What are the critical care guidelines for diabetic ketoacidosis (DKA)?

What are the critical care guidelines for diabetic ketoacidosis (DKA)?

Diabetic Ketoacidosis (DKA) Critical Care Guidelines continued Transition to SQ Insulin Guidelines for Transition 1) PH > 7.3 2) Serum Bicarbonate ≥ 17 3) Child demonstrates the desire and ability to eat a. Patient is alert and demonstrates interest in eating b. Time is appropriate for meal or snack c. Demonstrates positive bowel sounds Orders

What are diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar state (HHS)?

Diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar state (HHS) are acute metabolic complications of diabetes mellitus that can occur in patients with both type 1 and 2 diabetes mellitus.

What is the resolution of DKA and HHS?

The resolution of DKA is reached when the blood glucose is < 200 mg/dl, serum bicarbonate is ≥15 mEq/L, pH is >7.30 and anion gap is ≤12 mEq/L (17). HHS is resolved when serum osmolality is < 320 mOsm/kg with a gradual recovery to mental alertness. The latter may take twice as long as to achieve blood glucose control.

What is the pathophysiology of DKA?

DKA is a state of a relative or absolute insulin deficiency that is worsened by hyperglycemia, dehydration, and acidosis. In most cases, the trigger is an infection, new-onset diabetes, or lack of compliance with treatment.

What is the typical bicarbonate level of a sick DKA patient?

Sick DKA patients typically have extremely low bicarbonate levels, for which they are compensating with a respiratory alkalosis (for example, consider a patient with bicarbonate of 2 mEq/L, PaCO215 mm, and pH 6.75).

What drives insulin titration in DKA?

Insulin titration in DKA may be driven by either ketoacidosis or glucose (above). For example, the American guidelines recommend titrating the insulin based on the glucose level ( Kitabchi 2009 ).

Should normal saline be used in DKA resuscitation?

Pearl #1: Avoid normal saline A common phenomenon observed when starting a DKA resuscitation with normal saline (NS) is worsening of the patient’s acidosis with decreasing bicarbonate levels (example below). This occurs despite an improvement in the anion gap, and is explained by a hyperchloremic metabolic acidosis caused by bolusing with NS.

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