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!