Diabetic crises: Recognition and management (Proceedings)

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Diabetes mellitus occurs in both dogs and cats and is the most common endocrine disorder in the emergency setting.

Diabetes mellitus occurs in both dogs and cats and is the most common endocrine disorder in the emergency setting. Three types of diabetic emergencies may occur: (1) Insulin overdose, (2) Diabetic ketoacidosis, and (3) Non-ketotic hyperosmolar diabetes. Historical findings may be similar in all 3 cases, and may include polyuria, polydypsea, weight loss, anorexia, weakness, ataxia, severe depression, stupor, coma, or seizures. Diabetes most commonly occurs in middle-aged female dogs and in older male cats.

The initial approach to an animal with suspected diabetic crisis is aimed toward differentiating between the 3 types of diabetic emergencies and determining how "sick" the patient is. An intravenous catheter is placed and 4 capillary tubes of blood are collected to run the hematocrit and total protein, blood glucose (using a Dextrometer, Ames Laboratories, Ames IA), blood urea nitrogen (using a reagent stick), and serum electrolytes. Blood for serum electrolytes must be collected in a lithium heparin capillary tube rather than in a sodium heparin tube. Evaluation of the laboratory work will reveal whether the animal is hypoglycemic or hyperglycemic, and whether or not ketones and glucose are present in the urine, and whether the animal is dehydrated, anemic, azotemic, or has a serious electrolyte imbalance. Other tests which can be run rapidly in an emergency setting include serum osmolality and venous or arterial blood gases. Within a few minutes after the animal is presented to the hospital, the clinician should be able to determine which type of diabetic crisis is occurring and to manage it accordingly.

I. Insulin Overdose

Insulin overdose can occur through owner error (for example, switching from low dose insulin syringes to tuberculin syringes) or through change in the animal's insulin requirements. Insulin requirements will decrease following treatment for hyperadrenocorticism or after estrus is completed, and the insulin dosage must be lowered accordingly.

Problems in insulin regulation can also result in hypoglycemia, especially if insulin dosage is based on morning glucose readings. The "Somogyi overswing" occurs when an overdose of insulin is given resulting in hypoglycemia. Working owners often miss the signs of hypoglycemia which occur in the afternoon following the morning insulin dose. Release of stress hormones causes a rebound hyperglycemia to occur with accompanying signs of polyuria, polydypsea, and glucosuria. If the owner continues to increase the insulin dose based on morning urine glucose readings, clinically significant hypoglycemia will result. A similar problem can occur with rapid insulin metabolism. Animals with this problem should receive insulin injections twice daily, instead of increasing the insulin dosage based on morning glucosuria.

Clinical signs of hypoglycemia include lethargy, depression, ataxia, weakness, stupor, coma, or seizures. If an owner recognizes these signs at home, he or she should be instructed to give Karo syrup orally (rub it on the gums if the animal is comatose or seizuring) and bring it directly to the veterinary hospital. If significant hypoglycemia is present, the animal should be given a slow intravenous bolus of 50% Dextrose (0.5 g/kg diluted 1:4). Then, to prevent recurrent hypoglycemia, 5% dextrose can be administered by continuous IV infusion. Mild or subclinical hypoglycemia may be treated by simply feeding the animal.

Blood glucose must be monitored closely and insulin can be re-administered when hyperglycemia occurs. Sometimes, following an extreme insulin overdose, insulin therapy is not required again for several days. If poor insulin regulation is the cause of the hypoglycemia, the animal should be hospitalized for a glucose curve.

II. Diabetic Ketoacidosis (DKA)

Diabetic ketoacidosis is a medical emergency involving extreme alterations of metabolic parameters. The syndrome is characterized by hyperglycemia, metabolic acidosis, ketonemia, dehydration, and loss of electrolytes. Treatment goals include: (1) Restoration of electrolyte and acid-base balances, (2) Replacement of body fluids, (3) Reduction of blood glucose and (4) Identification of underlying or precipitating factors in the disease process.

DKA commonly occurs when there is a relative excess of stress hormones in an insulin deficient animal. Therefore, every effort should be made to detect underlying disease factors contributing to stress. The work-up should include bloodwork (CBC, chemistry panel, blood gases, electrolytes, osmolality); chest radiographs if dyspneic (rule out congestive heart failure, neoplasia, dirofilariasis, pneumonia); abdominal radiographs (rule out pancreatitis, pyometra, urolithiasis, etc.); urinalysis (including culture and sensitivity); and amylase and lipase in vomiting dogs.

