42: Dry As a Bone: Acute Kidney Injury

His kidneys did not perk up like I had hoped they would but the additional fluids. He had only urinated 100 ml, the entire night shift. When I got to him, he was still a thargic. His blood pressure was 88 over 50. He was more puffy. His lungs had crackles. He was deceptic. He was tachycardic in the 120s. He was not going the right direction. At this point, all of his lungs were out of whack and he needed emergent dialysis. Hey there. I'm your host, Sarah Lorenzini, a rapid response nurse and educator who loves telling stories to teach critical thinking. This podcast is for nurses who want the knowledge, skills, and confidence to respond to any emergency. With almost 20 years of experience in the ER and critical care nursing and a master's degree in nursing education, I have a lot of stories to share and I love to nerd out and break down the pathophysiology, pharmacology, and nurses' role in emergencies. Stories bring learning to life. It is way easier to learn from and remember the stories that my colleagues and mentors have told me than anything I've read in a textbook. And that is why I made this podcast. Every episode is packed full of exactly what you need to know to handle whatever crisis that could arise on your shift. It's one thing to get the right answer on the test, but knowing how to detect when your patient is declining and what to do when your patient is crashing is what will make or break your day and might just save your patient's life. Today we're talking about a patient who was so dehydrated, so dry that his kidneys just stop filtering. And I want to talk you through a case, a specific rapid response that I went to, but honestly, I see cases like this all the time. Acute kidney injury is really common in the hospital setting, and so I think it's so important that as nurses we know what to look for, what to expect, when to anticipate, and how to prevent it if possible. So by the end of this episode, I hope that you walk away feeling more empowered to advocate for your patient who either came to you with an AKI or is developing one while in the hospital. All right, so I arrived to find a pale diaphoretic man in his 60s. The blood pressure on the portable bottles machine says 60 over 40. His heart rates in the 130s, he's breathing like 30 times a minute, laying the bed with his eyes closed. So I approached the patient say, "Hello, my name is Sarah. I'm from the rapid response team." He barely opened his eyes and falls right back asleep. When I touched his skin, it was cool and clammy. So I start scanning the room to see what's going on while I'm asking the nurse to give me the history. So I go feel four radio pulls, and I can't feel one, but I do feel a strong carotid. I see some fluid bolus infusing. It's on the pump at 999 mLs per hour, which is as fast as our pumps can infuse. I see some antibiotics hanging and his IV catheter is pink, which for our hospital that denotes a 20-gauge IV catheter. So I immediately pulled the fluids off the pump and proceeded to place them on a pressure bag that I had pulled on my backpack, and the nurse is kind of telling me the story as I'm doing this. He says, "The patient was admitted last night from the ER. He came in for a generalized malaise, nausea, vomiting, diarrhea. He was hypotensive and had an elevated white count, so the ER gave him a 30 cc spokane bolus and his blood pressure improved." It sounds like he kind of perked up in the ER, so they admitted him to the floor. His initial BUN and carotidin was elevated in the ER, but that's new for him. He has no history of renal failure. They still haven't determined the source of his sepsis. Blood cultures are pending, but it wasn't your sepsis or pneumonia according to the urinalysis or the chest x-ray. He has a history of a heart attack, a cabbage, hypertension, and diabetes. I got a blood glucose right before you got here and it was totally normal. Great report from the nurse. He answered all the things that I wanted to know. So I cycles blood pressure again. Now it's a whopping 68/46, but only like 500 cc's have gotten so far. So I start mixing up a norepinephrine drip just in case, but I'm still hoping the fluids will turn his blood pressure around. So I put the patient on my portable cardiac monitor and it shows AFib RVR in the 130s. I asked the nurse if he'd been in AFib and it sounds like this was also new for his admission. By that time, the critical care resident had arrived and has started looking through his history in labs. I started a second IV since he only had the one and after a liter of fluids, his blood pressure had improved to 80/50. The ICU resident gave me an order to give a second liter of fluids because his morning lab showed a worsening BUN and creatinine, even from his initial bad labs in the ER. Now