Page 132 - Clinical Small Animal Internal Medicine

100 Section 2 Endocrine Disease

VetBooks.ir Box 12.2 Home blood glucose monitoring protocol for glargine or detemir using a preinsulin blood glucose concen­
tration measured using a glucometer calibrated for feline blood, used in a feline‐only practice for the last 8 years
Newly diagnosed diabetics (<2 months insulin therapy)

Blood glucose concentration >235 mg/dL (>13 mmol/L) Increase the dose by 0.5 IU
Blood glucose concentration 126–235 mg/dL (7–13 mmol/L) Keep the dose the same
Blood glucose concentration 72–<126 mg/dL (4–<7 mmol/L) Decrease the dose by 0.5 IU
Blood glucose concentration <72 mg/dL (<4 mmol/L) Do not give insulin and call the clinic to discuss

Longer‐term diabetics (>2 months insulin therapy)

Blood glucose concentration >450 mg/dL (>25 mmol/L) Increase the dose by 1 IU
Blood glucose concentration 270–450 mg/dL (15–25 mmol/L) Increase the dose by 0.5 IU
Blood glucose concentration 108–<270 mg/dL (7–<15 mmol/L) Keep the dose the same
Blood glucose concentration 90–<126 mg/dL (5–<7 mmol/L) Decrease the dose by 0.5 IU
Blood glucose concentration <90 mg/dL (<5 mmmo/L) Do not give insulin and call clinic to discuss, check
for remission depending on dose

If using a glucometer calibrated for human blood, decrease target glucose concentration by 20% (approximately 18 mg/dL; 1 mmol/L).
Source: Adapted from Rand 2017.

cats subsequently shown to have acromegaly, and is glucagon and other counterregulatory hormones, free
caused by pituitary oversecretion. Cats that have poor fatty acids are broken down into ketoacids. As ketoacids
glycemic control despite adequate or increased insulin and glucose accumulate in the blood, metabolic distur-
doses should have insulin‐like growth factor (IGF) bances occur, which can be profound and life‐threatening,
measured and, if possible, brain imaging. Occasionally, and include dehydration, hypovolemia, elevated anion
diabetic cats with acromegaly are not insulin resist- gap, metabolic acidosis, electrolyte disturbances,
ant at the time of diagnosis, but this is atypical. azotemia, elevated liver enzymes, hyperlactatemia, and
Hyperadrenocorticism causes clinically significant clinical signs of vomiting and anorexia. Treatment involves
endogenous insulin resistance and is more common in rehydration and the use of short‐ and long‐acting insulins
dogs than cats. Approximately 1 in 20 dogs with hyper- to reduce ketone production and establish euglycemia.
adrenocorticism develops diabetes. Hyperosmolar hyperglycemic state is another syn-
Clinically significant insulin resistance occurs when drome of decompensated diabetes mellitus. It is charac-
concurrent disease causes upregulation of glucocorti- terized by profound hyperglycemia greater than 600 mg/
coids, epinephrine, glucagon, and other counter regulatory dL (33.3 mmol/L) and hyperosmolality >320 mOsm/kg,
hormones. Any concurrent infection or inflammatory with a normal pH and no or mild ketonemia or ketonu-
disease, endocrine or cardiac disease, or neoplasia can ria. It is less common than diabetic ketoacidosis. In the
contribute to insulin resistance. In dogs, common con- classic form, animals are not ketotic or acidotic, but
current diseases that can contribute to insulin resistance mixed forms occur with severe hyperosmolality, com-
include hyperadrenocorticism, acute pancreatitis, urinary pounded by ketoacidosis.
tract infection, neoplasia, hypothyroidism, kidney dis-
ease, severe obesity, and oral infection. In cats, common
concurrent diseases include pancreatitis, hepatic lipido- Prognosis
sis, cholangiohepatitis, urinary tract infection, kidney dis-
ease, hyperthyroidism, acromegaly, inflammatory bowel Improved diets, insulin types, and the availability of home
disease, obesity, oral infection, and heart disease. monitoring have led to improvements in canine and
feline diabetes management in recent years. Most impor-
tant of these is diabetic remission, thought to be attaina-
Diabetic Ketoacidosis
ble in 80% or more of newly diagnosed feline diabetics if
Diabetic ketoacidosis is a form of decompensated diabetes managed to achieve normal or near normal blood glucose
mellitus in which cells use free fatty acids as an energy concentrations. Current data on prognosis that incorpo-
source, because they cannot access glucose due to absolute rates recent improvements in management are lacking.
or relative insulin deficiency. In the presence of elevated Older data suggest that in diabetic animals managed with