Diagnosis and assessment
These guidelines describe different approaches to DM diagnosis and assessment depending on the level of hyperglycemia and the presence of clinical signs.
For cats and dogs who present with clinical signs suggestive of DM, perform a physical exam and full laboratory evaluation (complete blood count [CBC]), chemistry with electrolytes, urine analysis with culture, urine protein:creatinine ratio (UPC), triglycerides, blood pressure (BP), and thyroxine (T4) in cats; to confirm the diagnosis as well as to rule out other diseases. Elevated BG can sometimes be identified on blood work in the absence of consistent clinical signs. In such cases, if stress hyperglycemia can be ruled out, the patient may be classified as at-risk for developing DM. Clinical signs of PU/PD do not develop until the BG concentration exceeds the renal tubular threshold for spillage of glucose into the urine.
Glucosuria will typically develop when the BG concentration exceeds approximately 200 mg/dL in dogs and 250–300 mg/dL in cats.
Clinical signs of DM will typically be present when there is persistent hyperglycemia and glucosuria. Clinical signs are usually absent with glucose levels ranging between the upper reference levels and the renal threshold values noted above. Blood glucose concentrations in these ranges may occur for a variety of reasons, including stress hyperglycemia in cats, corticosteroid administration, the presence of concurrent insulin-resistant disease (hyperadrenocorticism, obesity), or as part of the early stage of developing DM.
Dogs and cats in the early stages of nonclinical DM appear healthy, have a stable weight, and are usually identified as a result of routine laboratory evaluation. They do not have clinical signs of DM. Stress hyperglycemia needs to be ruled out, as well as correction of any insulin-resistant disorders and discontinuation of drugs associated with impaired insulin release or sensitivity. Reassessing BG or monitoring urine glucose (UG) levels once the patient is no longer stressed at home or measuring serum fructosamine concentrations may help differentiate between stress hyperglycemia and DM, and determine if further action should be taken.
Clinical DM is diagnosed on the basis of persistent glucosuria, persistent hyperglycemia, and presence of characteristic clinical signs.
Documentation of an elevated serum fructosamine concentration may be necessary to confirm the diagnosis in cats.9Fructosamine levels may be only mildly elevated with lower levels of persistent hyperglycemia, and should be interpreted as part of a complete evaluation.9
Animals with clinical DM will present with PU, PD, PP, and weight loss. Some may present with lethargy, weakness, and poor body condition. Dogs may have cataracts, and cats may present with a complaint of impaired jumping and abnormal gait. Some patients will present with systemic signs of illness due to diabetic ketosis/ketoacidosis, such as anorexia, vomiting, dehydration, and depression.
The initial evaluation of the diabetic dog and cat should:
- Assess the overall health of the pet (history including diet and concurrent medications, and a complete physical exam).
- Identify any complications that may be associated with the disease (e.g., cataracts in dogs, peripheral neuropathy in cats).
- Identify any concurrent problems often associated with the disease (e.g., urinary tract infections, pancreatitis).
- Identify any conditions that may interfere with the patient’s response to treatment (e.g., hyperthyroidism, renal disease, hyperadrenocorticism).
- Evaluate for risk factors such as obesity, pancreatitis, insulin-resistant disease, diabetogenic medications, and diestrus in female dogs.
Physical exam results of the diabetic cat or dog can be relatively normal early in the course of the disease. As the disease persists without treatment, the physical exam may reveal weight loss, dehydration, poor hair coat, abdominal pain if concurrent pancreatitis is present, or cataracts. Some cats with longstanding hyperglycemia can develop peripheral neuropathy, which manifests as a plantigrade stance. If ketosis is present, a sweet odor may be noticed on the breath of the pet.
Laboratory evaluation includes a basic minimum database (CBC, chemistry with electrolytes, urine analysis with culture, triglycerides, UPC, BP, and T4 level in cats). Typical findings include hyperglycemia, glucosuria, and stress leukogram, as well as increased cholesterol and triglycerides. Dogs frequently show increased levels of alkaline phosphatase (ALP) and alanine aminotransferase. Cats, however, show more variability in the presence of a stress leukogram and elevated ALP. Elevated liver enzymes in a cat may warrant further evaluation for concurrent liver disease.10 Pancreatitis is a common comorbidity and may need to be addressed.10
Cats and dogs with diabetic ketoacidosis may show very elevated BG concentrations, azotemia, and decreased total CO2 secondary to metabolic acidosis, osmotic diuresis, dehydration, and, in the case of profound hyperosmolarity, coma.
Urinalysis will reveal the presence of glucose. It may also show presence of protein, ketones, bacteria, and/or casts. Because a urinary tract infection cannot be ruled out by the absence of an active urine sediment, a urine culture should always be performed in glucosuric animals, because infection is commonly present.
If thyroid disease is suspected in a dog, it is best to perform thyroid testing after DM is stabilized because of the likelihood of euthyroid sick syndrome. Cats over 7 yr of age with weight loss and PP should be tested for hyperthyroidism because DM and hyperthyroidism cause similar clinical signs and can occur concurrently.
ALP (alkaline phosphatase); BG (blood glucose); BGC (blood glucose curve); BP (blood pressure); CBC (complete blood count); DM (diabetes mellitus); HAC (hyperadrenocorticism); NPH (Neutral Protamine Hagedorn); PD (polydipsia); PP(polyphagia); PU (polyuria); PZI (protamine zinc insulin); T4 (thyroxine); U (units); UG (urine glucose); UPC (urine protein:creatinine ratio)