Nursing Care and Pathophysiology of Diabetic Ketoacidosis (DKA)
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Outline
Overview
- Severe Hyperglycemia with Ketoacidosis
Pathophysiology:
Diabetic Ketoacidosis (DKA) occurs with severe hyperglycemia and ketoacidosis. This occurs because the blood sugar is so elevated and there is not enough insulin to take the sugar to the cell. The cell needs energy. Since the cell can not get the energy from the sugar (because no insulin) it uses fatty acids for energy. As the body burns up fatty acids to produce energy, it produces a by-product. The by-product of this process is ketones which is acidic. As acids build up this will cause metabolic acidosis. As the ketones build up in the body the patient will spill ketones into the urine showing positive ketones in the urine. The body will do Kussmaul respirations to try and breathe out the CO2 and get rid of the acid.
Nursing Points
General
- Type I Diabetes Mellitus – Acute Exacerbation
- Body has NO insulin→ can’t get glucose into cell → breaks down fatty acids for energy → Ketones (Acids)
- Sudden onset → stress, infection
Assessment
- Ketoacidosis
- Acidosis (pH <7.35, HCO3- <22)
- Ketones in Urine
- Fruity Breath (due to ketones)
- Kussmaul Respirations
- Trying to breathe off Co2 to compensate for acidosis
- Patients can tire easily
- Hyperkalemia
- K+ leaves the cell to compensate for acidemia
- Hyperglycemia
- Blood Glucose 400-600 mg/dL
- Severe Dehydration
- Osmotic Diuresis
- Polyuria
- ↑ BUN, Creatinine
- Altered LOC (cellular dehydration)
Therapeutic Management
- First nursing action = begin fluid replacement and check electrolytes
- Treatment Priority = correct acidosis
- Insulin therapy → so the body can STOP breakdown of fatty acids
- Without insulin, DKA will continue to progress, despite fluid replacement
- Insulin therapy continues until anion gap acidosis has fully resolved
- Continue replacing fluids as needed
- Helps manage the dehydration caused by the hyperosmolarity
- Monitor neurological status
- Monitor and treat electrolyte imbalances
Nursing Concepts
- Acid-Base Balance
- Monitor Arterial Blood Gases and Anion Gap
- Monitor Respiratory status
- Glucose Metabolism
- Blood sugar checks q1h
- Intensive insulin therapy (IV – Regular Insulin)
- May continue even after blood sugar down (goal = correct acidosis)
- Evaluate urine for glucose/ketones
- Fluid & Electrolytes
- Give IV Fluids (IVF)
- Monitor electrolytes & replace as needed
- Potassium may ↓ with insulin therapy
- May add KCl to IVF
Patient Education
- Continue to monitor blood sugars and take insulin even on a sick day
- Do not skip doses of insulin
- Signs and symptoms of hyperglycemia (before DKA) to alert to a problem earlier
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Transcript
Hey guys, my name is Brad and welcome to nursing.com. And in today’s video, we’re going to be discussing diabetic ketoacidosis, also known as DKA, a lot of the pathophysiology behind it, some signs and symptoms, as well as how we’re going to treat our patient. Let’s dive in.
So in DKA, what we’re essentially looking at here is too much sugar and too much acid, right? We call it diabetic ketoacidosis. Okay. Another way to think about it is diabetes causing acidosis. That’s essentially exactly what we have here. We have an acidosis which is brought on by diabetes, right? Remembering that diabetes is too much blood glucose. So we’re having too much sugar and this, through the release and break down of something called ketones, ends up causing acidosis.
So let’s actually discuss some of the pathophysiology of diabetes. Well, the first thing to know is that insulin is produced in the pancreas, right? From something in the pancreas called a beta cell. Beta cell is directly responsible for releasing insulin from the pancreas. Okay. And in instances where patients have diabetes, we basically have a breakdown in our beta cells and issues with insulin production. So as a result, we don’t have enough insulin being made. Now, why is this important? So here’s the way that I like to think about it. Right? Think about the cell of our body being a club, a nightclub and insulin is a bouncer at the front door, sitting on the surface of that cell, sitting outside of that nightclub. The only way that our friend glucose can get into the cell or get into the club is through this bouncer, insulin. Insulin is directly responsible for allowing glucose into the cell. Now, what would happen in cases such as diabetes, if insulin were not getting produced, if insulin called into work sick that night, and he’s not showing up at the club, he can’t allow glucose into the cell. If there’s no insulin on the surface of that cell glucose cannot get into the cell. And as a result, glucose is just going to build up in our vessels in our blood. And this is hyperglycemia. Now, what’s important to know here is two different kinds of concepts that would actually normally occur in a normally functioning pancreas, a person who does not have diabetes. Basically, how is glucose stored in instances of hyperglycemia, where we have too much blood sugar and how is glucose released into the blood in times of hypoglycemia, where we don’t have enough glucose in the blood. So there are two different things, right? The first one here is something called gluconeogenesis. Okay. This is essentially, in instances where we have hyperglycemia, where we have too much sugar in the blood, we’re going to lock some of this glucose away, right? We’re going to lock it away, in a glucose reserve, in a glucose storage container called glycogen. And then there is a second process called glycogenolysis. Okay. We already said that we’re, we’re storing glucose in these storage containers called glycogen. In glycogenolysis, we’re breaking open those storage containers, right? All in an attempt to release that glucose into the bloodstream. This is done by breaking down the glycogen reserves in the liver, breaking down the glycogen reserves in those fatty cells in order to release extra glucose into the bloodstream.
