves, but the mixture had not been dis-
pensed. The veterinarian was concerned that the bottle might have been sold inadvertently to the owner of the dog.
VetBooks.ir bottle contained 5,317 mg selenium/l. Subcutaneous tissue at the injection site contained 129 mg of selenium/kg. The calculated
Two liquid phases, one oily and the other watery, were visible in the vitamin preparation bottle. The water-base liquid from the

dose of selenium that had been administered to the dog was 2.5 mg/kg.The minimal lethal dose of selenium administered by intra-
muscular injection in dogs is 2.0 mg/kg.

Comments
Selenium toxicosis in cattle, sheep, horses, swine and poultry has been documented and usually develops as a subacute to chronic
disease resulting from ingestion of seleniferous plants or feeds that contain high concentrations of selenium because of errors in
ration formulation. Lesions of subacute to chronic selenium toxicosis have also been produced in dogs by long-term parenteral sele-
nium administration. Acute selenium toxicosis causes increased vascular permeability, which is manifested as hemorrhages and
edema in many tissues.

Bibliography
Janke BH. Acute selenium toxicosis in a dog. Journal of the American Veterinary Medical Association 1989; 195: 1114-1115.

CASE 6-5

Cervical Rigidity in a Cat
Patient Assessment
A 10-year-old, castrated domestic shorthair cat weighing 7 kg was examined for lethargy, decreased appetite and weight loss of sev-
eral months’ duration. Weight loss of 2 kg over the preceding 12 months was evident from the medical record.
The cat appeared depressed, had a matted, unkempt coat and extended its cervical region and held its head low and directly in
front of its body.The cat was afebrile, obese and dehydrated. On palpation, the cervical region was rigidly extended with tense mus-
culature. A hard mass was palpable in the midcervical region. The rigidly extended neck was the only neurologic abnormality.
Evaluation included a complete blood count (mild leukocytosis with mature neutrophilia), serum biochemistry analysis (mild
hyperglycemia and hypercholesterolemia), feline leukemia virus antigen test (negative) and cervical and thoracic radiographs.
Radiography revealed a bone-dense, cervical mass ventral to the C -C intervertebral space. Much of the normal vertebral archi-
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tecture appeared to be obliterated and the trachea and soft tissues were deviated ventrally and laterally. Thoracic radiography
revealed ventral, bony proliferations extending from thoracic vertebrae T through T . Marked bony proliferation was evident along
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the sternum and several of the costal cartilages.
The cat’s serum vitamin A concentration was markedly high (315 µg/dl, normal 20 to 80 µg/dl).
Assess the Food and Feeding Method
The cat was fed a commercial dry cat food ad libitum supplemented with fresh beef liver daily.

Treatment and Feeding Plan
A tentative diagnosis of hypervitaminosis A was made based on the dietary history, clinical signs and radiographic lesions.The daily
liver supplementation was considered the source of the excess dietary vitamin A.The cat was given a single intramuscular injection
of dexamethasone and an oral analgesic was prescribed. The owner was advised to discontinue feeding beef liver and to feed only a
balanced commercial cat food. The owner was further advised to encourage the cat to eat with hand feeding.

Reassessment
Six months later, the cat was euthanatized for reasons unrelated to the hypervitaminosis A. The cat had been eating fairly well,
although its stiff-necked posture remained.
Bibliography
Goldman AL. Hypervitaminosis A in a cat. Journal of the American Veterinary Medical Association 1992; 200: 1970-1972.