02.04 Diabetic Ketoacidosis (DKA)

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DKA Treatment (Mnemonic)
DKA Pathochart (Cheat Sheet)
DKA vs HHNS (Cheat Sheet)
Symptoms of Diabetes Mellitus (Image)
Treatment for DKA and HHNS (Image)
140 Must Know Meds (Book)

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This lesson is going to talk about Diabetic Ketoacidosis or DKA.

Diabetic Ketoacidosis is a state of severe hyperglycemia WITH ketoacidosis. This is essentially an acute exacerbation of Type I Diabetes Mellitus. Remember in Type 1 Diabetes, the body has NO insulin. Normally, insulin allows glucose to enter the cell and that creates energy or ATP. The insulin is the key that unlocks the cells for glucose to come in. Without the key, the cells have to find another way to get energy. It’s like a burglar - the door is locked, there’s no key - so what does he do? He breaks a window. So that process is called gluconeogenesis and it involves breaking down fatty acids for energy. A byproduct of that process is Ketones, which are acids. So we end up with this buildup of acids in the system - leading to a metabolic acidosis. Specifically, it’s what’s known as an anion gap acidosis. It is usually a sudden onset and can be caused by stress or infection. Or it could be a medication issue - if they aren’t taking their insulin, or if their insulin pump malfunctions, that can lead to DKA.

So what will we see? Well we’re going to see two MAIN sets of problems. First, we see hyperglycemia - elevated blood glucose levels around 400-600, maybe a little higher. That causes hyperosmolarity, where the fluids are shifting out of the cells into the bloodstream to try to balance this concentration. That leads to severe cellular dehydration. When blood glucose is that high, the kidneys can’t hold onto all of it, so they’ll begin dumping the sugar into the urine. Not only is there more water in the vessels, but the water now follows glucose out into the urine, so we see polyuria. The dehydration causes their BUN and Creatinine to elevate, and we could also see altered LOC because of that cellular dehydration in the brain.

The second set of problems is due to the Ketoacidosis. Their pH will drop below 7.35 and their Bicarb could be less than 22. We’ll see ketones in their urine - either on a UA or a dipstick. They’ll also have fruity breath because of those ketones - that’s one of your classic signs of DKA in addition to the lab values. We also see Kussmaul Respirations. This is when patients are breathing very fast and very deep. Why? Well their body is acidotic and they’re trying desperately to compensate. So they’re trying to blow off as much CO2 as they can. Remember CO2 is acidic, so if they can get rid of some, it might correct the pH. Problem is, patients can only breathe this way for so long before they get fatigued and worn out. And finally we see hyperkalemia. This is a result of the acidosis and it’s another one of the body’s attempts to balance out electrical charges. Hydrogen ions (those are your acids) and potassium ions both have the same charge, so the body tries removing the hydrogen from the bloodstream and replacing it with potassium - except we know how dangerous hyperkalemia can be for our patients, right?

So what are our priorities for management of DKA? Well, of course we want to identify and treat the cause, especially if it’s an infectious source. But our #1 priority is going to be to correct the acidosis. The only way to really do this is to give IV Insulin therapy with Regular insulin. Not only will this bring the sugars down, but it will also let the body know it’s okay to stop using the fatty acids and stop making ketones. So, sometimes, we keep giving insulin even after their sugars come down to keep working on getting the acidosis reversed. We’ll just give them sugar to balance the process. Our secondary priority is going to be to replace the lost IV fluids. Remember they have polyuria and cellular dehydration, so we still need to address the fluid situation. We want to monitor their LOC and respiratory status during the treatment - remember they can get very tired with that heavy breathing or have some neuro changes, so we want to make sure we keep them safe. And we monitor electrolytes, specifically potassium, as well as our ABGs, glucose, and anion gap levels to know where we’re at and how they’re responding to treatment.

Our top nursing concepts for a patient with DKA are acid-base balance, glucose metabolism, and fluid & electrolytes. Check out the care plan attached to this lesson to see more detailed nursing interventions and rationales.

Let’s recap for DKA - It’s an acute exacerbation of Type 1 Diabetes where the body is breaking down fatty acids for energy instead of glucose - this causes ketones to buildup in the bloodstream, leading to a severe metabolic acidosis. Remember that’s a pH off less than 7.35 and a bicarb less than 22. This causes an altered LOC, deep, fast Kussmaul respirations, and hyperkalemia. The severe hyperglycemia causes a hyperosmolar state which pulls fluid out of the cells and into the bloodstream - causing severe cellular dehydration and osmotic diuresis. Our number one goal is to correct the acidosis through insulin therapy. That helps reverse the gluconeogenesis process so the body stops making ketoacids. Then, we’ll make sure we give IV fluids and monitor potassium levels. Insulin actually drives potassium INTO the cells, so with intensive insulin therapy, we can actually see their potassium levels drop significantly. So sometimes we’ll just add 20 mEq of KCl into their IV fluids to keep those levels up.

So those are the things you need to know for DKA - you’ll see in the HHNS lesson that they’re very similar, but the priorities are different, so check out that lesson as well. Don’t miss all the resources attached to this lesson, including a cheatsheet on the differences between DKA and HHNS. Now, go out and be your best selves today. And, as always, happy nursing!
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