Ckd lectures

Talk a little bit already about AKI, and you've learned a little bit about CKD, especially when you learned about diabetes back in the second semester courses.

And so now we're really going to elaborate more. When you're studying and you're thinking about AKI and CKD, we're not really comparing, like, oh, this is AKI and this is CKD, because really it's the same thing, but it's that one is happening very quickly, acutely, and the other is happening over a prolonged period of time.

Since one is happening more acutely, the priorities and the concerns can be elevated as well as slightly different than when we're looking at a patient who is dealing with this from the chronic perspective.

And what I mean by that is there are some medications that are different because for chronic, we're trying to slow down the progression of chronic.

Whereas with acute, we're simply trying to manage the patient and keep them stable in that acute time period. So I don't want you to think like a Venn diagram, let's compare.

But we do need to know that AKI, our priorities are going to be a little bit different and they're going to be heightened, right? When we think about AKI, when the kidneys start to fail, what is it that leads to someone's demise?

What changes in bodily function? Think about the properties that the kidneys are responsible for. We worry about the buildup of waste products. Okay, what else do we worry about?

In AKI, think about essentially what could kill the patient, right? What could result in their deterioration or demise? Ashley? I was just going to say on like fluid management.

So fluid, like fluid overload, we worry about acute fluid overload, especially with AKI. Remember, it's happening quickly. If the kidneys start to shut down, all of that fluid that should become urine, isn't becoming urine.

It's being retained. Okay, it's being retained in the vasculature. What else? You mentioned waste products, but let's get really specific. What in particular can lead to their demise?

Necrosis. What do you say? Synecrosis. Necrosis, kale. Potassium. Yes, electrolytes, right? So electrolyte disturbances. That's going to be one major focus, especially with AKI.

With CKD as well, right? But again, CKD a little bit different. It's happening slower over time. So we talked about fluid changes, so the buildup of fluid, electrolyte disturbances.

You mentioned the buildup of waste products. So when we think about waste products, what are we thinking about? Ukraine. Yes, the azoemia, right?

The buildup of urea in B UN, the increase in creatinine that we see. And then what's another major function that the kidneys are responsible for that if we become altered can result in an imbalance in our homeostasis.

We talked about it a lot with respiratory pH. PH, right? Acid-based balance. So we know that's another big key component when we're thinking about kidney function.

There are other things too, right? And we've talked about, especially as you listen to that pre-recorded lecture in the very beginning, about some of the A and P, some of the calcium regulation, right?

The erythropoietin, which we'll talk about too, especially as we get into CKD. Alright, AKI. It's happening quickly. It's an abrupt change, an abrupt decrease in the GFR.

Where do we want GFR to be? 90, right? So when we start to fall below that, that's when we can start to recognize ooh, is our patient developing AKI.

What else will we see though? It's not just GFR. We'll see changes in which lab values. EON and creatinine, those are the ones we pay really close attention to.

So when you come in on shift, right, you've got a few more weeks left of clinical. When you're in your med surge rotation, that's why when you're getting that report from the nurse, you want to be looking at all of your labs.

We're looking at electrolytes, we're looking at BUN creatinine, we're looking at hemoglobin, and we're trending, right? We're seeing where is my patient now, and what does that tell me about their current status?

When we think about AKI, if we can put it in a nutshell as far as what causes AKI most frequently, it's hypoperfusion. It is a decrease in our net perfusion, because remember, we've talked about the kidneys a lot already.

They're very pressure dependent, right? Not only are they pressure dependent, but they use a lot of our blood supply at one time. And so when our blood pressure drops and they're not getting enough flow, they can start to decrease in their functionality.

When we talk about AKI, you're gonna hear different terms. Okay, they're all used interchangeably. So whether I say it's AKI or it's acute renal dysfunction or acute renal insufficiency or acute renal failure, we're talking about the same thing.

And so when you go into your chart at clinical and you see all the necrologists used this term, but pulmonology used a different term. That's fine, they're talking about the same thing.

