Diabetic ketoacidosis is a life-threatening condition caused by insulin deficiency and resistance, leading to excessive production of ketoacids by the liver and metabolic acidosis. It commonly affects older dogs and cats and has an acute onset of lethargy, vomiting, and dehydration. Treatment involves aggressive fluid therapy, insulin administration, and electrolyte replacement to slowly correct blood glucose and acidosis over 24-48 hours, monitoring for complications like hypoglycemia. Long-term management focuses on insulin therapy, diet, exercise and monitoring to control blood glucose levels.

1. Diabetic Ketoacidosis
Dr. Aimee Jalkanen

2. What is Diabetic Ketoacidosis (DKA)?
 Life-threatening metabolic condition
 Result of insulin deficiency and resistance
 Excessive production of ketoacids by the liver
 Leads to metabolic acidosis, hyperosmolality,
electrolyte imbalances, systemic illness
http://petdiabetes.wikia.com/wiki/Ketoacidosis

3. Etiology and Pathophysiology
 Shift in hepatic metabolism
from fat synthesis to fat
oxidation and ketogenesis
produces ketone bodies
(acetoacetic acid, β-
hydroxybutyric acid,
acetone)
 Insulin deficiency and
resistance leads to
increased production of
ketones
 Lipolysis increases, thus
more FFAs are available for
the liver to produce ketones
http://petdiabetes.wikia.com/wiki/Ketoacidosis

4. Etiology and Pathophysiology
 Accumulation of ketones overwhelms the body’s
buffering system leading to metabolic acidosis
 Renal tubules are unable to have complete
resorption leading to ketonuria
 Osmotic diuresis ensues leading to increased loss of
Na+, K+ in urine
 Loss of electrolytes and fluid through urine and
vomiting leads to azotemia, cellular dehydration

5. Common Signalment
 Older dogs (7-9) and cats
(9-11)
 Female dogs 2x > males
 Male cats > females
 Multiple dog breeds
commonly affected include:
Schnauzer, Poodle, Bichon
Frise, Keeshond
 Cats: no breed disposition
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6. Pertinent History
 May or may not be a previously diagnosed
diabetic
 Have shown signs of diabetes including
PU/PD, weight loss despite increased
appetite
 Recent history includes vomiting, weakness,
anorexia

7. Physical Exam Findings
 Dehydration-often moderate to
severe
 Weakness
 Respiratory pattern changes:
tachypnea or Kussmaul’s
respiration (slow, deep
breathing)
 Abdominal pain (associated
with pancreatitis)
 Strong acetone odor to breath
(sweet smell)
 Cataracts (more common in
dogs)
 Diabetic neuropathy (dropped
hocks, more common in cats)

8. Diagnostics
 Complete blood count
 Biochemical profile
 Electrolyte panel
 Urinalysis and culture
 Radiographs, ultrasound, and further
diagnostics may be needed

9. Results
 CBC
– Variable, may show high white blood cells
 Profile
– High blood glucose, low sodium, low potassium
– High cholesterol
– Liver enzyme elevation
– Azotemia
 Urinalysis
– Positive ketones
– Glucosuria
– Pyuria and bacteria common if concurrent UTI
 cPL positive if concurrent pancreatitis

10. Treatment-Fluid Therapy
 Crystalloid, type based on electrolytes
 Supplement with potassium
– Usually 30-40 mEq/L
 Supplement phosphorus if <1.5mg/dL
– Necessary to avoid hemolytic anemia
 Add 2.5-5% dextrose to fluids once BG
approaches 250 mg/dL

11. Treatment-Insulin
 Begin after starting fluid therapy
 Intermittent IM technique:
– 0.2 U/kg IM initially
– Then, 0.1 U/kg IM hourly
 Insulin CRI
– 0.05 U/kg/h (cat) 0.1 U/kg/h
(dog) in 0.9% NaCl
 Adjustments made based on
BG
– Switch to every 0.1 U/kg 6 to 8
h SQ once BG ~ 250 mg/dL
 Goal is to slowly decrease BG
until between 100-300 mg/dL

12. Treatment-Other
 Bicarbonate supplementation
– Use with caution
– Supplement if bicarb is < 12mEq/L
– HCO3
-
= body weight (kg) x 0.4 x (12 - patient’s HCO3
-
) x 0.5
– Add to fluids and given over 6 h
 Anti-emetics if needed to control vomiting
 Nutrition: Very important to encourage patient’s to
eat to avoid hypoglycemia
 Antibiotics: Many patients have concurrent UTIs

13. Monitoring
 Frequent blood glucoses
– Initially every 1 to 2 hours
– May begin to decrease when BGs stabilize
 Hydration status
– Monitor inputs (fluids) and outputs (urine, vomit, diarrhea)
– Make adjustments as needed
 Electrolyte concentrations
– Adjust fluids and additives as necessary
 Patient’s weight, temperature, blood pressure

14. Potential complications
 Goal is to correct blood glucose, acidosis,
and electrolyte abnormalities SLOWLY (24-
48 hours)
 Hypokalemia, hypoglycemia, hypernatremia,
hemolytic anemia commonly occur
 Neurologic signs related to cerebral edema

15. Long-term Care and Follow-up
 Treat concurrent diseases
– Urinary tract infections
– Diarrhea
– Pancreatitis
– Cushing’s disease
 Establish good control over
blood glucose levels
– Regular check-ups
– Blood glucose curves to help
establish insulin dose
free-glucose-meter.com

16. Long-term Care and Follow-up
 Dietary changes
– Controlled weight loss
– High fiber, low calorie, low-fat
diets
– Hill’s w/d, r/d, or m/d, Purina’s
OM or DM, other senior or
weight loss diets
– Avoid giving treats or snacks
high in fat and sugar
 Encourage regular exercise
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17. At home care and monitoring
 Owners of diabetics need to be aware of
DKA and its life-threatening nature
 Have owners contact a veterinarian if:
– Patient is vomiting or having diarrhea
– Stops eating
– Becomes lethargic
– Urine and/or breath smells “funny”

18. DKA on ER
 May be a stat triage-many of these patients
are very ill
 Brief history from owner-if known diabetic,
ask about insulin, when and how much last
given and has patient been eating
 Ask permission for IV catheter, diagnostics
(about $150 to $200 to start)

19. Once in treatment room
 Obtain blood for CBC/profile
and a urine sample
 Run an I-stat 8
– Glucose, pH, electrolytes
 Check urine dipstick
– Look for ketonuria (if
negative, does NOT rule
out DKA)
 Place IV catheter
 Prepare fluids
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20. Sources
 Côté, Etienne (ed): Clinical Veterinary
Advisor. St. Louis, Mosby, Inc. 2007.
 Hill’s Key to Clinical Nutrition 2007-2008.

21. Thanks for your attention!