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Vol. 19, No.

1 January 1997 V HEINZ SYMPOSIUM 1996

Continuing Education Article

Endocrine
Emergencies. Part I.
FOCAL POINT Endocrine Pancreatic
★Diabetic ketoacidosis is a
common emergency in small
animal practice.
Disorders
KEY FACTS Colorado State University
Deborah S. Greco, DVM, PhD
■ In diabetic ketoacidosis, serum
potassium is usually elevated but

P ancreatic disorders often cause emergencies in small animal practice.


the body stores of potassium are
typically depleted. This article reviews the signs and immediate medical management of
emergencies related to high or low blood glucose.
■ Hemolysis in diabetic cats
may be caused by Heinz-body DIABETIC KETOACIDOSIS
formation. Pathophysiology
Diabetic ketoacidosis is probably the most common endocrine emergency in
■ Hyperosmolar nonketotic small animal practice. Diabetes mellitus results from impaired glucose utili-
syndrome is usually preceded by zation, increased gluconeogenesis, and increased hepatic glycogenolysis. De-
the classic signs of diabetes creased peripheral utilization of glucose leads to accumulation of glucose in
mellitus. serum, followed by osmotic diuresis. Osmotic diuresis drives polydipsia, and
inadequate intake of fluid results in dehydration.
■ Attempts to restore euglycemia Insulin is anabolic; therefore, insulin deficiency leads to protein catabolism
in a patient with insulinoma may and contributes to the clinical signs of weight loss and muscle atrophy. As a
result in rebound hypoglycemia. consequence of protein catabolism, amino acids are utilized by the liver to pro-
mote gluconeogenesis. Stress hormones, such as cortisol and epinephrine, stim-
ulate protein catabolism and glycogenolysis, respectively.1
Some of the most profound changes associated with the ketoacidotic diabetic
state occur in lipid metabolism. Because of increased lipase activity, adipose tis-
sue is broken down at an accelerated rate into nonesterified fatty acids. Hepatic
assimilation of these fatty acids, which depends on the rate of lipolysis, is also
accelerated.2 Nonesterified fatty acids are released into the bloodstream and de-
livered to the liver for repackaging as triglycerides or are used extrahepatically
as oxidative fuels.1
With insulin deficiency, lipid metabolism in the liver becomes deranged and
nonesterified fatty acids are converted to acetyl coenzyme A rather than being
incorporated into triglycerides. Acetyl coenzyme A accumulates in the liver and
is converted into acetoacetyl coenzyme A and then ultimately to acetoacetic
acid. Finally, the liver starts to generate large amounts of acetoacetic acid, β-
hydroxybutyrate, and acetone.1,2
Small Animal The Compendium January 1997

As insulin deficiency culminates in diabetic ketoaci- lar catheter to avoid overhydration.