And we know that AKI affects a large percentage of our patients that we see in the hospital setting, up to 20%. That's huge. Many of you have seen it already.

Yes. Can you explain why AKI causes disruptions in coronavirus production? So because when we think about hormones in particular, like erythropoietin, okay, erythropoietin, we depend on the kidneys to produce it.

And we need erythropoietin to do what? Make our red blood cells. And so this is why in a little bit when we talk mostly about CKD patients. When patients come in experiencing chronic kidney disease, we know that their hemoglobin is going to run low.

Okay, we expect that when we look at their labs. When we look at those labs, then again, we're looking at it through that lens, understanding that their hemoglobin of 7.2 doesn't necessarily mean they're hemorrhaging somewhere.

Could they be? Maybe. Let's look at their trends, right? But if they come in and they're 7.2, that can all be linked to that dysfunction of the kidney.

Does that help, Juliette? So causes. I mentioned hypoperfusion being the most common cause. So when we think about pre-renal, intranal and post-renal, those are the three different insults essentially that can result in AKI.

And we want to be able to identify when we have a problem, is it pre intra or post? So pre-hypoperfusion. It's the vast majority of all types of AKI.

Intra is the next most common, and it involves direct damage to the kidney. And post would be least common, although something we definitely see, which could result or or be a result of obstruction, some type of blockage, occlusion that's causing issues with the urine flow, distal to the kidneys.

So let's look. I like this image because I think it just helps people to remember. Okay, pre-intra post. So pre, look at which body system we're thinking about with pre.

We're thinking about hypoperfusion. What drives perfusion? The heart, right? So reduced cardiac output, reduced blood pressure. Those would be prime examples of a prerenal cause of AKI.

So really when we talked way back when, for exam one, and we learned all about cardiac. We talked about MIs. We were remiss in a way to not tie in and talk more about the kidneys.

Because remember that cardiorenal connection, right? When we drop our cardiac output from an MI, we're gonna see now a renal insult or injury. Okay, and that is why so many patients come in with myocardial infarction or a sudden reduction in their cardiac output and then develop acute kidney injury after the fact.

Intravenal. We've talked about some intranal things already. Last week, when we talked about glomerulone nephritis, that's a good example here. It's something happening inside of the kidney.

In a couple minutes, we're going to talk about medications and how medications can be nephrotoxic. You've learned about necrotoxic meds already.

And how that can cause acute kidney injury by causing acute tubular necrosis. And then jumping to postrenal, I mentioned it could be an obstruction.

We talked about calculi last week, right? If we have a calculi that's blocking the ureter, or maybe it's blocking the urethra. Now we have hydronephrosis, right?

That's going to cause acute kidney injury. So AKI from the prerenal cause, hypoperfusion, hypotension, reduced cardiac output. This also includes some other conditions that we haven't talked a lot about yet, but we've mentioned so far, like sepsis.

The sepsis can spread to septic shock, right? And when it turns into septic shock and our hemodynamics drop suddenly, that reduces perfusion to the kidneys.

Those of you that aspire to work in a critical care setting, emergency department setting, you're getting patients coming in who are severely dehydrated.

You're getting patients who are traumas, right? Gunshot wounds, stabbing victims, lost blood. Maybe it's a post-op patient who's lost blood in the OR.

Those are all examples of situations where a patient could progress into a prerrenal AKI. We talked about how dependent those kidneys are on getting the blood flow and circulation that they need.

And one of the most important things about AKI is if we recognize it early, we can stop it and we can reverse the damage. But if we don't pick up on it and we can't recognize it, this can continue to worsen and to progress.

So I mentioned how AKI and CKD, one is acute, one is chronic, right? Have you heard the terms though? Acute on chronic kidney disease. What does that mean?

I mean that's an acute exacerbation in somebody who already has history of the chronic. Yeah, so essentially we have both things that are going on, right?

The patient comes in and they have underlying chronic kidney disease. So let's say their creatinine runs 1.5. Okay, that's their baseline. But now they've come in for some type of procedure or surgery.

