Diabetic Ketoacidosis (DKA)

Most Common cause of DKA

Total body potassium is depleted due to increased GI losses and osmotic diuresis, but

paradoxical hyperkalemia due to

  1. extracellular shift of potassium in exchange to H+ ion, with resultant intracellular potassium deficit
  2. Impaired insulin-dependent cell entry of the potassium ion

Winter's formula is used to assess expected pCO2 during resp: compensation for a primary metabolic acidosis

PaCO2 = 1.5 (HCO3-) + 8

The best markers indicating resolution of ketonemia are the serum anion gap and direct assay of beta-hydroxybutyrate (BH), which is the predominant ketone in DKA.

That's why anion gap is used to guide conversion from IV insulin to SC insulin

Despite normal or elevated serum potassium levels, patients with HHS or DKA have a total body potassium deficit due to excessive urinary loss caused by glucosuria-induced osmotic diuresis. Aggressive insulin therapy for HHS can lower serum potassium levels further and cause severe hypokalemia.

N.B.

If the baseline/first potassium is already low in HHS, the initial fluid of choice should be 0.45%N/S with added Potassium, instead of 0.9% NS

Potassium repletion affects the saline solution that is given, because potassium is as osmotically active as sodium.

If 40 mg of potassium is added to each liter, one-half isotonic saline should be used if the patient is hemodynamically stable, because this solution contains 117 mEq of cation (77 mEq of sodium and 40 mEq of potassium) and is therefore equivalent to approximately three quaters isotonic saline. In contrast, the addition of potassium to isotonic saline results in the generation of a hypertonic fluid that does not correct the hyperosmolality.