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Why Is Potassium Given In Dka?

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Management Of Diabetic Ketoacidosis In Adults

Management of diabetic ketoacidosis in adults Management of diabetic ketoacidosis in adults Insulin (blue dots) promotes glucose uptake in the liver and muscles, controlling blood sugar. Despite these losses, the increased delivery of potassium to the ECF from the intracellular space usually causes the serum concentration of potassium to be normal and, in some cases, high. This regular concentration of the ECF potassium creates the illusion of normalcy, despite the fact that total body potassium stores are almost always low. This concept becomes important in understanding the risk of potentially devastating hypokalemia in treating DKA. Insulin administration causes a rapid shift of potassium out of the ECF and into the cells. In addition, fluid resuscitation can be expected to cause a dilutional decrease in serum potassium concentration. For this reason, the ADA recommendations encompass a three-tiered approach to potassium regulation during fluid and insulin therapy for DKA: Patients with a serum potassium concentration >5.2 mEq/L should receive insulin and IV fluid without potassium, but the level should be checked every two hours.3 Patients with a serum potassium concentration Continue reading >>

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Popular Questions

  1. metalmd06

    Does acute DKA cause hyperkalemia, or is the potassium normal or low due to osmotic diuresis? I get the acute affect of metabolic acidosis on potassium (K+ shifts from intracellular to extracellular compartments). According to MedEssentials, the initial response (<24 hours) is increased serum potassium. The chronic effect occuring within 24 hours is a compensatory increase in Aldosterone that normalizes or ultimatley decreases the serum K+. Then it says on another page that because of osmotic diuresis, there is K+ wasting with DKA. On top of that, I had a question about a diabetic patient in DKA with signs of hyperkalemia. Needless to say, I'm a bit confused. Any help is appreciated.

  2. FutureDoc4

    I remember this being a tricky point:
    1) DKA leads to a decreased TOTAL body K+ (due to diuresis) (increase urine flow, increase K+ loss)
    2) Like you said, during DKA, acidosis causes an exchange of H+/K+ leading to hyperkalemia.
    So, TOTAL body K+ is low, but the patient presents with hyperkalemia. Why is this important? Give, insulin, pushes the K+ back into the cells and can quickly precipitate hypokalemia and (which we all know is bad). Hope that is helpful.

  3. Cooolguy

    DKA-->Anion gap M. Acidosis-->K+ shift to extracellular component--> hyperkalemia-->symptoms and signs
    DKA--> increased osmoles-->Osmotic diuresis-->loss of K+ in urine-->decreased total body K+ (because more has been seeped from the cells)
    --dont confuse total body K+ with EC K+
    Note: osmotic diuresis also causes polyuria, ketonuria, glycosuria, and loss of Na+ in urine--> Hyponatremia
    DKA tx: Insulin (helps put K+ back into cells), and K+ (to replenish the low total potassium
    Hope it helps

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