And we look at their post-op labs, and now their creatinine is 1.7, 1.8. Right? That shows us there's some type of acute issue happening that has caused that creatinine to bump even more.

So that is acute kidney injury on top of chronic kidney disease. And we see it all the time. If we think about intra-renal causes, so we're thinking about things inside of the kidney.

I mentioned nephrotoxic drugs, specifically our aminoglycosides. So when you hear your myosins, your gentomyosin, your vancomycin, your neomyosin, your tobromyosin, those are all aminoglycoside medications, which can be very taxing on the kidneys.

So I had someone this morning ask, well, if they're so harsh on the kidneys, then why would we have them prescribed for a patient? Right? Is there something else we can just use instead?

What are your thoughts on that? Chandra? I was thinking like VENCO is like broad spectral antibiotic. So it's kind of like a risk benefit type deal, like we want to treat whatever is going on right away, but at the same time, that risk of AKAI is there.

Yeah, right. They're prescribed it because they have some type of infection, right? Whether we think they're septic or it's they've got a known pylone nephritis, right?

And they've ordered this specific antibiotic because we need to make sure we have ample coverage. Coverage meaning it's going to work on the bacteria that's present.

So they're prescribed it because they need it. But you're right, now it's risk versus benefit, where we need to be really watchful on these patients to make sure that they don't develop AKI as a result.

Contrast eye, we've talked about this already when we talked about MI, right? Going to the cath lab, we talked about contrast dye with PE, getting a chest CT with contrast, and contrast eye can be damaging to the kidneys as well.

Now we're talking about acute. So we're going to talk about NSAIDs in the acute sense. If someone is exposed to high doses of NSAIDs in a very short time span, that can lead to acute kidney injury.

Okay, so an example of this might be someone who, whether intentional or unintentional, consumes too many NSAIDs. Okay, whether this is a type of self-harm event or an accident, but they're exposed now to high levels of NSAID medication.

Because when we think about NSAIDs, remember how it impairs prostaglandin synthesis in the kidneys. So when we have high levels of NSAID, it can result in acute kidney injury.

This is going to be similar when we get to CKD for patients taking NSAS chronically. Patients who take NSAT medications every day. Maybe it's to help with pain.

Maybe it's for conditions like lupus, right? That can also lead to chronic kidney disease. But in the acute sense, it's someone taking a large amount in a short time span.

We talked about glomerulone nephritis. We talked a little bit about rhabdomyolysis, and I know you've heard it before. So refresh my memory. Tell me what rhabdo is.

Muscle breakdown. Okay, what happens? Let's continue to talk through it. Myoglobin ends up in your blood. Yes, results in the release of myoglobin.

So myoglobin is now free in circulation. Then what?

Holly, are you holding back? No. I'm just trying to pull. I like talked about it before, but in the blood. Because it's blood. Yeah, it can cause damage now to this specific nephrons, the filtering system within the kidneys.

So that myoglobin can clump and block that area, which can lead to acute kidney injury. How do we know someone has rhabdo? We can't look at someone and be like, oh, you have muscle breakdown.

What do we look for? We look in the labs for something in particular. Amanda? Creatine kinase. Creatine kinase, CK, right? Remember our CKs? When someone has really high CKs, creatine kinase values.

We're talking in the thousands. Okay, that can tell us that someone has rhabdo. So what causes rhabdo? You mentioned muscle breakdown. From what though?

How do we get muscle breakdown? Ashley, can we see like over exertion? Some medications that's like also the side of so over exertion, extreme physical activity, maybe it's someone who went and ran a marathon or someone who went and did an endurance activity with maybe not as much training as necessary, or it might have been very hot.

You mentioned medications. Can you recall a medication that you've learned about up to this point? Not the top of my head right now. Statins. Yes, statins.

Okay, can be a medication that can lead to rhabdo. Can you think of any other situations that could cause rhabdo? Anyone want to work in neuro? Uh NMS.

Neuromalignant syndrome. Something else too, I'm thinking of. Can you think of anything else where you'd have a lot of muscle breakdown, a lot of muscle activation happening?