let me pause here to talk through this dilemma that I'm often faced with responding to hypotension rapid response calls. So when the BP drops, I don't actually know what the culprit is. I mean, I can make a good guess based on history and assessment findings, but without advanced, hydrodynamic monitoring, we're all just guessing. Like, is his BP low from low preload? Is it just a volume problem? Maybe. He has been vomiting. Is his BP low because he's septic in his low afterload? Maybe. Septic patients do tend to vasodilate. His blood pressure could be low because the vessels are all dilated out from sepsis. Is his blood pressure low because he has some underlying heart failure? Is the contractility of his heart poor? Is his blood pressure low because his heart just isn't squeezing adequately? I mean, maybe. But I would need an echo and some advanced hydrodynamic monitoring to know that for sure. Additionally, he's an AFib RVR. So we know that AFib alone decreases cardiac output. And to add to that, his fast rate doesn't allow for enough fill time and that too will decrease cardiac output. So that is likely contributing to his hypotension as well. Plus, I don't know what mess he's perceived that morning. All of those could be contributing to his hypotension. So when the doctor orders another leader of fluids, I always pause and think through all of the possible reasons for hypotension because we may improve the blood pressure for a minute with another leader, Ravi fluids. But I want to actually fix the problem, not just put a fluid band-aid on it. So for this guy, though, all science pointed towards hypovelemia. I mean, he came in for nausea, vomiting, diarrhea. He did respond to the first leader I gave him going from 60 over 40 to 80 over 50. But I could also make things worse with fluids. So giving them the caution. We gave the second leader, since, you know, he did have an acute kidney injury, likely from vomiting depletion, and his blood pressure corrected to 95 over 60. Sweet. So even though his blood pressure had improved and his heart rate also came down to like the 90s, low 100s, I asked that he be transferred to the Progressive Care Unit. The doctor said that he didn't meet PCU criteria, which was true. I hadn't started vasopressors. He wasn't requiring high levels of oxygen. He had no cardiac drips infusing. But I knew where this was going. So they agreed and I transferred him to the PCU. But that is not the end of the story. We have this watch list where we keep track of patients and check on patients who have a high risk for deterioration for one reason or another. I put him on the list and went back the next morning to check on him in the PCU. And he was not better. His kidneys did not perk up like I'd hoped they would with the additional fluids. He had also gotten normal saline at 100 ml per hour overnight. So that's an additional 1500 ml since I had last seen him the day prior. And he had only urinated about 100 ml the entire night shift. When I got to him, he was still lethargic. His blood pressure was 88 over 50. He was more puffy. His lungs had some crackles. He was tachycardic. He was tachycardic in the 120s. So I called the primary doctor and asked that she could reach out to the critical care team again because he was not going the right direction. At this point, all of his lads were out of whack. He needed dialysis, but he would not be able to tolerate the regular human dialysis. His blood pressure was 88 over 50 to start with. He would likely require some vasopressors and need continuous renal replacement therapy or continuous, like a more gentle dialysis. In the next 30 minutes, I started a norepinephrine drip and I took him to the ICU. I stayed to help get an outline in him so that we could place that advanced humanamic monitoring. Sure enough, he was very vasoplegic, an SBR of 400. For those of you that don't routinely deal with advanced human dynamics, SBR stands for systemic vascular resistance. Normal SBR is 800 to 1200, and he was only 400. So low systemic vascular resistance means the vessels are very dilated. Norepinephrine was just what he needed to bridge the gap until we could get his sepsis under control and get his kidneys back to filtering. He was in the ICU for weeks, but his kidneys did recover and he was discharged home. Now, there's so much to unpack here, so let's just start with basic definitions. Acute kidney injury is characterized by an acute reduction of glomular filtration rate, or GFR. We can confirm that this is going on when there's a rise of serum creatinine concentration or a decline in urine output, and our patient had both. Okay, so we have a diagnosis of AKI based on urine output and lab values. The next question is, why are the kidneys failing to filter and produce urine? So there's three basic categories. First