Name
Diabetic
Ketoacidosis, Canine
Short Description
Diabetic ketoacidosis
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 include polyuria, polydipsia,
polyphagia, weight loss, lethargy, anorexia, and vomiting.
Complications may include anemia, electrolyte abnormalities,
neurological disorders, and acute renal failure.
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.
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.
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.
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.
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.
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.
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.
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