Seizures. Seizures. Status epilepticus, right? After seizure activity. Patients can also go into rhabdo. And perhaps another example that I have seen most often in practice, especially in a critical care setting, is we would get a call, right?

A patient. EMS had a call for a patient, found down. You hear it all the time, right? They were found down. They were laying down at home for 24, 48, 72 hours, and that period of being down, it's normally an elderly person, but could be anybody.

They experience dehydration, low blood pressures, right? Then their CKs increase because now they start to have muscle breakdown and they experience rhabdomyelysis.

So it's not atypical to see someone come in for that type of scenario as well, experiencing rhabdo. So we know rhabdo can cause AKI. We talked about pylonephritis last week.

And as I mentioned, a lot of these nephrotoxic medications can lead to acute tubular nephrosis. So then it comes down to how do we protect our patients?

What are some things we as the nurse can do to keep our patients safe? So you mentioned aminoglycosides. Some patients just need them, right? It's not like we can DC them.

It's not like we're gonna hold them. But what can we do related to, let's start with aminoglycosides to help protect our patient? Juliette. Okay, how do we do that?

Yes, labs, right? When you learned way back in 1060 about peak and trough, right, and drawing drug levels. And if you haven't already had a patient on one of these antibiotics, you will be drawing a drug level, whether it's peak trough or a randomized level.

So when would we draw a peak? We're gonna give an Ivy piggy back medication. It's vancomycin. And we know that that day we need to draw a peak and a trough.

When would we draw the trough? And when would we draw the peak? Before? Okay. You said before. What are we gonna draw before? We give the middle.

Is it the trough or the peak? Trough before. Trough before, why? That's given the medication time.

It's after subsequent doses. Yeah. So they would give medication time to think of the word only for. Be removed. Yeah. And a peak we would want to do during like the an hour, two hours, whatever the time of the medication concentration.

After giving the medication. So think of trough, right? When we think of trough, we're thinking of the valley, right? When is it at its lowest? So a medication is going to be at its lowest, right before we're getting ready to give it again, right?

And a medication will be at its peak. Now it can vary based on pharmacodynamics, but shortly after giving it, right? We give the medication, it gets absorbed, and then it goes into the patient's circulation.

Yes, so trough would be before and peak would be after. Sometimes we have a randomized drug level, which is literally what it sounds like. It's random.

And so that does not need to be drawn at a certain time. But it's important that we're drawing them when they need to be drawn, because if we're drawing it at the wrong time, they're basing the dose off of the information we're giving in the lab value.

What about contrast dye? We had a patient share this morning that a family member had to have a cardiac catheter. And they have underlying renal concerns.

How do we protect a patient who needs to have a cardiac calf and receive contrast dye? How do we keep them from developing an AKI? Juliette? Dialysis.

That would only be if someone is dialysis dependent. Sully? Would you flush them? Flush them. So we want to give fluids, right? We want to help to excrete and remove that contrast dye more effectively so we can give some fluids.

Alright, what else? Hold their metformin, very good. We talked about that earlier this semester. Monitor the labs. Okay. We can also give other medications too to help in the process.

Sometimes we can administer some steroidal medications. And we can administer things like dicenhydrane to help as they're introduced to that contrast dye.

Jess, did you have a question? Oh, I was gonna say shoes seed metaphyn over and said post renal. Postrenal, after the kidneys. So, of course, blockages, obstructions.

It could be calculi, it could be a tumor or a mass. Could be spinal cord injury, right? Neurogenic ladder. We talked last week about hydro nebrosis, so if we can't get the urine out and it continues to back up, it can cause acute kidney injury that way.

We had a patient a few semesters ago at clinical, a male patient with very extensive scrotal and penile edema. It was really bad, probably the worst case that I've ever seen.

And they had him hooked up to an external catheter. And we got looking at his I's and O's, and he was admitted the previous day, there was no documentation of any output, and there was nothing in the external catheter canister.

So, of course, we got thinking well, has he voided and it just hasn't been captured or collected or documented, or is he not voiding? So, what do we do?