dosis, accumulation of ketones and lactic acid in the Fluid rates depend on the severity of dehydration,
blood and loss of electrolytes and water via urine result maintenance requirements, continuing losses (vomiting
in profound dehydration, hypovolemia, metabolic aci- and diarrhea), and the presence of concurrent disease
dosis, and shock. Nausea, anorexia, and vomiting result (e.g., congestive heart failure). Use of hypotonic solu-
when ketonemia and hyperglycemia stimulate the tions is controversial because serum hyperosmolality
chemoreceptor trigger; they contribute to the dehydra- often causes idiogenic osmoles in the brain, which are
tion caused by osmotic diuresis. Ketonuria and osmotic trapped when serum osmolality decreases and rapidly
diuresis result in sodium and potassium loss via urine, produce cerebral edema.5
thus exacerbating hypovolemia and dehydration.
Eventually, severe dehydration may result in hypervis- Insulin
cosity, thromboembolism, severe metabolic acidosis, re- Insulin therapy should be initiated as soon as possi-
nal failure, and finally death. ble. Either intravenous insulin or low intramuscular
doses are given.5 The protocol outlines the intravenous
Diagnosis insulin fluid rate, which should preferably be adminis-
The clinical signs and physical examination findings tered via a separate peripheral catheter. Approximately
in animals with acute diabetic ketoacidosis are dra- 50 ml of fluid and insulin is allowed to run through the
matic. These dogs and cats typically have a history of intravenous drip set and then discarded because insulin
anorexia, weakness, depression, and vomiting that was binds to the plastic tubing.5
preceded by polydipsia, polyuria, and weight loss.3,4 The species of regular insulin (beef, pork, or human)
Animals suffering from diabetic ketoacidosis are often does not affect response; however, the type of insulin
presented in shock. given is critical. Regular insulin must be used; insulin
Physical examination findings may include depres- zinc suspension, extended insulin zinc suspension, and
sion, tachypnea, dehydration, weakness, and vomit- isophane insulin suspension should never be given intra-
ing.3,4 Diabetic cats may exhibit clinical icterus as a re- venously. Intravenous insulin reduces blood glucose to
sult of hemolysis, hepatic lipidosis, biliary obstruction below 250 mg/dl within approximately 10 hours in
due to pancreatitis, or acute pancreatitis. The gastroin- dogs and after about 16 hours in cats.5 Once eugly-
testinal signs (e.g., vomiting, abdominal distention, and cemia has been achieved, the animal is maintained on
abdominal pain) are similar to those of pancreatitis subcutaneous regular insulin (0.1 to 0.4 U/kg subcuta-
(which can occur concurrently with diabetic ketoacido- neously every 4 to 6 hours) until it starts to eat and/or
sis) and peritonitis.1 Diagnosis of diabetic ketoacidosis the ketosis has resolved.
is based on hyperglycemia, glycosuria, and ketonuria or An alternative, as shown in the protocol, is to use
ketonemia. low-dose intramuscular insulin. However, blood glu-
cose levels may drop precipitously as depots of intra-
Treatment muscular insulin are absorbed from muscle tissue that
Treatment, as outlined in Treatment of Diabetic Ke- had been poorly perfused.
toacidosis, includes the following steps (in order of im-
portance): Electrolytes
Electrolyte (specifically potassium) balance may be
■ Fluid therapy with 0.9% saline difficult to manage during a ketoacidotic crisis. Potassi-
■ Insulin therapy (low-dose intramuscular or um should be supplemented as soon as insulin therapy
intravenous)5 is initiated. Although serum potassium may be normal
■ Electrolyte supplementation (potassium chloride or elevated in animals with diabetic ketoacidosis, the
and/or potassium phosphate, magnesium) animal’s total body stores of potassium are actually de-
■ Reversal of metabolic acidosis pleted.

Fluid Therapy Metabolic Acidosis


Fluid therapy should consist of 0.9% saline supple- Correction of the metabolic acidosis tends to drive
mented with potassium when insulin therapy is initiat- potassium intracellularly in exchange for hydrogen
ed. A large central venous catheter should be used to ions. Insulin facilitates this exchange. The net effect is a
administer the fluid because the animals are severely dramatic decrease in serum potassium, which must be
dehydrated and require rapid fluid administration; cen- attenuated with appropriate potassium supplementa-
tral venous pressure may also be monitored via a jugu- tion in fluids. Refractory hypokalemia may be compli-

CENTRAL VENOUS CATHETER ■ REGULAR INSULIN ■ POTASSIUM


The Compendium January 1997 Small Animal

Treatment of Diabetic Ketoacidosis

Step One: Fluid Therapy

■ Place intravenous catheter, preferably central venous.

Administration rate:

■ Estimate dehydration deficit (ml): ■ Estimate maintenance needs:

Deficit (ml) = Dehydration (%) × body weight (kg) 2 ml/kg/hr × hours required to rehydrate (24 hours)
× 1000 ml
■ Estimate losses (vomiting, diarrhea)

Fluid dose = Dehydration deficit + maintenance needs + losses


Hourly fluid administration rate (ml/hr) = Fluid dose (ml) ÷ 24 hours

Fluid composition:

Blood Glucose (mg/dl) Fluids Rate Route Monitor Frequency

> 250 0.9% saline Up to 90 Intravenous Packed cell Every 4 hr


ml/kg/hr volume, total
to rehydrate solids, sodium,
potassium,
osmolality

200–250 0.45% saline Up to 90 Intravenous Packed cell Every 4 hr


plus 2.5% ml/kg/hr volume, total
dextrose to rehydrate solids, sodium,
potassium,
osmolality

150–200 0.45% saline Up to 90 Intravenous Central venous Every 2 hr


plus 2.5% ml/kg/hr pressure, urine
dextrose to rehydrate output

100–150 0.45% saline Up to 90 Intravenous Central venous Every 2 hr


plus 2.5% ml/kg/hr pressure, urine
dextrose to rehydrate output

<100 0.45% saline Up to 90 Intravenous Central venous Every 2 hr


plus 5% ml/kg/hr pressure, urine
dextrose to rehydrate output
Small Animal The Compendium January 1997

