Page 272 - WSAVA2018
P. 272

 25-28 September, 2018 | Singapore
· Hereditary
· Pyruvate kinase deficiency (Abyssinian, Somali, other
· Increased osmotic fragility (Abyssinian, Somali, other purebred and DSH cats)
· Porphyria (Siamese and DSH cats)
C. Ward1
1University of Georgia College of Veterinary Medicine, Small Animal Medicine and Surgery, Athens, USA
Cynthia R. Ward, VMD, PhD, DACVIM
University of Georgia College of Veterinary Medicine Athens, GA USA
Diabetes mellitus is a common endocrinopathy in dogs in cats. Dogs usually get type 1 or the insulin-dependent form. This occurs from loss of pancreatic beta cells such that adequate amounts of insulin are not produced and secreted. Cats usually get type 2 or the non-insulin dependent form of diabetes mellitus. This occurs as
a result of insulin-resistance, often from obesity. The pancreatic beta cells are forced to produce increasing amounts of insulin to over come the resistance, resulting in ultimate loss of function in the cells. Additional loss results from direct glucose toxicity of the beta cells. Cats can go into diabetic remission a syndrome in which insulin requirements diminish or cease to be necessary after initial treatment. This is probably due to correction of a condition causing insulin resistance.
Diabetes mellitus is relatively easy to diagnose.
Clinical signs include polyuria/polydipsia, weight loss, persistent or recurrent urinary tract infections, weakness and muscle wasting, cataracts (usually dogs), and peripheral neuropathies (usually cats). Diagnosis can
be made by recognition of appropriate clinical signs,
and demonstration of persistent hyperglycemia and glucosuria. One confounding factor to this diagnosis
is stress. Stress, alone, can cause hyperglycemia, that can be high enough to be cause spill over into the
urine and glucosuria. Should the clinician have any
doubt of whether hyperglycemia and glucosuria are
due to diabetes mellitus, s/he should check a serum fructosamine level. This value gives the average of the blood glucose over the preceding 2-3 weeks. If elevated, then diabetes mellitus can be diagnosed. If not elevated, then the hyperglycemia/glucosuria was probably due to stress.
Initial evaluation will decide how intensively the patient should be managed as diabetic treatment is begun. If
the animal is eating and drinking normally and is well hydrated, there is no reason to hospitalize him/her while insulin therapy is initiated. If the animal is ketotic, acidotic, hyperosmolar, or dehydrated, s/he should be admitted
 purebred and DSH cats)
 There are several important differential diagnoses for hemolytic anemias and thus treatment options depend on the cause of hemolysis. Various triggers such as drugs and chemicals can be rapidly removed. However, other diagnoses may require tests at reference laboratories, such as for serology and real-time PCR for infectious diseases and genetic tests for hereditary diseases.
It is therefore not unusual to start with a combination
of prednisolone (fortunately even at high doses well tolerated) and doxycycline as initial treatment of hemolytic anemias to cover the bases until test results are back
and specific and proper therapy can be instituted. For hereditary hemolytic anemias it is most important to avoid harmful treatments and offer a safe (indoor) environment.
Lastly, non-regenerative anemias due to decreased erythro- or overall hematopoiesis can be associated with a variety of disorders. Indeed, mild non-regenerative normochromic normocytic anemia is commonly seen
with many organ diseases and is mostly well tolerated. However, many middle-aged to older cats with chronic renal failure develop a moderate to severe anemia. The main cause is a lack of renal production of erythroproietin, but uremic toxins affecting red cell stability and bone marrow production as well as blood loss from ulcers
also play a role. Transfusion or human recombinant erythropoietin (darbepoetin) can reverse the anemia and associated clinical signs. However, repeat transfusions are generally needed and cats may become refractory,
as they develop alloantibodies against the transfused
red cells. Moreover, cats can develop antibodies against the recombinant human erythropoietin, which leads to
a severe and hardly reversible pure red cell aplasia. Renal transplantation from a carefully selected donor cat has effectively reversed not only the anemia but also restored kidney function. While rarely truly deficient, iron, folate, and cobalamin may be replenished as needed. FeLV infections may end in a pure red cell aplasia (C
type) or myelodysplasia to aplasia, while FIV exhibits less effects on the bone marrow. Cancer associated anemias may have many causes but may result in aplastic or myelophistic bone marrows.
Finally, many anemic cats need transfusion support during the initial management. There is no specific trigger PCV, but rather the overall clinical picture with a PCV of <20% is used. It should be noted that cats need to be AB blood typed before the first and crossmatched before the second transfusion (>4 days from first transfusion).

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