Hey Glucose, what are you doing there

You're on the right track as to why patients in DKA are started on a GIK infusion. This is not a comprehensive guide to DKA management, and I'm going to be a bit simplistic to make things easier to understand. Managing DKA is not often an easy undertaking.

Often when a patient that's in DKA seeks help, they're pretty well into the problem. These patients are often dehydrated. There often are electrolyte shifts so the labs may show the patient is hyperkalemic. What the body "sees" is the hyperglycemia and it tries to limit the glucose level by dumping it overboard through the kidneys. The end result is the patient urinates a LOT and frequently. Potassium unfortunately also goes out too. The dehydration concentrates what's left and the body shifts potassium out of the cells. There's often a total body depletion of potassium.

What we do for our DKA patients is rehydrate them. We use insulin to get the body's cells to take up the glucose. These two things result in a lower glucose and extracellular potassium level. We start replacing the potassium early and may start a glucose infusion early or we may wait until the glucose level reaches a certain level before we switch to a glucose infusion to prevent hypoglycemia. This is because the insulin infusion is likely a bit high compared to what the body normally needs and if glucose isn't added, hypoglycemia (and possibly death if too low) can result. Where I'm at, we only titrate the insulin infusion based on frequent serial finger stick blood glucose checks. The other stuff isn't titrated and we usually change to a D10 NS or 1/2 NS infusion once the blood glucose level reaches between 250 and 300. Now, why might we slowly correct the glucose level? If we rapidly corrected the blood glucose level while rehydrating the patient, we can cause damage to neurons as they can swell.

The majority of the correction might only take a few hours, but sometimes getting the patient back to normal can take a few days.

Just to expand or slightly explain why I say that we "start potassium early" is that as the potassium is shifted back into the cells, the extracellular potassium level (which is what we can measure, because we can't measure intracellular potassium) drops and can swing very quickly from a level that would normally look like a hyperkalemia (5.5 or greater) to a hypokalemia (3.4 or lower) and we haven't changed the actual amount of potassium in the body. We often start replacing potassium early because then we might be able to keep the body from truly becoming hypokalemic, with all the problems that come with it.

Incidentally, the potassium shift from extracellular to intracellular that happens when insulin and glucose are both present is also what we do to "normal" people when they're in a hyperkalemic state. Glucose and insulin work together as a "key" that causes cells to also uptake potassium, thus "hiding" potassium there where it's less of a problem for the body as a whole.