Here’s a quick review of the general management principles for DKA.

Fill the tank

This begins with a 10ml/kg 0.9%NS bolus. This accomplishes the following:

  • Restores circulation
  • Increases glucose uptake in the periphery
  • Increases glomerular filtration
  • Reverses the mounting acidosis

In many cases blood glucose rapidly declines following initial fluid resuscitation. Once you’ve improved perfusion, then start 0.45% saline for maintenance and replacement .

Kick ketogenesis to the curb

The insulin drip at 0.1 Units/kg/h (after initial fluid expansion of course) reverses proteolysis and lipolysis and promotes glucose uptake and utilization, thereby further normalizing blood glucose concentrations. Insulin’s haf life is super short – so boluses are not necessary. Just start the drip as soon as you’ve restored perfusion.

Sugar, ah sugar!

The prevent the glucose from dropping too precipitously add 5% glucose to the fluids when the blood glucose is approximately 300 mg/dL. In order to avoid wasting fluids you can employ the 2-bag system.

Bag 1: D10 1/2 NS +20KCl + 20 KPhos

Bag 2: 1/2NS + 20KCl & 20KCl KPhos

Here’s an example. If your rate is 130ml/hr, and you want to deliver a dextrose concentration at 5%, run both Bag 1 and Bag 2 at 65ml/hr. See, simple!

Lyte up your life

Patients with DKA have a total body potassium deficit regardless of what the serum level is. Recall that insulin is also going to drive K into the cells Pied Piper style. Therefore, your fluids must include potassium phosphate and potassium acetate or potassium chloride.

Also remember that the serum sodium concentrations is not a reliable indicator of extracellular fluid deficit. Why? Well recall that extreme hyperglycemia generates potent osmotic effects because of the osmotic effects and causes dilutional hyponatremia (pseudohyponatremia). You would do well to commit the corrected sodium equation to memory:

Add 1.6 mEq (1.6 mmol) to the measured Na value for every 100 mg/dL (5.6 mmol/L) blood glucose above normal

I’m also much more worried about the hypernatremic patient in DKA than the hyponatremic one. This generally indicates that they are much more dry than you think.

Watch the brain

Cerebral edema is the most dangerous complication of DKA and can lead to seizures, coma and death – which are all bad. Things that can increase the risk of CE include:

  • Bicarb administration  – so don’t give it – no matter how low the pH is!
  • Younger age (especially <5 years)
  • Severity of acidosis (especially <7)
  • Degree of hypocapnia
  • Elevated BUN
  • There is also the suggestion that the risk is increased when serum sodium fails to increase appropriately during treatment