We bladder scan, right? So we did a bladder scan. He had over a thousand mLs of urine in his bladder. Guess what he developed the next day? AKI from scrotal and penile edema.

Not something you think of, but makes sense, right? Because everything was so swollen that the urethra was essentially completely occluded. So none of that urine could get out.

So he developed a pretty extensive AKI. How do we fix it? Straight cap or indwelling. In this case, they had to go indwelling because it was going to be an issue after straight capping them as well.

Question, Ashley? No, I was just gonna ask. Yeah. So if we can open up and allow the passage of urine, then we can stop this post-renal AKI. We're still going to have to deal with the consequences though, right?

He continued to have BUN creatinine rise, but at least now we're starting to fix it. Yes. In that case of how they're falling, like how do you get the capital in it?

Like how would you even so urology had to come up and help pass that catheter. You haven't seen a coup d'eau, though, a c often works better. It has that curved, firm tip on it, which is good for males with BPH, but it's also good if you're just having issues passing as you go to insert.

You don't need an order for a few days, you can grab a two day and use that instead. Alright, you're familiar with these terms. These are just here as a reminder, we're not going to go over these in depth.

But for most patients with AKI that fall in that oligaric phase where they are producing lower amounts of urine versus an urea or polyuria. Not important for you to memorize these different phases, but let's talk it through so that we can understand what's happening with our patient with AKI.

So we have that initial insult or injury, whether it's low blood pressure or exposure to contrast dye, whatever it may be that happens. We're not going to see changes in the patient right away, right?

It's going to take time. Just like that patient who had the severe swelling. Okay, it wasn't until the next day that we could really see the BUN and the creatinine bump, and that we started to see now electrolyte changes.

It's in the maintenance phase where we start to see those changes. So now the patient may become more hemodynamically unstable. And this maintenance phase typically persists for days, sometimes even weeks.

So we have lower output. Most patients are falling into that oliguric category where we have changes or decreases in our urinary output. We start to see now the physical changes we would expect when someone has renal failure, right?

We see the edema, we're hearing the edema, and now we're noticing those electrolyte disturbances. We talked about potassium being one of the most important electrolyte changes because it's one of them that's most lethal.

We talked about acidosis earlier, right? We talked about erythropoietin. Now the asterisk, I'll say with erythropoietin is when someone develops AKI, we're not going to see on Monday their hemoglobin is 13, and on Tuesday their hemoglobin is seven, right?

You're not going to see a distinct change like that with AKI. Typically, with AKI, it will happen over a prolonged period of time, right? We need time to see that change in red blood cell production.

But we can also see related to the anemia, it can change from hemodilution. Because with AKI, that hemodilution happens more quickly than the acute drop in our red blood cells due to erythropoietin.

We have more fluid retention, electrolyte disturbances, which can lead to neurologic changes. Most AKIs patients are going to get better from. Sometimes, though, they're not.

And they may become dialysis dependent. So we'll talk about that in just a little bit. But for the vast majority of our patients, they are going to improve.

And what we will notice as they start to improve, they enter this recovery phase. And with the recovery phase, one of the first things that we will notice is they're starting to produce more urine.

It's called autodiuresis. They are automatically starting to diurese themselves. Now it's good because it tells us the kidneys are waking up, but it can also come with other consequences where they autodiurese too much.

This recovery phase can take a very long time, up to a year for some patients to recover from their AKI. So how do we know that they're recovered?

What are we looking for? GFR. An increase in their GFR, so we're trending the GFR. What else? Right, we're looking for that B UN and creatinin to trend back to their baseline, right?

So whether they had AKI on CKD, we're looking for them to hit their baseline again. Or if they came in without any renal compromise, we're looking for them to go back in the normal range for BUN and creatinin.

So remember, being a nurse is like being a detective. We've got to look for those signs and symptoms that tell us that our patient is at risk for something and developing a new problem.

This is why at clinical, when you do those clinical judgment worksheets, although I know you may not love them, especially in the beginning. It is helping you to recognize its potential problem recognition.

