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Diabetes Mellitus, Uncomplicated

basics

definition :

Disorder of carbohydrate, fat, and protein metabolism caused by an absolute or relative insulin deficiency. Type I (insulin-dependent diabetes mellitus [DM]) is characterized by very low to absent insulin secretory ability. These patients die if not treated with insulin and are prone to ketoacidosis. Type II (noninsulin- dependent DM) is characterized by inadequate or delayed insulin secretion relative to the needs of the patient. Many of these patients live without exogenous insulin and are less prone to ketoacidosis.

Pathophysiology:

Insulin deficiency causes an impaired ability of tissues, especially muscle, adipose tissue, and liver, to utilize carbohydrates, fats, and proteins. Impaired glucose utilization and ongoing gluconeogenesis cause hyperglycemia. Glucosuria develops, causing osmotic diuresis, polyuria, and compensatory weight loss. Mobilization of free fatty acids to the liver causes both hepatic lipidosis and ketogenesis.

Systems Affected :

• Endocrine/metabolic--electrolyte depletion and metabolic acidosis
• Hepatobiliary- -hepatic lipidosis. Liver failure may develop, particularly in cats.
• Ophthalmic--cataracts in dogs
• Renal/urologic--urinary tract infection and osmotic diuresis
• Nervous--peripheral neuropathy in cats
  

Genetics:

Familial associations in some breeds of dog

Incidence/Prevalence :

Prevalence in both dogs and cats varies between 1:400 and 1:500.

signalment :

• Breed Predilections
• Higher risk than other breeds--keeshond, puli, miniature pinscher, and cairn terrier
• Possible higher risk than other breeds--poodle, dachshund, miniature schnauzer, and beagle
• No breed predilections in cats

Mean Age and Range :

Dogs--mean about 8 years; range, 4-14 years (excluding rare juvenile form)

Cats-- 75% are 8-13 years; range, 1-19 years

Predominant Sex:

• Dogs--female predisposition
• Cats--male predisposition
  

signs :

• Signs are more often noticed in the early stages of disease in dogs than in cats.
• Early signs--polyuria and polydipsia (PU/PD), polyphagia, and weight loss
• Later signs--anorexia, lethargy, depression, and vomiting
• Obesity with recent weight loss is typical.
• Dorsal muscle wasting and an oily coat with dandruff common in cats
• Hepatomegaly in both species, but jaundice more prevalent in cats
• Less common findings-- cataracts in dogs and a plantigrade stance in cats (diabetic neuropathy)
  

causes :

• Genetic susceptibility
• Infectious (viral) diseases
• Immune-mediated beta cell destruction
• Pancreatitis
• Predisposing diseases (e.g., hyperadrenocorticism and acromegaly)
• Drugs (e.g., glucocorticoids and progestagens)
  

risk factors :

• Obesity for type II DM
• Diestrus in the bitch

diagnosis :

differential diagnosis :

• Renal glucosuria--usually does not cause PU/PD, weight loss, or hyperglycemia
• Stress hyperglycemia in cats--no PU/PD or weight loss. Blood glucose concentration normal if sample taken when cat is not stressed.
  

CBC/Biochemistry/Urinalysis

• Results of hemogram usually normal
• Glucose > 200 mg% in dogs; > 250 mg% in cats
• High SAP, ALT, and AST activities and hypercholesterolemia and lipemia common
• Electrolytes vary, but hypernatremia, hypokalemia, and hypophosphatemia indicate severe decompensation.
• Total CO2 or HCO3 are low if the patient has ketoacidosis or severe dehydration.
• Glucosuria is a consistent finding.
• Ketonuria is common.
• Urine specific gravity often is low.
  

other laboratory tests :

• Anion gap--high in patients with ketoacidosis
• Plasma insulin--may be helpful in differentiating type I from type II DM. Normal or high insulin concentration with hyperglycemia found in patients with type II DM. Low insulin concentration suggests type I DM but may be an incorrect diagnosis because persistent hyperglycemia can impair insulin secretory activity, even if functional beta cells are present.
• Glucose tolerance test--best way to differentiate types of DM but impractical
  

imaging :

