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The special challenge of patients with diabetic ketoacidosis (Proceedings)

October 1, 2011
Cynthia Ward, VMD, PhD, DACVIM

Ketone bodies: acetoacetate, beta hydroxybutyrate, acetone

Pathophysiology

  • Ketone bodies:  acetoacetate, beta hydroxybutyrate, acetone

  • Oxidation of free fatty acids

  • Mobilization of fatty acids from adipose tissue

  • Shift from fat synthesis to fat oxidation in the liver

  • Relative/absolute deficiency in insulin

  • Mitigating factor

  • elevation in glucose counter-regulatory hormones, especially glucagon

  • glucagon:insulin ratio

  • metabolic acidosis

  • elevations in plasma free fatty acids and amino acid concentrations

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  • Hyperketonuria enhances osmotic diuresis and electrolyte loss into the urine

  • Severe volume depletion

  • Severe acidosis

  • Pre-renal azotemia

Clinical presentation

  • Previously diagnosed diabetes mellitus

  • Previous clinical signs of diabetes mellitus

  • Anorexia

  • Vomiting

  • Weight loss

  • Tachypneic

  • Tachycardic

  • Lethargy

  • Depression/obtundation

  • Poor perfusion, weak pulses, pale mm

  • Hypotension

Initial Diagnostic Assessment

  • PCV/TS/AZO/DEX

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

  • Osmolality, blood gas

  • CBC, Chemistry, Urinalysis, Urine culture

Diagnosis

  • Hyperglycemia

  • Glucosuria

  • Ketonemia

  • Ketonuria

Clinical Pathologic Abnormalities

  • Elevated WBC +/- left shift if pancreatitis or underlying infection

  • Elevated liver enzymes

  • Icterus in some cats

  • Azotemia, pre renal

  • Sodium concentration normal/low

  • Potassium concentration normal/low

  • Acidosis

  • Bacteriuria, pyuria

 

Treatment (in order of importance)

  • Fluid Therapy

  • Correct hypovolemia and poor perfusion

  • Combat lactic acidosis

  • Correct electrolyte abnormalities

  • Preserve cardiac output and renal perfusion

  • Dilute hyperglycemia

  • 0.9% NaCl +/- potassium

  •  

  • Potassium Replacement

Serum K (mEq/L)

KCl/L (mEq)

Maximum rate (mL/kg/h)

3.6-5.0

20

24

3.1-3.5

30

16

2.6-3.0

40

11

2.1-2.5

60

8

<2.0

80

6

  • Insulin Therapy

  • Rregular crystalline insulin

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

  •  

  • CRI Insulin Therapy using Regular, Crystalline Insulin

Glucose (mg/dL)

Fluid

Insulin rate (2.2 U/kg in 250 ml) mL/hr

>250

0.9% NaCl

10

200-250

0.45% NaCl + 2.5% dextrose

7

150-200

0.45% NaCl + 2.5% dextrose

5

100-150

0.45% NaCl + 5% dextrose

5

<100

0.45% NaCl + 5% dextrose

Stop infusion

  • Intermittent IM insulin technique with regular insulin

  • 0.2 U/kg IM initially

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

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

  • Bicarbonate Therapy

  • Only give initially if pH < 7.0

  • Otherwise wait to see if reperfusion will correct acidosis

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

  • Phosphorous Therapy

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

  • can cause myopathies, hemolysis, encephalopathy

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

  • Magnesium Therapy

  • Often worsens with initial treatment

  • 2.  Difficult to correct other electrolyte abnormalities until hypomagnesemia is addressed

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

Initiation of Longer Acting Insulin

  • Dehydration corrected

  • Animal eating/drinking normally

  • Electrolyte abnomralities corrected

 

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