Clinical signs are useful in the diagnosis and monitoring of canine and feline
diabetes. Other laboratory tests are also necessary for diagnosis
of Diabetes mellitus and the monitoring of treated diabetic pets.
There are three distinct clinical pictures in diabetes mellitus:
The classical signs are polyuria, polydipsia, polyphagia, cachexia and increased susceptibility to infections (e.g. urinary tract infections). In long term diabetes complications due to protein glycosylation can be seen: cataracts (mainly in dogs) and peripheral neuropathy (mainly in cats).
Diabetic ketoacidosis (DKA) is a serious metabolic emergency.
DKA develops due to long standing undiagnosed diabetes mellitus, insufficient insulin dose in treated diabetics and impaired insulin action and/or resistance, caused by obesity, concurrent illness or drugs. This is the cause of more than two thirds of cases of DKA.
Due to the lack of insulin, glucose cannot be used as an energy source. Fats are broken down to provide energy. During lipolysis, high levels of ketones are produced. Ketosis and acidosis develop and are accompanied by electrolyte imbalances. Ketosis causes anorexia, nausea and lethargy.
Treatment
DKA is an emergency and treatment must be started as soon as possible.
The goals of treatment are to correct fluid deficits, acid-base balance and electrolyte balance, lower blood glucose and ketone concentrations and recognize and correct underlying and precipitating factors.
Therapy includes intravenous fluid therapy with isotonic fluids, e.g. 0.9% saline, and intravenous administration of rapid-acting insulin. If possible the electrolyte concentrations and acid-base balance should be measured and corrected. Caninsulin is an intermediate-acting insulin and is not suitable for intravenous administration.
When blood glucose is lowered and maintained between 11 and 14 mmol/L (198 and 252 mg/dL) for at least 4-10 hours, insulin therapy with Caninsulin administered subcutaneously can be initiated.
Hyperglycemic, hyperosmolar syndrome or hyperosmolar non-ketotic syndrome (HHS) is an uncommon complication of untreated diabetes mellitus. It is an emergency and has an extremely guarded prognosis.
HHS is characterized by very marked hyperglycemia (e.g. >36 mmol/l or >650 mg/dL) and osmolality (>380 mOsm/L). Blood glucose concentrations as high as this shift water from brain cells by osmosis and result in coma.
Diagnosis
Initially, before HHS develops, the typical clinical signs of Diabetes mellitus will have been seen. These animals become progressively
weaker, anorexic, and lethargic and drink less. Physical examination often
reveals profound dehydration, lethargy and severe depression or coma. There appears to be a direct relationship between the severity of the hyperosmolality
and the severity of the clinical signs.
There is no ketoacidosis in HHS and plasma glucose concentrations are much higher (>36 mmol/l) in HHS than in DKA.
Treatment
The goal of treatment is correction of the hyperglycemic, hyperosmolar
state. This is achieved by aggressive intravenous fluid therapy
and reduction of the blood glucose concentration. For the first 4-6 hours,
fluid therapy is critical. Insulin therapy can be delayed until
the condition of the animal has improved.
Prognosis
The prognosis for full recovery is extremely guarded. Even with
appropriate treatment, many animals die within the first 24 hours;
the long-term survival rate is in the region of 12%.
The diagnosis of DKA is based on the presence of ketonuria along with signs of systemic illness.