• Radiography--useful to evaluate for concurrent or underlying disease (e.g., cystic or renal calculi, emphysematous cystitis or cholecystitis, and pancreatitis)
• Ultrasonography--indicated in selected patients, particularly those with jaundice, to evaluate for hepatic lipidosis, cholangiohepatitis, and pancreatitis

other diagnostic procedures :

Liver biopsy (percutaneous)--indicated in some jaundiced patients

gross and histopathologic findings :

Usually no gross necropsy changes

Histopathologic findings may be normal or reveal vacuolar degeneration of the islets of Langerhans or low numbers of islet cells. Immunohistochemical staining is necessary to show low numbers of beta cells. In cats, amyloid deposits in the islets are usually seen.

treatment :

inpatient versus outpatient

Compensated dogs and cats can be managed as outpatients. They are alert, hydrated, and eating and drinking without vomiting. For management of decompensated patients, see Diabetes Mellitus, Ketoacidotic.

activity

Strenuous activity may lower insulin requirement. Consistent amount of activity each day is helpful.

diet

• Avoid soft, moist foods because they cause severe postprandial hyperglycemia.
• Nonobese dogs and cats--feed a consistent diet that the pet will reliably eat. Keep daily calorie intake constant.
• Obese dogs and cats--gradual weight reduction improves insulin sensitivity and reverses diabetes in some cats with type II DM. Technique 1--reduce the calorie intake to 70% (cats) or 60% (dogs) of the caloric requirement for the animal's ideal body weight. Technique 2--feed a high-fiber, low-calorie food in a quantity similar to what the pet is accustomed. Try to achieve the target weight over 2-4 months. Rapid weight loss is inadvisable, especially in obese cats with DM because they are prone to hepatic lipidosis.
• Thin dogs and cats--avoid reduced calorie diet. Starvation exacerbates ketoacidosis and poor immune function.
• Role of fiber--key role is in weight loss and obesity prevention. Another beneficial effect may be improved glycemic control. Recommended diet is high in fiber, low in fat, and high in complex carbohydrates.
• Feed the pet half its daily food every 12 hours to coincide with twice-daily insulin injections or orally administered hypoglycemic agent. For animals on once-daily insulin injections, half the food is given with the injection and the remainder in 8-10 hours or at the time of peak insulin activity, if that has been determined. For nibblers, dry food can be fed ad libitum, and two small meals of canned food given as described.

client education

Discuss daily feeding and medication schedule, home monitoring, signs of hypoglycemia and what to do, and when to call or visit veterinarian. Clients are encouraged to keep a chart of pertinent information about the pet, such as urine dipstick results, daily insulin dose, and weekly body weight.

surgical considerations

Intact females should have an ovariohysterectomy when stable. Progesterone secreted during diestrus makes management of DM difficult.

medications

drugs and fluids

Fluid therapy--see Diabetes Mellitus, Ketoacidotic

Insulin--treatment of choice for all dogs and most cats

• Regular crystalline insulin has rapid bioavailability, short duration of action, and can be given by any parenteral route. Used for patients with anorexia, vomiting, or ketoacidosis. Can be mixed with other insulins.
• NPH (Isophane) insulin--intermediate in duration; given SQ q12h in all cats and most dogs; initial dosage--dogs, 0.5 unit/kg; cats, 0.25-0.5 unit/kg; adjust the dosage according to individual response
• Lente insulin--intermediate in duration; given SQ; initial dosage same as for NPH. Often given q12h but may be suitable q24h in some animals.
• Ultralente insulin--long acting insulin; given SQ, usually q24h. Some animals require injections q12h.

Insulin mixtures add rapid bioavailability to longer duration insulins. The lente series can be mixed in any combination. NPH and regular insulin mixtures are commercially available. A combination of 25% regular and 75% ultralente can be used after it equilibrates in the vial for 24 hours. Most animals can be managed without insulin mixtures.

Species of origin of the insulin may affect pharmacokinetics. Beef, pork, beef/pork, and human recombinant insulin are options. Animal-origin insulins are being phased out. Keep the pet on the same type and species of insulin if possible. When changing from an animal origin to human recombinant insulin, lower the dosage and reregulate the animal.

