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Name
Diabetic Ketoacidosis, Canine
Short Description
Diabetic ketoacidosis
Affected Animals:
Dogs and cats.
Overview:Diabetic ketoacidosis, or DKA, is one of
the most serious metabolic disorders seen in both human and
veterinary medicine. A severe complication of diabetes mellitus, DKA
is characterized by an elevated concentration of blood sugar, the
presence of substances called ketones in the urine, and reduced
concentrations of bicarbonate in the blood. Some dogs with DKA will
be affected mildly, but the majority will be seriously ill and may
have severe complications such as neurological problems due to brain
swelling, acute kidney failure, pancreatitis, and anemia. DKA will
lead to death in many cases, but aggressive diagnostics and
treatment can be life saving.
DKA often develops in dogs with diabetes that had previously been
unrecognized or untreated. Thus, it is essential to identify
diabetes mellitus or the development of additional symptoms in a dog
that is known to be diabetic to prevent DKA from occurring.
Clinical Signs: Clinical signs include polyuria, polydipsia,
polyphagia, weight loss, lethargy, anorexia, and vomiting.
Complications may include anemia, electrolyte abnormalities,
neurological disorders, and acute renal failure.
Symptoms: Symptoms include increased thirst, appetite, and
frequency of urination; weight loss; tiredness; vomiting; loss of
appetite; and symptoms related to any of a large number of disorders
that can accompany or trigger DKA.
Description: Diabetic ketoacidosis is probably the most
serious complication that can develop in association with diabetes
mellitus. Used for energy production in most body tissues, ketones,
also called ketone bodies, normally form when fatty acids are
released from fatty tissue and are transported to the liver. The
liver then makes ketones from the fatty acids. Excessive production
of ketones can occur in uncontrolled diabetes mellitus, and as they
accumulate, ketosis, and eventually acidosis, develop. The four
major factors that contribute to ketone formation in DKA are insulin
deficiency, fasting, dehydration, and increased levels of "stress"
hormones such as epinephrine, cortisol, glucagon, and growth
hormone.
DKA occurs more commonly in animals with previously undiagnosed
diabetes mellitus, but it can also be seen in dogs with established
diabetes that are not receiving enough insulin. In these dogs, there
may be an associated inflammatory or infectious disease. Other
canines may develop conditions associated with insulin resistance
such as hypothyroidism or Cushing's disease. Dogs may be only mildly
affected by DKA, or they may be close to death at the time of
diagnosis. DKA develops at an unpredictable rate, and some diabetic
dogs may be able to live fairly normal lives for several months with
no treatment at all. However, once DKA develops, most dogs become
seriously ill within one week.
The aggressiveness of treatment depends on how sick the dog is.
While dogs with mild DKA may be successfully treated with
intravenous fluids and insulin, dogs with severe manifestations of
disease will need more significant intervention. Fluid therapy,
potassium, bicarbonate, and phosphorus supplementation can be
vitally important. Any accompanying disorders must be identified and
treated specifically where possible to enhance resolution of DKA.
Complications during DKA treatment are common, and can include the
development of hypoglycemia, neurological signs due to brain cell
swelling, and severe electrolyte abnormalities. Anemia due to red
blood cell breakdown can occur if the serum phosphorus concentration
drops too low. Acute kidney failure also is possible.
DKA is one of the most serious metabolic disorders seen in both
human and veterinary medicine. Many patients will die from it.
However, the majority of patients can pull through a crisis
successfully with aggressive diagnostics and treatment.
Diagnosis: The diagnosis of DKA is based on the clinical
signs and the presence of elevated serum glucose concentrations and
ketones in the urine, and reduced serum bicarbonate concentrations
within the blood stream. Mild DKA is present when dogs with high
serum glucose concentrations and ketones in the urine appear
healthy, or have only mild clinical signs, or have mild decreases in
serum bicarbonate concentration. These dogs do not require extremely
aggressive treatment, and should be distinguished from dogs with
severe DKA. Dogs with severe DKA have high serum glucose
concentrations, ketones in the urine, extreme reductions in serum
bicarbonate concentration, and often show severe signs of illness.