Step Two: Insulin


Intravenous insulin (regular only) is mixed in 250 ml of 0.9% saline; 50 ml is allowed to run through the administration
set and discarded. See the text for treatment recommendations for hyperosmolar coma.
Blood Glucose (mg/dl) Rate Route Dose Monitor Frequency
(U/kg)
Intravenous (regular only)
>250 10 ml/hr Intravenous Cats: 1.1 Blood glucose Every 1–2 hr
Dogs: 2.2
200–250 7 ml/hr Intravenous Cats: 1.1 Blood glucose Every 1–2 hr
Dogs: 2.2
150–200 5 ml/hr Intravenous Cats: 1.1 Blood glucose Every 4 hr
Dogs: 2.2
100–150 5 ml/hr Intravenous Cats: 1.1 Blood glucose Every 4 hr
Dogs: 2.2
<100 Stop Subcutaneous 0.1–0.4 Blood glucose Every 2 hr
intravenous
insulin; begin
subcutaneous
insulin every
4 hours

Intramuscular (regular only)


>250 mg/dl Initial dose Intramuscular 0.2 Blood glucose Hourly
Every hour Intramuscular 0.1 Blood glucose Hourly
<250 mg/dl Every 4–6 hr Intramuscular 0.1 Blood glucose Every 4–6 hr
Every 6–8 hr Subcutaneous 0.1–0.4 Blood glucose Every 6–8 hr

Step Three: Electrolytes

Electrolyte Concentration Amount Added to Fluid Maximum Fluid Administration


(mEq/L) Rate (ml/kg/hr)
Potassium
3.6–5.0 mEq/L 20 26
2.6–3.5 mEq/L 40 12
2.1–2.5 mEq/L 60 9
<2.0 mEq/L 80 7

Phosphorus
1–2 mg/dl 0.03 mmol/kg/hr Monitor serum phosphorus
every 6 hr

<1.0 mg/dl 0.1 mmol/kg/hr Monitor serum phosphorus


every 6 hr
Magnesium
<1.2 mg/dl 0.75–1 mEq/kg/day (magnesium Use 5% dextrose; magnesium is
chloride or sulfate) in a constant- incompatible with calcium and
rate infusion sodium bicarbonate solutions
Small Animal The Compendium January 1997

Step Four: Acid–Base Balance

pH Bicarbonate Concentration Dose of Bicarbonate Rate


(ml)

< 7.1 <12 mEq/L 0.1 × body weight (kg) Over 2 hr


× (4 – bicarbonate [mEq/L])

