Canine diabetes mellitus diagnosis, insulin therapy and monitoring

Doses on this pageEvery dose below is quoted from the cited source. Verify against the current label/formulary and the patient's full clinical picture.

Causes and predisposed dogs

Merck describes diabetes mellitus as a chronic disorder of carbohydrate metabolism caused by relative or absolute insulin deficiency, with most spontaneous canine cases occurring in middle age [1]. In dogs, Merck attributes reduced insulin production mainly to islet cell destruction, either immune-mediated or secondary to severe pancreatitis; chronic relapsing pancreatitis can progressively replace exocrine and endocrine tissue with fibrous tissue [1].

Merck also describes insulin resistance and secondary diabetes in dogs with spontaneous hyperadrenocorticism or chronic glucocorticoid or progestin administration, and notes that pregnancy, diestrus, and obesity can predispose [1]. In dogs, but not cats, Merck explains, progesterone triggers growth hormone release from mammary tissue, producing hyperglycemia and insulin resistance [1].

The review by Shiel and Mooney adds that some diabetic dogs carry anti-insulin antibodies before treatment begins, which may reflect naturally occurring autoantibodies as part of type 1 diabetes, and that certain breeds and dog leukocyte antigen haplotypes are associated with antibody development [2]. The authors state the clinical significance of these antibodies is unknown [2].

Clinical signs and complications

Merck lists polyphagia, polyuria, polydipsia, and weight loss as the characteristic signs, with an onset that is often insidious and signs that usually progress over weeks to months [1]. Merck places the canine renal threshold for glucose at approximately 180 mg/dL; the 2012 review gives a range of 160 to 220 mg/dl [1][3]. Some dogs show reduced appetite, and hepatomegaly from hepatic lipid accumulation and lethargy are also described [1].

Cataracts develop frequently in dogs with poorly controlled diabetes, Merck says, and it links them to the sorbitol pathway of glucose metabolism in the lens [1]. The 2012 review goes further, stating it is widely accepted that most diabetic dogs will develop cataracts even at commonly used glycemic targets, while retinopathy, vascular injury, and nephropathy are not expected in the species [3].

Merck notes reduced resistance to bacterial and fungal infection, with chronic or recurrent cystitis, prostatitis, bronchopneumonia, and dermatitis, possibly related to impaired neutrophil function [1]. Emphysematous cystitis is rare, and gas in the gallbladder wall can occur in diabetic dogs, per Merck [1].

Diagnosis and testing pitfalls

Merck bases the diagnosis on persistent hyperglycemia and glucosuria and gives a normal fasted blood glucose of 75-120 mg/dL for dogs and cats [1]. It also advises taking a thorough history to rule out drugs or diseases that predispose to diabetes [1]. Merck discusses serum fructosamine mainly as a way to separate stress hyperglycemia from diabetes in cats [1]. The 2012 review describes fructosamine, glycated serum proteins that are mostly albumin, as reflecting persistent hyperglycemia over the previous 2 weeks, and cautions that changes in serum protein levels or turnover can affect accuracy [3].

The cited sources do not describe a formal staging system for canine diabetes. Merck does classify two decompensated forms. Diabetic ketoacidosis (DKA) arises when insulin deficiency forces cells to burn free fatty acids, producing ketoacids, and it brings dehydration, metabolic acidosis, electrolyte disturbances, vomiting, and anorexia [1]. Hyperosmolar hyperglycemic state (HHS) is defined by Merck as "severe hyperglycemia (serum glucose concentration> 600 mg/dL) and hyperosmolality (> 320 mOsm/kg)," is less common than DKA, and carries a worse prognosis [1].

Insulin options for dogs

Merck names NPH or lente as the usual initial insulin for dogs and notes that most dogs need two doses a day [1]. For dogs with poor control on NPH or lente, Merck says detemir "(0.1 U/kg, SC, every 12 hours) should be considered," with reassessment 1 week after starting because of its potency [1].

The Shiel and Mooney review explains that canine and porcine insulin share an identical amino acid sequence, and reports that over 50% of dogs given bovine insulin were anti-insulin antibody positive, compared with 12.6% of dogs given porcine insulin [2]. The authors caution that many insulin studies in dogs are small, often ten dogs or fewer, and that differing designs, diets, and definitions of control make comparison difficult [2].

On lente frequency, the review notes the manufacturer advises starting once daily, but several studies favour twice-daily dosing and most clinicians use it from the outset, with a possible higher hypoglycemia risk in dogs whose insulin action lasts beyond 12 hours [2]. Most insulins are 100 U/mL, the review notes, while the licensed veterinary lente and PZI products are 40 U/mL [2].

Diet, concurrent disease and client communication

Merck states that diet and weight loss alone will not control the disease, so initial insulin is required [1]. With twice-daily injections, Merck describes feeding two meals of equal calories, each given immediately before insulin [1]. For dogs, Merck prefers diets high in fiber and complex carbohydrates and says semimoist foods high in simple sugars should be avoided [1]. Merck also recommends spaying intact diabetic females to achieve insulin regulation [1].

Merck lists excellent client communication first among the factors for successful treatment and ties long-term success to the owner's understanding and cooperation [1]. The 2012 review adds that monitoring plans should reflect the owner's finances, motivation, and expectations, and that owner perceptions of quality of life will determine outcome [3].

Monitoring after diagnosis

The 2012 review defines success as stable body weight, control of thirst, urination, and hunger, and avoidance of ketosis and hypoglycemia [3]. It describes monitoring every 7 to 14 days while dose and insulin type are worked out, then every 4 to 12 weeks [3]. Merck suggests reassessment every 4-6 months once a patient is stable on maintenance treatment [1].

Indirect measures carry known limits, according to the review. Water intake roughly tracks glucose but can miss periods of hypoglycemia, so raising a dose solely because polydipsia persists can result in overdose. The review also warns against raising a dose simply because glycosuria persists, since the Somogyi effect (prolonged rebound hyperglycemia after a steep glucose drop) can occur [3]. A prolonged period without glycosuria in a dog suggests insulin overdose, the review states, and ketonuria in an established diabetic suggests substantial insulin deficiency or resistance [3].

For blood glucose curves, the review describes sampling every 2 hours from just before insulin until the next dose, with the next sample within 60 minutes if glucose falls quickly or nears 100 mg/dl [3]. It notes poor day-to-day repeatability of curves and says curve data should not be read in isolation from thirst, urination, and body weight [3]. Owners can collect capillary samples at home from the ear edge, paw pad, elbow callus, or outer lip [3]. Hematocrit affects meter readings: breeds with high hematocrits such as greyhounds and dachshunds read low, and anemic patients read high, so hypoglycemia may be missed [3].

Merck states that studies in dogs and cats show at-home monitoring improves glycemic control [1]. It describes continuous glucose monitoring (CGM) systems that read interstitial glucose every 15 minutes for up to 14 days and can reveal nocturnal hypoglycemia, and it advises confirming low CGM readings with a blood glucose measurement [1]. The 2012 review describes CGM systems that needed two or three blood glucose measurements for initial calibration and could not be calibrated when blood glucose was above 400 mg/dl or below 40 mg/dl [3].

Before using any dose aboveVerify against the current label/formulary and the patient's full clinical picture.