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Pathophysiology Of Hypokalemia In Dka

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Management Of Diabetic Ketoacidosis And Other Hyperglycemic Emergencies

Understand the management of patients with diabetic ketoacidosis and other hyperglycemic emergencies. ​ The acute onset of hyperglycemia with attendant metabolic derangements is a common presentation in all forms of diabetes mellitus. The most current data from the National Diabetes Surveillance Program of the Centers for Disease Control and Prevention estimate that during 2005-2006, at least 120,000 hospital discharges for diabetic ketoacidosis (DKA) occurred in the United States,(1) with an unknown number of discharges related to hyperosmolar hyperglycemic state (HHS). The clinical presentations of DKA and HHS can overlap, but they are usually separately characterized by the presence of ketoacidosis and the degree of hyperglycemia and hyperosmolarity, though HHS will occasionally have some mild degree of ketosis. DKA is defined by a plasma glucose level >250 mg/dL, arterial pH <7.3, the presence of serum ketones, a serum bicarbonate measure <18 mEq/L, and a high anion gap metabolic acidosis. The level of normal anion gap may vary slightly by individual institutional standards. The anion gap also needs to be corrected in the presence of hypoalbuminemia, a common condition in the 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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