A. Fluid therapy

The initial fluid of choice is 0.9% NaCl. Isotonic saline prevents the rapid fall in osmolality which may occur if hypotonic fluids are used. Fluid requirements should be calculated to restore hydration over 10 - 12 hours (see Table I). Hypokalemia is a common problem in animals with anorexia and vomiting. In addition, potassium levels may drop precipitously with insulin therapy and correction of metabolic acidosis. Clinical signs associated with hypokalemia include muscle weakness, paralytic ileus, respiratory paralysis, and cardiac arrhythmias. Ideally, potassium should be monitored closely during therapy and added to the fluids as described in Table II. If monitoring equipment is not available and renal function is normal, potassium can usually be safely added to the fluids (20 - 40 mEq/L) after the first 4 hours.

The use of sodium bicarbonate to correct acidosis in DKA is controversial. Treatment with insulin and fluids will correct the acidosis via oxidation of ketone bodies and excretion of hydrogen ions in the urine. Administration of sodium bicarbonate may cause decreased serum potassium, hyperosmolality, rebound alkalosis, or impaired oxygen delivery to tissues by increasing hemoglobin affinity for oxygen. Therefore, bicarbonate therapy is not recommended unless the pH < 7.100, and a conservative approach is always justified.

Hypophosphatemia may occur in some animals being treated for DKA. Clinical signs include muscle weakness, rhabdomyolysis, hemolysis, respiratory failure, and impaired cardiac function. Phosphate replacement is not indicated in asymptomatic animals, however, since over-supplementation may be dangerous if hypocalcemia occurs.

B. Insulin therapy

Regular insulin is used at an initial dosage of 2.2 U/kg/24 h as a continuous intravenous infusion. Low dose continuous intravenous insulin infusion affords a safe and effective treatment by providing a gradual but consistent reduction in blood glucose while acid-base, electrolyte, and hydration abnormalities are corrected. The method is particularly efficacious for treating dogs with concurrent acute pancreatitis, or other causes of vomiting and anorexia, since the insulin infusion may be continued for several days with no adverse effects. When ketones are negative and the animal is eating, therapy can be initiated with longer acting insulin as in routine uncomplicated diabetics.

The drip is very easy to prepare. For a 20 lb dog, 20 units of regular crystalline insulin are added to 250 ml of 0.9% NaCl. Since insulin binds to the plastic IV tubing, the first 50 ml should be run through and discarded. The drip is administered at 10 ml/hr in a separate line from the fluids, preferably through an infusion pump. The rate of insulin infusion is adjusted according to Table III. When the blood glucose drops to ≤ 250 mg/dl, 2.5% dextrose is added to the intravenous fluids and the infusion rate is slowed by 25 - 50%. Blood glucose should be monitored q 2 hours, and hematocrit, total protein, and electrolytes every 4 hours. Hypokalemia and hypoglycemia are potential problems that can be avoided with careful monitoring and appropriate supplementation. The mortality rate for DKA in animals is 25 - 30%, even with aggressive treatment. There is a high incidence of serious underlying disease factors, such as acute pancreatitis and hyperadrenocorticism, which undoubtedly contribute to the high mortality rate.

III. Non-ketotic Hyperosmolar Diabetes (NKHD)

This syndrome is characterized by severe dehydration, abnormal brain function, marked hyperglycemia, and lack of significant ketoacidosis. Central nervous system signs associated with hyperosmolality include restlessness, convulsions, hyperthermia, ataxia, muscle twitching, nystagmus, and death.

In human beings, NKHD generally develops in older nursing home residents with underlying renal or cardiovascular disease. They are commonly type II, maturity onset, non-insulin dependent diabetics. It is thought that endogenous insulin secretion in these patients maintains anti-lipolytic and anti-ketogenic effects, but is too low to allow for adequate glucose uptake. The most striking feature of NKHD is marked dehydration. Persistent hyperglycemia results in osmotic diuresis. When dehydration is of such magnitude that urine flow is impaired, serum glucose levels rise sharply. In addition, pre-renal azotemia develops. The extremely elevated blood glucose and hyperosmolality which develop cause an alteration of sensorium. NKHD is uncommon in dogs, but may occur in up to 50% of diabetic cats.