Because when you get report on someone, your wheels should already be turning, and you should have a list in your head. Okay, I'm worried about this and this today.

Because we're tying it all together. And so if our patients here with calculi or a tumor, or they're on amino glycosides, or we know they have a reduced ejection fraction from heart failure.

All of those things should come into play and helping us to use our clinical judgment and figure out what they're at risk for today. We want to try to prevent it.

We know we actually meet with the practice partners and we talk with our practice partners, so Cleveland Clinic, UH, the VA, Metro, and we find out what is it that you want to see, not just rebrads, but improvement in in your nursing staff.

And when we think about disease processes, complications, AKI is one of those things because patients experience it so frequently in the hospital setting that they've mentioned before, nurses in general and their institutions need to continue to work on and identify early, as well as the health care providers.

But we're the ones who see the labs at three in the morning, right? We're the ones who determine do we reach out about that or do we let that lab go?

So we're looking at that history, and we're looking at our own assessment as well as our labs. We talked about creatinine B UN. We're looking at our output, we're looking at the color, the clarity, we're looking at our hemodynamics like blood pressure, we're listening to the patient, and we're trending our weight.

And that's why weight can be so important. All of these things are telling us and informing us about the patient's volume, electrolyte, and waste product balance.

So we're maintaining adequate hydration. We know that oftentimes we're dealing with too much fluid, right? We need to try to get some of that fluid off because those kidneys are not working well enough.

We talked about electrolytes, we talked about our drug levels, and when we look at our B UN and creatinine, as we trend those, we're also keeping in mind that simply a high B UN, but a normal creatinin tells us our patient is dehydrated, versus when we're seeing now that trend where both values are continuing to increase.

So we need to identify what type of AKI it is so we can fix it. So for example, if it's post-renal, we put in the foley, right? Or we fix the obstruction.

If it's from lack of volume, we can give volume. If it's a lack of cardiac output, we give medications to boost cardiac output. And we've talked about dopamine before.

So remind me, what is dopamine? How does it work? What does it do for a patient? It's a positive inotrope. What else? Yep, so it gives us more squeeze, right?

What about its chronotropic effect? Positive, negative, positive chronotropic effect, so that's going to increase heart rate, good. When did we talk about dopamine before?

What scenario or what type of disease process would we use dopamine? We talked about it after cardiac arrest. Which dysrhythmia might it be good for?

Boosts cardiac output, it boosts heart rate. Arboritocardias, right? It can increase heart rate there and increase our blood pressure. But dopamine also has some unique properties.

We can give it at two different dosages. So that high dose dopamine is what we've talked about up to this point. We've talked about giving dopamine at higher levels to boost cardiac output and to boost blood pressure and to boost heart rate.

But if we give it at a lower dose, it has a different therapeutic effect. It actually helps in improving renal perfusion. And so dopamine is a medication that we can give at a low dose when someone is having AKI, and it can minimize and help reverse some of those effects of our acute kidney injury.

We talked about fluid, and we're really worried about fluid overload, right? So when we think about patients, whether they have kidney injury, chronic kidney disease, adjusted heart failure, right?

Those are all conditions where we have too much fluid. So we think about utilization and integration of a fluid restriction in our care. Treat elevated electrolyte levels.

Someone this morning said, well, how do we do that? How do we know if we're doing it adequately? Well, we look at our labs, right? Our labs are driving the decisions that we make when it comes to electrolytes.

Careful diuresis. So we can give diuretics, right, to help pull off fluid because we know we have too much fluid. They're holding on to too much because the kidneys can't release it.

So we go with perhaps that favorite class of diuretic that we've been talking about a lot this semester, our luck diuretics, ferosamides, what are other loops?

Torcemide, eumetonide, right? Those are our loop diuretic medications. We like them because they're potent. They give us a lot of oomph when we go to give a diuretic.

But in the same regard, they're potent. And we need to be really careful when someone has AKI and those kidneys are fragile. If we give them too much, as far as lute diuresis in particular, we can tip them over the edge and cause that AKI to worsen.

