Special challenges of the diabetic ketoacidotic cat (Proceedings)

I. Pathophysiology

      A. Ketone bodies: acetoacetate, beta hydroxybutyrate, acetone

      B. Oxidation of free fatty acids

      C. Mobilization of fatty acids from adipose tissue

      D. Shift from fat synthesis to fat oxidation in the liver

      E. Relative/absolute deficiency in insulin

      F. Mitigating factor

           a. elevation in glucose counter-regulatory hormones, especially glucagon

           b. glucagon:insulin ratio

           c. metabolic acidosis

           d. elevations in plasma free fatty acids and amino acid concentrations

      G. Hyperketonuria enhances osmotic diuresis and electrolyte loss into the urine

      H. Severe volume depletion

      I. Severe acidosis

      J. Pre-renal azotemia

II. Clinical presentation

      A. Previously diagnosed diabetes mellitus

      B. Previous clinical signs of diabetes mellitus

      C. Anorexia

      D. Vomiting

      E. Weight loss

      F. Tachypneic

      G. Tachycardic

      H. Lethargy

      I. Depression/obtundation

      J. Poor perfusion, weak pulses, pale mm

      K. Hypotension

III. Initial Diagnostic Assessment

      A. PCV/TS/AZO/DEX

      B. Na, K, UA (dipstick and S.G.), serum ketones

      C. Osmolality, blood gas

      D. CBC, Chemistry, Urinalysis, Urine culture

IV. Diagnosis

      A. Hyperglycemia

      B. Glucosuria

      C. Ketonemia

      D. Ketonuria

Potassium Replacement

V. Clinical Pathologic Abnormalities

      A. Elevated WBC left shift if pancreatitis or underlying infection

      B. Elevated liver enzymes

      C. Icterus in some cats

      D. Azotemia, pre renal

      E. Sodium concentration normal/low

      F. Potassium concentration normal/low

      G. Acidosis

      H. Bacteriuria, pyuria

VI. Treatment (in order of importance)

      A. Fluid Therapy

           1. Correct hypovolemia and poor perfusion

           2. Combat lactic acidosis

           3. Correct electrolyte abnormalities

           4. Preserve cardiac output and renal perfusion

           5. Dilute hyperglycemia

           6. 0.9% NaCl ± potassium

      B. Insulin Therapy

           1. regular crystalline insulin

           2. 2.2 U/Kg/24 hr (dog); 1.1 U/kg/24 hr (cat) IV in separate IV bag

           3. Intermittent IM insulin technique with regular insulin

                a. 0.2 U/kg IM initially

                b. 0.1 U/kg IM hourly until blood glucose < 250 mg/dl

                c. Regular insulin SQ 0.5-1 U/kg q 4-6 hours after patient hydration achieved

CRI Insulin Therapy using Regular, Crystalline Insulin

      C. Bicarbonate Therapy

           1. Only give initially if pH < 7.0

           2. Otherwise wait to see if reperfusion will correct acidosis

           3. 0.1 x base deficit x BW(kg); add slowly over 2 hours – only 1/3 replacement amount to prevent overcorrection

      D. Phosphorous Therapy

           1. patients will often get hypophosphatemic within 1-3 days after initiation of therapy

           2. can cause myopathies, hemolysis, encephalopathy

           3. 0.01-0.03 mmol phosphate/kg/h over 6 hours and recheck

      E. Magnesium Therapy

           1. Often worsens with initial treatment

           2. Difficult to correct other electrolyte abnormalities until

                hypomagnesemia is addressed

           3. 0.75-1.0 mEq/kg/day IV in 5% dextrose for 24-48 hours

VII. Initiation of Longer Acting Insulin

      A. Dehydration corrected

      B. Animal eating/drinking normally

      C. Electrolyte abnomralities corrected