Normal serum osmolality is between 285-310 mOsm/kg. Neurologic signs occur when the osmolality is greater than 350 mOsm/kg. Serum osmolality can be measured directly with a freezing point depression osmometer, or osmolality can be calculated by the following formula:

serum osmolality (mOsm/kg) = 2(Na) + glucose/18 + BUN/2.8

The object of therapy is to slowly and steadily lower the blood glucose and correct dehydration and electrolyte imbalances. Basically, the treatment is similar to the DKA protocol, but the insulin dosage is lower and the rate of rehydration is slower.

1. Insulin - Regular insulin is administered in a continuous intravenous infusion at 1 U/kg/24 h. The blood glucose should be monitored closely, and should not drop below 250 mg/dl within the first 12 hours, since rapid decreases have been associated with cerebral edema and worsening of neurologic status. Generally, the insulin infusion is not initiated until 2 - 4 hours after the start of fluid therapy. Even without insulin, the blood glucose will drop as hyperglycemia is diluted and renal perfusion is restored.

2. Fluids - The fluid of choice is again 0.9% NaCl, unless the serum sodium is very elevated. Caution must be exercised if a hypotonic fluid such as 0.45% NaCl is chosen, since it may lower the serum osmolality too rapidly, resulting in cerebral edema. Fluid requirements are estimated, and 80% of the calculated dose should be given over 12 hours.

Table 1 - Diabetic Ketoacidosis Emergency Treatment Protocol

I. Initial data base

1. Immediate PCV, TS, Azostick, Dextrometer, Na, K, UA (dipstick and specific gravity), osmolality, blood gases

2. CBC, chemistry panel

3. Rule out underlying infection - (radiographs, urine culture, amylase/lipase, etc.)

II. Fluid therapy

1. Place IV catheter - preferably central venous.

2. Calculate fluid requirements and replace 80% of deficit over 10 hours.

i. Estimate % dehydration x BW(kg) x 1000 ml/L = # ml to rehydrate

ii. Estimate maintenance needs - 1 ml/lb/hr

iii. Estimate # ml lost with vomiting or diarrhea

3. Begin with 0.9% NaCl.

4. Change fluids to 0.45% NaCl and 2.5% Dextrose when glucose ≤ 250 mg/dl.

5. Add potassium to drip according to potassium replacement chart (Table 2).

6. If pH < 7.000, give NaHCO3

- x base deficit x BW(kg) = # ml slowly over 2 hours

7. If serum phosphorus < 1 mg/dl, and related clinical signs (hemolysis, myopathy, respiratory paralysis, encephalopathy) are evident, give 0.01 - 0.03 mmol phosphate/kg/hr over 6 hours and recheck phosphorus.

III. Insulin Therapy

1. Use regular crystalline insulin in separate IV drip.

2. Dose: 2.2 U/kg/24h (dog) or 1.1 U/kg/24h (cat).

3. Add insulin to 250 ml NaCl or Ringer's solution. Run 50 ml through IV tubing and discard. Begin drip at 10 ml/h with infusion pump.

4. Slow insulin infusion rate by 25-50% according to insulin therapy chart (Table 3) when glucose ≤ 250 mg/dl.

5. Continue IV insulin infusion until ketones are negative and patient is eating.

6. Begin long acting insulin (NPH, Lente, or Ultralente) at 0.5 U/kg SQ when ketones are negative and patient is stable.

IV. Miscellaneous

1. Antibiotics if fever/systemic infection.

2. NPO if pancreatitis

3. Monitor Dextrometer q 1-2 h initially

- PCV, T.S., Na, K, osmolality q 4 h

- Blood gases q 6 h

- Urine output q 2 h

Table 2 - Potassium Replacement*

Table 3 - Insulin Therapy Adjustments

Table 4 - Guidelines for Treating Hyperosmolar Diabetes Mellitus in Dogs and Cats.

Follow protocol for DKA except:

1. Estimate fluid needs and replace 80% of deficit over 12-24 hours.

2. Do not begin insulin therapy until 2-4 hours after initiation of fluid therapy.

3. Lower insulin dosage to 1.1 U/kg/24 h.

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