In addition to the serum glucose concentrations and urinalysis
results, other key diagnostic procedures include measurement of
venous total carbon dioxide, blood gas evaluation, and analysis of
electrolytes and serum kidney values. In addition to a routine
urinalysis, a urine culture should be performed on any dog with DKA,
as urinary tract infections are very common complicating factors for
this condition. A complete blood count, serum liver and pancreatic
enzyme measurements, and cholesterol and triglyceride levels should
also be obtained. X-rays of the chest and abdomen, and ideally an
abdominal ultrasound, should also be used to investigate underlying
or associated factors, as well as other abnormalities that might
require specific treatment.
Prognosis: The prognosis for DKA is guarded. As many as five
to 10 percent of humans with DKA die from this condition. Death
rates for dogs may be as high as 30 to 40 percent in some
environments.
Transmission or Cause: DKA usually occurs in either dogs with diabetes
that has been present but unrecognized and untreated for a long
time, or in previously diagnosed diabetic dogs that have become ill
with another problem or that are taking inadequate amounts of
insulin.
Treatment:
Relatively healthy dogs with DKA can be treated
with potent but regular short-acting crystalline insulin injections
to help get the serum glucose levels back under control. It may take
a few days for serum glucose and urine ketone levels to fall, but
aggressive treatment may not be needed as long as the dog's
condition is basically stable.
Treatment of sick diabetic dogs needs to be more aggressive.
Paramount to the treatment of DKA is the gradual replacement of
fluid deficits, as well as the maintenance of normal fluid balance.
Many dogs will seem substantially better after being treated by
intravenous fluids alone. Phosphate supplementation may also be
needed, since serum phosphorus concentrations can drop to
dangerously low levels during the treatment of DKA leading to
serious complications such as a red blood cell breakdown that
results in anemia. Bicarbonate is given to help correct acid-base
disturbances. Insulin also is vital in the treatment of DKA. In some
situations, fluids need to be replaced quickly, while the glucose
levels will need gradual adjustment.
Until safer serum glucose concentrations are obtained, most dogs
with DKA are treated first with regular crystalline insulin, the
most potent and shortest acting form of insulin, which may be given
intravenously or on an hourly basis in the muscle. If the dog is not
eating on its own, dextrose may be added to the fluids to keep the
serum glucose level from dropping too low after insulin is started.
Concurrent illnesses must be identified and
treated specifically where possible. Pancreatitis is extremely
common in DKA, but there is no specific treatment for this disorder.
Bacterial infections need to be identified and treated in a timely
manner. Antibiotics usually are given even if a bacterial infection
has not been confirmed, due to the problems that infections cause in
DKA. Acute kidney failure may also accompany DKA, and needs to be
treated aggressively with fluids. Drugs may be needed to stimulate
urine production if it appears inadequate.
Complications during treatment of DKA that occur most frequently
include the development of hypoglycemia, central nervous system
signs, electrolyte abnormalities, and anemia. The best way to
prevent these side effects is to aim for gradual correction of the
multiple abnormalities associated with DKA. Excessively rapid
correction of glucose concentrations and electrolyte abnormalities
often leads to brain cell swelling and neurological signs.
Electrolyte concentrations need to be monitored very carefully
during the treatment of DKA, as frequent adjustments of fluid type
and rate, and the amount of potassium supplementation, are often
needed. Also, close attention must be paid to the serum phosphorus
concentration, as supplementation with phosphorus is often needed to
prevent the development of severely low serum phosphorus
concentrations and the anemia that can result from this.
Once the dog is stabilized and eating and drinking on its own,
longer-acting insulin types can be initiated. In addition, the
supportive measures, such as fluid therapy and medications, can be
tapered, as long as no other complicating issues surface and
improvement continues. Eventually, the animal should be able to go
home with an insulin regime designed for at home use, as well as any
other treatments necessary to address additional disorders that
might be present.
Prevention: There is no specific method for preventing DKA,
but careful treatment and monitoring of diabetic dogs is essential.
Recognition of the common signs of diabetes mellitus in a
dog--increased thirst and urination, increased appetite, and weight
loss--also is important so the diagnosis of uncomplicated diabetes
mellitus can be made, and appropriate treatment can be started
before DKA develops. The feeding of high fat foods, which can
trigger pancreatitis and then lead to DKA, should be avoided. In
diabetic dogs, steroids such as prednisone should be used very
carefully, if at all, because of the risk of insulin resistance and
the frequent association of steroid administration with the
development of DKA.