Oral administration of hypoglycemic agent--glipizide is useful with dietary therapy in some cats with type II DM. The cat should have uncomplicated DM and no history of ketoacidosis. Initial dosage, 2.5 mg PO q12h. Monitoring is the same as for patients on insulin. If hyperglycemia is not controlled, 5 mg q12h may be tried. Potential side effects are hypoglycemia, hepatic enzyme alterations, icterus, and vomiting.

precautions

• Glucocorticoids, megestrol acetate, and progesterone cause insulin resistance.
• Hyperosmotic agents (e.g., mannitol and radiographic contrast agents) if the patient is already hyperosmolar from hyperglycemia

possible interactions

Many drugs (e.g., NSAIDs, sulfonamides, miconazole, chloramphenicol, monoamine oxidase inhibitors, and beta blockers) potentiate the effect of hypoglycemic agents given orally. Consult the product insert.

alternate drugs

Dietary therapy or oral administration of hypoglycemic agents or both can be tried if owners are unwilling or unable to give insulin. This is more successful in cats than dogs.

follow-up

patient monitoring

Glucose curve--the best method of monitoring. The owner feeds the pet, injects the insulin, and then brings the patient to the hospital for serial blood glucose testing every 1-2 hours, beginning about an hour after the injection. Animals receiving insulin q12h are followed for 12 hours, and those on insulin q24h are followed for 24 hours. The goal is to maintain blood glucose between 100 and 200 mg% for at least 20-22 hours per day in dogs, and between 100 and 300 mg% in cats. The curve is performed every few weeks until the disease is regulated, and then every few months or whenever a problem arises.

Urine glucose monitoring--urine is tested for glucose and ketones before the meal and insulin injection. To use this as a regulatory method, the pet must be allowed to have trace to 1/4% glucosuria to avoid hypoglycemia. Animals regulated by urine alone may be more hyperglycemic than ideal, and insulin overdose with rebound hyperglycemia is an inherent risk with this method. It is most useful to combine urine monitoring with intermittent glucose curves. Owners should seek veterinary attention if ketonuria is detected.

Clinical signs--owner can assess degree of PU/PD, appetite, and body weight. If these are normal, the disease is well regulated.

prevention/avoidance

Prevent or correct obesity. Avoid unnecessary use of glucocorticoids or megestrol acetate.

• possible complications
• Cataracts (dogs) and diabetic neuropathy (cats) with poor glycemic control
• Seizure or coma with insulin overdose
• Anemia and hemoglobinemia with severe hypophosphatemia, which can occur after initial insulin therapy
  

expected course and prognosis

Some cats recover but may relapse at a later time. Dogs have permanent disease. Prognosis with treatment is good. Most animals have a normal life span.

miscellaneous

Urinary tract infection

age related factors

Juvenile DM is rare and may be more difficult to manage.

pregnancy :

Diabetes mellitus can develop during pregnancy, in which case the pregnancy is difficult to maintain. Exogenous insulin administration may cause fetal oversize and dystocia. Insulin resistance develops, making hyperglycemia difficult to control. The pregnant bitch is prone to ketoacidosis. An emergency ovariohysterectomy may be necessary. Dogs with DM should not be used for breeding.

abbreviations :

• ALP = alkaline phosphatase
• ALT = alanine aminotransferase
• AST = aspartate aminotransferase
• NSAID = nonsteroidal antiinflammatory drug
• PU/PD = polyuria and polydypsia
• DM = diabetes mellitus

references :

Nelson RW. Diabetes mellitus. In: Ettinger SJ, Feldman EC, eds. Textbook of veterinary internal medicine. Philadelphia: WB Saunders, 1995:1510-1537.

Wallace MS, Kirk CA. The diagnosis and treatment of insulin-dependent and non-insulin-dependent DM in the dog and the cat. Prob Vet Med 1990;2:573-590.

Author Melissa S. Wallace

Consulting Editor Rhett Nichols

The majority of the information in this page is has been taken from VetMedCenter.com. For further information about this useful source of informtion follow the link or look, on the internet, at www.vetmedcenter.com.