Diabetic Ketoacidosis (DKA) is associated with a wide variety of metabolic abnormalities, and the most common ones are sodium and potassium irregularities. I will try to explain in brief, the sodium and potassium imbalances in DKA and their causes.
Due to excess glucose in the blood, which acts as an osmotically active substance at such high concentration, fluids will be absorbed into the vascular space from the interstitial and intracellular space. The increase in the volume of intravascular compartment leads to dilutional hyponatremia. Also, urine output will be high in a DKA case due to the osmotic diuresis resulting from high glucose levels. Some amount of sodium is also lost due to this high urine output. When the DKA settles with insulin infusion, sodium level normalizes. If sensorium worsens during treatment, suspect cerebral edema which might have occurred as a result of overzealous fluid therapy. Hypertonic saline infusion might be helpful as it is an effective anti-edema measure.
Potassium levels can be high, normal or even low in DKA. As DKA causes metabolic acidosis at the cellular level, potassium ions are pushed out of the cell due to excess hydrogen ions and it results in hyperkalemia. But, due to very high urine output, a major chunk of this potassium is excreted. So, even though there is hyperkalemia, intracellular potassium is quite low in DKA. What is trickier is that, when insulin infusion is started for acidosis correction, hypokalemia can precipitate as a result of an intracellular shift of potassium by insulin and partly by correction of metabolic acidosis. Hence, the maintenance and deficit correction fluid given intravenously need to have 40mEq/L of potassium, unlike the normal maintenance fluid which has only 20mEq/L.
You will be perplexed to see the serum creatinine levels in DKA. Usually, serum creatinine in the initial renal function test will be higher than normal in DKA cases and the doctor would be in a dilemma of whether to add potassium to the intravenous fluid. But, more often than not, the elevated creatinine value is due to the positive interference of high glucose levels and ketone bodies in the laboratory estimation of serum creatinine. Both enzymatic and Jaffe’s methods of creatinine estimation may suffer from positive interference of glucose and ketone bodies. So, if the patient doesn’t have a history of chronic kidney disease or any other suggestive history of renal pathology, we can conveniently ignore a slightly higher creatinine value.
One common pitfall which happens in the monitoring of serum electrolytes is that the health care staff may do phlebotomy for serum electrolytes from the proximal end of the vein through which the intravenous fluid is flowing. Remember, that fluid has a potassium content of 40mEq/L. This will result in sky-high values of potassium and the doctor will be tempted to stop the potassium component in the maintenance fluid which will give rise to hypokalemia.
So, the take-home messages are, both sodium and potassium levels in the blood will be altered in DKA and a good understanding of the pathophysiology is necessary for the management.
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