So you'll see here it says the newest recommendation is to limit the use. So typically what you'll see is a lower dose, like 20 milligrams of ferosamide, IV push, and the purpose is to try to remove that fluid.

For some patients with AKI, it doesn't work. The kidneys are too damaged. And in that case, we don't keep going back and trying, oh, let's give more corosamide and more carosamide.

If it's not working, we need to stop and develop another plan. Julia. Which phase of AKI repases in? Because recovery phase is usually when they're diurasing themselves and sometimes too much.

So we use it in that phase, or would it just be like maintenance? It's typically in that maintenance phase. Because that's the phase where they're still holding on to all that fluid, and we're trying to treat those related problems, right?

The pulmonary edemas, the pleural effusions, the heart failure that they're starting to develop because they have too much fluid on board. Whereas you're right, when they're autodiures, blood pressure's low.

Do we want to give ferosamide? Yeah. This goes along hand in hand with the fluid challenge. Okay, fluid challenge. The point of giving fluids is to see if we can perk the kidneys up when they have AKI.

It's a test. It works for some patients, it doesn't work for others. So if we talk for a minute about a typical patient, they have no renal issues.

Okay, BUN creatinine look great, they're normal. That patient develops hypotension while you're at clinical. And you call a rapid response. When the team comes, they're probably going to decide to give what?

Fluids, right? Normal saline or what other crystalloid? LRs. LR. Okay. We're anticipating normal saline or LR. How much volume would you expect for that patient in their fluid bolus?

One liter? Maybe 500. We'd at least give 500, right? Probably a liter. And how are you going to run it? Wide open. Wide open, or maybe we hook it to a pressure bag, or maybe we hook it through the pump and we run it at 999, right?

We're running it fast. But now we're talking about the patient in AKI. Okay. Creatinin is 1-7. B UN is 45. We're going to give this fluid challenge.

How much volume are we going to give? Are we given a liter? No. No. We're going to give much less. It's usually 250 mLs. Why are we going so small?

Yeah, the last thing we want to do is flood them with 500 or a liter, and then they can't get rid of it, right? And now we have all this extra volume in circulation.

So it's typically 250, it's sometimes 500. It's going to be provider dependent, right? They're making the call. But we would anticipate a fluid challenge.

And with the fluid challenge, what we hope to see if it's going to work is you're going to see that increase in urinary output. And so sometimes it takes, they'll actually combine these.

We're going to give a little bit of ferrosamide, we're going to give a little fluid challenge, and we're going to see if those kidneys can perk up and show more activity with their production of urine.

You can see here with AKI, it's a delicate balance because so many of these problems can become lethal quickly, like too much fluid and electrolyte changes, which brings us to the hyperkalemia piece.

When someone is hyperkalemic, so we've got a high potassium, the treatment that we are going to anticipate is typically multimodal. We're doing more than one medication to treat this problem.

So let's start first if we look right at the top. Our medication of choice is typically called the K cocktail, but in it, it includes D50, so we're giving dextrose, and we're giving regular insulin IV push.

Now they don't come together. You don't get it from pharmacy in one syringe. You pull each one separately. This is the only time in your life you are ever going to push insulin IV.

And it's always regular insulin. You never give any other type of insulin IV. So you're standing there with your dextrose and your insulin. Which one are you going to push first?

Who said extrose? Kale. Why are we pushing dextrose first? You're going to push someone if you're going to push insulin really quickly through the bottom out our blood sugar.

Exactly. If we were to give the insulin first, we could cause the death or serious harm of our patient, which we do not want to do, right? So we're giving the dextrose.

The dextrose actually doesn't do any of the work in decreasing our potassium. It's just there to boost sugar, right? It boosts that blood sugar so that, like you said, we don't automatic the patient.

Now, how does the insulin work? Well, it really works by masking the hyperkalemia. Because what the insulin does is it pushes it intracellular. So it takes that free serum potassium and it pushes it into the cell so that now when we recheck our potassium level, it appears lower on the laboratory results, but it's temporary.