cated by hypomagnesemia. The article by Dr. Macintire Approximately one third of ketoacidotic diabetic cats
on disorders of potassium, phosphorus, and magnesium are presented in recumbency and with a serum osmolal-
in this issue of Compendium provides guidelines for the ity in the range of 388 mOsm/L; this may be a mani-
supplementation of serum potassium and other elec- festation of mixed hyperosmolar syndrome.5
trolytes in patients with diabetic ketoacidosis. Treatment of hyperosmolar coma is difficult. Several
Serum and tissue phosphorus may also be depleted guidelines, which differ from the treatment of diabetic
during a ketoacidotic crisis, and some of the potassium ketoacidosis, should be followed. First, fluid therapy
supplementation (one third of the potassium dose) may should be approached cautiously by estimating the flu-
consist of potassium phosphate—particularly for small id needs (dehydration deficit) and replacing 80% of the
dogs and cats, which are most susceptible to hemolysis deficit over a 12- to 24-hour period.5 Isotonic, rather
caused by hypophosphatemia.5,6 Oversupplementation than hypotonic, solutions should be used. Hyper-
of phosphorus can result in metastatic calcification and glycemia should also be reversed very slowly. A lower
hypocalcemia. Cats with diabetic ketoacidosis may also dosage of insulin (1.1 U/kg over 24 hours) is recom-
have a mild increase in mean cell volume because hy- mended for hyperosmolar animals, and insulin therapy
pophosphatemia causes erythrocytes to swell.6 should be delayed until 2 to 4 hours after fluid therapy
Another cause of hemolysis in cats with diabetic begins.5
ketoacidosis is Heinz-body anemia.7 Although Heinz-
body anemia usually does not result in overt hemolysis HYPOGLYCEMIC SEIZURES
by itself, it probably shortens the erythrocyte life span. Causes of hypoglycemia include iatrogenic insulin
When coupled with low phosphorus levels, it may pre- overdose, insulinoma, sepsis, large tumors, hunting dog
cipitate a hemolytic crisis.6 and puppy hypoglycemia, hypoadrenocorticism, por-
The first three steps in the treatment of diabetic ke- tosystemic shunts, hypothyroidism, growth hormone
toacidosis usually correct serum acid–base status. How- deficiency, and (rarely) starvation.8–14 Insulin overdose,
ever, some patients with blood pH under 7.1 or serum hypoadrenocorticism, and insulinoma are the most
bicarbonate below 12 mEq/L need bicarbonate therapy common endocrine disorders that result in hypo-
(see the protocol).5 Caution is recommended because glycemia.
metabolic alkalosis may be difficult to reverse. Treatment should consist of administration of a
slow intravenous bolus of 50% dextrose (0.5 g/kg di-
HYPEROSMOLAR COMA luted 1:4). If no vein is readily accessible, corn syrup
In humans, nonketotic hyperosmolar diabetes is defined or pancake syrup may be applied to the oral mucous
as extreme hyperglycemia (serum glucose >600 mg/dl), membranes with a large syringe. Thereafter, animals
hyperosmolality (>350 mOsm/L), severe dehydration, with hypoglycemia of any cause should be given a
central nervous system depression, and a paucity of ke- continuous infusion of 5% dextrose until they can be
tones or metabolic acidosis.5 Hyperosmolar nonketotic fed.
syndrome in dogs and cats is an unusual syndrome Veterinarians should avoid the temptation to restore
characterized by neurologic and gastrointestinal abnor- blood glucose concentrations to the normal range in
malities (e.g., progressive weakness, anorexia, vomiting, dogs with insulinoma. Administration of higher and
and lethargy). These signs are usually preceded by the higher doses of 50% dextrose in an attempt to restore
classic signs of uncomplicated diabetes mellitus: poly- euglycemia may result in a cycle of rebound hypo-
dipsia, polyuria, weight loss, and polyphagia. glycemia by provoking insulin secretion. The goal of
Physical examination reveals severe dehydration, hy- intravenous glucose therapy is to stop the seizure rather
pothermia, extreme depression, lethargy, and coma.5 than to normalize blood glucose.

HEINZ-BODY ANEMIA ■ HEMOLYSIS ■ REBOUND HYPOGLYCEMIA


Small Animal The Compendium January 1997

Your comprehensive
Long-term management of hypoglycemia depends on
guide to diagnostic the cause. The veterinarian must therefore use appro-
priate diagnostics to identify the cause of the hypo-
ultrasonography glycemia.
The immediate therapy for hypoglycemia resulting
Nautrup and Tobias from insulin overdose is the same as for other causes of
hypoglycemia. However, endogenous glucose stores
may have been depleted by the insulin overdose; it may
take several days for hyperglycemia to recur.5 In these
cases, insulin therapy should be discontinued until hy-
perglycemia recurs. Insulin overdose in animals may
lead to cerebral edema and temporary blindness or be-
havior changes. These signs are often temporary and re-
solve after several weeks or months.

About the Author


Dr. Greco is affiliated with the Department of Clinical Sci-
ences, College of Veterinary Medicine and Biomedical

New Sciences, Colorado State University, Fort Collins, Col-


orado, and is a Diplomate of the American College of
Veterinary Internal Medicine.

$
149 REFERENCES
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Robert E. Cartee, Editor 2. Feldman EC: Diabetic ketoacidosis in dogs. Compend Con-
400 pages, hard cover tin Educ Pract Vet 2(6):456-463, 1980.
3. Schaer M: Insulin treatment for the diabetic dog and cat.
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■ Case illustrations using conventional 7. Christopher MM: Hematologic complications of diabetes
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Price valid only in the US, Canada, Mexico, and
JAVMA 186:53–55, 1985.
the Caribbean. Request international pricing.
Email: books.vls@medimedia.com

GLUCOSE STORES ■ CEREBRAL EDEMA ■ CNS SIGNS


The Compendium January 1997 Small Animal

13. Turnwald GH, Troy GC: Hypoglycemia. Part I. Carbohy- 14. Turnwald GH, Troy GC: Hypoglycemia. Part II. Clinical
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