So let’s dive into the pathophysiology of the ketoacidosis component of DKA, right? What exactly is occurring here? A patient has diabetes. So we have low insulin production. We have no insulin release. As a result, the insulin is not there on the surface of the cell, like a bouncer, allowing glucose into the cell. Therefore, glucose is going to build up in that bloodstream, as we’ve already mentioned, resulting in hyperglycemia. Okay. We got that. If we have no insulin allowing glucose into the cell and we have excess glucose building up in the bloodstream, instead of going to the cell, it’s building up in the bloodstream, how does our brain interpret this, right? How’s our brain interpreting this? Well, our brain is thinking, why the heck are these cells not getting glucose, right? Why is there no glucose in these cells? Basically, the brain is saying our cells are being starved of glucose although we have hyperglycemia. Although we have an extreme excess amount of glucose in our blood, we’re not getting that glucose into those cells where it needs to go. The brain says, wait a minute, our cells are starving for glucose, they need more glucose. And so what does the body do to compensate? It attempts to release more glucose. It’s saying, Hey, we don’t have, we must not have, enough glucose in our blood. Let’s release more so that these starving cells can get the glucose they need. And how does our body release the glucose from those glycogen storages, remember, it does it through glycogenolysis right? The actual breakdown of those glycogen storages. So what occurs, as I mentioned in the previous slide, we’re going to break down the glycogen reserves in the liver. We’re also going to break down the glycogen reserves in those fatty cells. Now, the problem is, whenever we actually break down one of these fatty cells where glycogen is being stored, sure, we’re going to release glucose, right? That’s what our brain is telling our body to do. A by-product of the glycogenolysis that occurs in these fatty cells is the release of ketones as well. Now, similar to CO2, if you have seen that video, CO2 is an acid. Okay? So are ketones, they are also an acid. This is important. As we mentioned in our ABGs video, we have a very narrow pH range, a normal pH range of 7.35 to 7.45. If we have an excess of release of ketones into the blood, this is going to drive our pH to become more acidic, therefore becoming less than 7.35. And we will recall from our ABGs video that because that range is so narrow, any alterations going below 7.35 or above 7.45 can lead to cellular destruction. It’s incredibly problematic in patients. And this is what the entire issue with the cascade of symptoms with diabetic ketoacidosis is. Again, we have too much blood glucose in our blood because we don’t have insulin. It can’t get to the cells. The cells are starving. The brain says, Hey, our cells are starving, we need to release more blood glucose. Glycogenolysis occurs. The release of glucose occurs leading to further hyperglycemia. Oh, and by the way, here’s some ketones on top, releasing those acidic ketones into the blood leading to acidosis.
So regarding some assessment findings of DKA, patients are going to have fruity breath. That’s a hallmark sign of patients who have DKA. Ketones because of that glycogenolysis, right? Dehydration can also occur, right? Also altered levels of consciousness, right? Our pH is low, less than 7.35, we are acidotic, we have cellular alteration in our blood pH. We can have altered levels of consciousness. We’re also going to see, again, hyperglycemia, typically a capillary blood glucose greater than 250. We’re also going to be doing, regarding our assessment, Q1 hour glucose checks, as well as frequent neuro checks related to that altered levels of consciousness. And we’re also going to be checking Q2 hour BMPs. We’re basically going to be looking at the amount of bicarbonate that their body is producing, wanting to make sure as we treat and correct their acidosis, we’re wanting to make sure that their bicarbonate levels are getting back to a normal range, as well as, again, you’ll remember from our ABGs video, bicarbonate is released to neutralize excessive acids and to restore a more normal blood pH level.
So how are we going to treat the patient in DKA? The first thing is we’re definitely going to use regular IV insulin. Again, we are insulin deficient in a patient who has diabetes, first of all, much less than one in DKA. We need insulin, right? So that, that excessive glucose in the bloodstream can go back into the cells where it belongs, but we’re going to be treating with IV insulin. We’re also going to be seeing hypotonic dextrose solutions. So imagine as you’re treating with IV insulin, patients blood glucose is to drop. And sometimes it can drop rapidly patients who are sitting there with a blood glucose of 400 for instance, if you drop them from 400 to 200, although 200 is still considered greatly hyperglycemic, you’re going to drop them too quickly. So one of the ways that we treat that is by using a hypotonic dextrose containing solution, it would be something like D5W (5% Dextrose in Water) or D5 ½ NS (5% Dextrose and 0.45 Sodium Chloride). The entire idea being that although we’re treating hyperglycemia with regular IV insulin, we don’t want their blood glucose to drop too rapidly as this is also dangerous. So we’re going to administer at a particular rate, some dextrose containing fluids to prevent their blood glucose from dropping too rapidly. Something else that’s also important to know is, not only is that insulin on that cell, you know, a bouncer to allow glucose in, also as a by-product insulin also allows potassium to go into the cells as well. Right? So what can actually occur as you’re administering insulin is you can have a depletion of your potassium levels. All of the potassium that was inside of your blood vessel is now going into the cell. And as a result, you can have hypokalemia. So we may end up seeing some electrolyte repletion being given as well.
And so to summarize some of our key points with DKA, remember in diabetic ketoacidosis, there’s too much sugar and there’s too much acid, right? Hyperglycemia resulting in ketoacidosis. This is why we call it diabetes causing acidosis. Also make sure that you’re familiar with the normal physiology that normally occurs, that fine balance of insulin production as well as glucose allocation, right? Through two different ways, right, either gluconeogenesis or glycogenolysis. Remember how those two work together to maintain that fine balance of blood glucose. And then taking that knowledge and applying it to the pathophysiology associated with DKA. Make sure that you’re familiar with the different assessment findings and understanding that they all come back to the fact that we do not have enough insulin being produced. And we have an abundant production of glucose within the blood, as well as the release of ketones and all of the therapeutic management that we just discussed.
Guys, that was diabetic ketoacidosis. And now, you know, I hope that you guys go out there and be your best selves today. And as always, happy nursing.
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