It's just taking it and it's pushing it somewhere else. It's not actually getting rid of that potassium. But it works really well, and it's IV push.

So it works fast, right? We can do this quickly. So you see this very frequently. Emergency department, in critical care settings, step-down units, when we have hyperkaalemia, we go with this because it works so fast.

We can give it very fast. Whereas sodium polystyrene sulfonate, help me out. What is the other name, the trade name for sodium polystyrene sulfonate?

Kylate. KXylate. Now you know NCLEX will only have generic names. But I like to bring it up because sodium polystyrene sulfonate doesn't exactly roll off the tub.

How do we give sodium polystyrene sulfonate? So it's either oral or it's rectal. We can actually give it rectally via a rectal tube. And sodium polystyrene sulfonate is unique because it actually pulls the potassium out.

So it pulls it into the gut, into the stool, and the patient will excrete it. Okay, so it truly drops the potassium level and gets rid of the potassium.

Whereas sodium bicarbonate is similar to our K cocktail, it is simply pushing potassium into the cell. It can work well, it doesn't mean that it doesn't work well, but again, it only works for a short period of time, and then that potassium starts to leak back out again into the serum.

The other drug I want to talk about as we talk about hyperkalemia is calcium gluconate. We know that high potassium levels can lead to what problem.

So this is why calcium gluconate is an important medication that's administered when a patient is hyperkalemic. Calcium gluconate stabilizes the cardiac cell membranes.

Essentially, if you think of it like stabilizing the heart. Tries to keep that patient from going into lethal dysrhythmias. What do we see on the telemetry?

Peaked T waves, peaked T waves are a hallmark early sign of hyperkalemia. You can see that late signs include more prolongation, so prolonged PRs, widened QRSs, and this can progress into lethal rhythms.

So I had a student this morning ask, okay? N CLEX likes to go with prioritization, right? Which medication are we going to give first? We did that already with our K cocktail.

Okay, but now let's pretend we've got our patient in front of us, and we have our dextrose, we have our regular insulin, and we have our calcium gluconate.

When would we push the calcium gluconate first? When they have late symptoms. Okay, you mentioned when they have late symptoms, so if you see these things on your telemetry, good.

What else might you see? Dizziness, synchrony. Other cardiac related symptoms, right? That's telling us that we have impaired cardiac perfusion.

So it could be things too, like couplets, right? We see a little run of V TAC. Now we're grabbing and pushing that calcium gluconate first to try to stabilize the cardiac activity for the patient.

And then we're very quickly thereafter giving our other medications that we have. So hyperkalemia is not treated with just one medication. It's treated with multiple.

Sometimes your orders will include giving all of these that are mentioned on this slide. Juliet. Did you say sodium by coveries are quick, or is that bird thanks as well?

Yeah. Because it just pushes it into the cell.

Okay. Couple other things to think about. When someone has AKI, it can progress into multi-system organ failure. Okay, so we're monitoring not only our kidney function, but we're looking at our other values as well.

And we know that elevated levels of blood sugar can also lead to diabetic nepropathy, which is a very common cause of CKD. So we're going to maintain normal glucose levels for our patient.

That might be new to them, right? They might say, I'm not diabetic. Why are you checking my sugar with every meal? I've never had an issue with blood sugar.

And it's all about keeping them safe and reducing further problems and further complications with their AKI. I mentioned how most patients are going to get better from AKI.

But a lot of them may need dialysis. And so when we think about dialysis, patients can have intermittent dialysis or continuous dialysis. We're going to elaborate more in just a little bit about those two treatments, which are types of dialysis.

We know nephrology will be following as these patients accumulate more fluid electrolyte disturbances, we worry about skin problems, blistering, pressure injuries.

We talked about monitoring and trending our daily weights, as well as fluid restrictions and dietary restrictions. Remember that renal diet that we talked about last week?

That also comes into play for our patients with AKI. Questions about acute kidney injury before we transition and talk more about chronic disease.

Okay. Chronic kidney disease. Is it your remote?