Diabetic Ketoacidosis

Question 1

What is diabetic ketoacidosis?

Answer 1

Rare, yet potentially fatal hyperglycemic crisis which can occur in patients with both Type 1 and Type II DM (especially those of African or Hispanic descent)

• Serum glucose concentration generally above 250mg/dL
• A state of excessive intracellular dehydration resulting from excessive hyperglycemia
• Hyperglycemia increases serum osmolality, causing shift of intracellular water into intravascular space.

Metabolic acidosis the major finding

DKA characterized by hyperketonemia and acidotic pH

Question 2

What are the triad findings associated with DKA?

Answer 2

• Triad of findings: hyperglycemia, high anion gap metabolic acidosis and hyperketonemia is due to the relative or absolute lack of insulin
• Presents within hours of onset

Question 3

What can cause DKA in a patient?

Answer 3

• Omission or lack of insulin, inadequate dosing
• Infection
• Medications affecting carbohydrate metabolism, such as:
  
  • Corticosteroids
  • Thiazides
  • Sympathomimetic agents (dobutamine, terbutaline, atypical antipsychotics)
  • Sodium-Glucose Co-transporter 2 inhibitors- increases risk of DKA
• Increased incidence in diabetics who have insulin pumps
• Substance abuse- cocaine, alcohol, marijuana
• Pancreatitis
• Surgery or trauma in a patient with co-existing DM

Question 4

What is the leading cause of death from DKA?

Answer 4

Cerebral edema

Question 5

What are the diagnostic criteria for DKA?

Answer 5

1. Blood glucose > 250mg/dL
2. Arterial pH of < or equal 7.30
3. Bicarbonate level (HCO3) < or equal to 18mEq/L
4. Ketones present in serum and urine - further lowering pH
5. Hyperkalemia – related to shifting of hydrogen ions intracellularly in an attempt to buffer acidosis; hydrogen ions are exchanged for potassium ions; must replace potassium stores even if serum potassium appears normal.

Question 6

In DKA why do you replace potassium if serum potassium appears normal?

Answer 6

• Patients with DKA undergo osmotic diuresis from the hyperglycemia and lose potassium in their urine. In DKA, insulin deficiency (decreased potassium uptake by cells) and hyperosmolarity (causing intracellular fluid contraction and outward potassium gradient) leads to the increased serum potassium concentration. This elevates the serum potassium level even though total body potassium becomes depleted through urinary losses. Administration of exogenous insulin causes a corresponding rapid intracellular shift of potassium and can lead to hypokalemia.
• Therefore potassium chloride should be administered alongside insulin in the treatment of DKA.
• Patient’s in DKA should receive IV fluids until the serum anion gap has normalized (less than 12 mEq/L)

Question 7

How do you calculate the anion gap in DKA?

Answer 7

Anion gap: AG = NA – (HCO3 + Cl)

• Normal anion gap (AG) = 7-17mEq/L
• The higher the AG, the higher the patient’s acuity. Increasing fluids will help reduce AG.

Question 8

How do you manage a patient with DKA?

Answer 8

1. Place them on tele

2. IV fluid replacement initially with 0.9NS at 1,000mL/hr x 1-2 hours, then 300-500 mL/hour x 4 hours to correct fluid deficit of 4-8 L

• Once dehydration improves, 250mL/hour recommended.
• Usually 4-8L of fluid is administered within initial 24 hour period of treatment.

3. Potassium: Check levels every hour and replace: Initiate IMMEDIATELY if serum potassium is < 5.3 mEq/L. Levels should be monitored closely during fluid resuscitation

• If initial serum K is < 3.3 mEq/L, give 20-40 mEq/hour as IV additive in replacement IVF
• If initial serum K is between 3.3 and 5.3 mEq/L, given 20-30 mEq/hour as IV additive in replacement IVF
• If initial serum K is > 5.3 mEq/L, delay replacement until serum level has fallen below this level.

4. Isotonic IV fluids utilized until patient is hemodynamically stable, then change to hypotonic solution (0.45NS) to promote intracellular hydration.

5. Once the patient’s glucose falls to 250mg/dL, IVF’s are changed to D5 0.45NS to prevent hypoglycemia and cerebral edema due to lowering glucose too rapidly.

6. Insulin:

• The only indication for delaying the initiation of insulin therapy is if the serum potassium is < 3.3 mEq/L, since insulin will worsen the hypokalemia by driving potassium into the cells. Patients with an initial serum potassium below 3.3 mEq/L should receive aggressive fluid and potassium replacement prior to treatment with insulin. Insulin therapy should be delayed until the serum potassium is > 3.3 mEq/L to avoid complications such as cardiac arrhythmias, cardiac arrest and respiratory muscle weakness.

Administer loading dose of regular insulin 0.1-0.15 units/kg IV, followed by continuous infusion (1:1 admixture) at 0.1 units/kg/hr

• Plasma levels should fall by 10% during first hour. If not, then repeat loading dose of insulin.
• Once serum glucose reaches 200mg/dL, insulin infusion should be decreased to 0.05units/kg/hour.
• The rate of insulin administration and the rate of infusion of D5W with 0.45NS are adjusted to maintain the glucose value at approx. 200mg/dL until the ketosis is resolved.
• Convert to subcutaneous insulin therapy when:
  
  • Serum anion gap < 12 mEq/L
  • Serum bicarbonate > or equal to 15mEq/L
  • Venous pH > 7.30

7. Sodium Bicarbonate rarely required, but if warranted, administer 50-100 mEq per liter of hypotonic saline if pH level is 7.0mol/L or lower OR if HCO3 levels are less than 9mEq/L

8. Monitor for other electrolyte abnormalities after treatment is completed – especially magnesium - as diuresis and acidosis can deplete magnesium & phosphorus. Monitor electrolytes at least every 2 hours during treatment

• Magnesium: Hypo K = Hypo Mg
  
  • Both electrolytes lost during osmotic diuresis
  • Cannot replace intracellular potassium without magnesium
  • Serum magnesium level may not correlate with total body stores
  • Dose: 1-2 gms MgSO4 IV
• Phosphorous:
  
  • If PO4 < 10 mEq, consider replacement with KPO4

9. If signs of cerebral edema exist, check blood glucose and obtain CT head; initiate treatment.

Question 9

When is ketoacidosis in DKA considered to be resolved?

Answer 9

The hyperglycemic crisis is considered to be resolved when the following goals are reached:

• The ketoacidosis has resolved, as evidenced by normalization of the serum anion gap (< 12mEq/L) and serum beta-hydroxybutyrate levels (measures ketoacid anions)
• The patient is able to eat