is pre-renal, meaning something has impaired the flow of blood or oxygen coming to the kidneys, like before the kidneys, there's an issue. The next is renal or intra-renal, and that's where there's something within the kidney that's damaged, like there's a tumor in there or there's certain medications that are nephrotoxic that have damaged the renal tubules and nephrons. Often, pre-renal offenders can turn into intra-renal injury, which I'll discuss in a bit. And finally, there's post-renal injury. Those are almost always some sort of obstruction south of the kidneys. So kidney stones, blood clots, you re-throw obstruction, like our patient from the last episode, his eight-day-long pripism had obstructive flow out and urine backed up causing renal failure. So here's the thing. When patients develop acute kidney injury, it dramatically increases their mortality and reduces the chance of them ever walking out of the hospital. So those eyes and nose that you hate charting, they are vital. That's how we know what's going on with our patient's kidneys. That's how we can know if they're going to renal failure. Acute kidney injury is a big deal, and as patient advocates, it's so important that we stay on top of it. I go to a lot of rapid responses, and when I ask about urine output, the nurse doesn't know how the urine output has been, because the nurse tech is often the one emptying the fully bag and taking the patient to the restroom, and I get it. The nurse-to-patient ratio is high, and it's really hard to stay on top of every detail for your patient. But I would say that looking after your patient's kidneys is a task to prioritize. So we're talking this week about a pre-renal kidney injury that turned into renal. Let's break down the pathophys of pre-renal injury. The most common cause of pre-renal injury is volume depletion. Hypovolemia caused from dehydration, gastrointestinal fluid losses like vomiting and diarrhea, hemorrhage or renal losses like overdiarrhesis can all cause the kidneys to take a hit, because there's just less volume coming to them. The kidneys need volume and pressure to allow them to even do their filtering job, and also to provide them the oxygen they need to keep doing their job. So whether it's low flow from low volume or low flow from low blood pressure, like patients who are in shock, either way, the kidneys get upset and stop working. Pre-renal injury can usually be reversed in 24 to 72 hours with correcting volume status and blood pressure. The kidneys perk back up and get back to work. The gold standard for distinguishing between pre-renal, the easily reversible volume depletion acute kidney injury, versus acute tubular necrosis is how the patient responds or doesn't respond to fluid depletion. So if you give fluids and the hypotension corrects, and the BU and a creatinine start trending back to normal, and the patient starts peeing more than 0.5 ml per kilogram per hour, then yay, you saved the kidneys. But if you have adequately fluid resuscitated and the BU and a creatinine are not improving and the patient's not peeing very well, and now you're seeing signs of fluid overload and electrolyte abnormalities, well then you have acute tubular necrosis. That's exactly what we saw on this patient. We were hopeful that the fluid resuscitation would turn things around, but on day two, 48 hours into his hospitalization, he was not peeing. He sounded wet to auscultation of his lungs, his BU and a creatinine were actually going up, and his potassium was climbing to critical levels requiring dialysis. Giving any more fluid to him at this point would have been harmful. So no one did anything wrong by giving fluids. He was septic, and that's what septic patients need, and that's what AKI patients need, but we have to watch these patients so closely to see how they're responding to our interventions because when they're no longer responding well, it's time to take a different approach. In his case, it was vasopressors for blood pressure control and dialysis. So how do patients recover from acute tubular necrosis? Well, a lot of them don't. They developed acute tubular necrosis for a reason, either sepsis or nephrotoxins or prolonged ischemia of the kidneys, but for those that do recover, it requires that whatever the underlying cause was is treated correctly and corrected. For example, his sepsis was treatable, but the initial broad spectrum antibiotics they started weren't touching it. Once the blood cultures came back and they switched up as antibiotics, then the bacterial load came down and the inflammatory cascaded awfulness that was causing him to be so sursy calmed down. Sorry, sursy is not actually a real word. It's a made-up word for when the body reacts to infection and the heart rate goes up and the blood vessels dilate so the blood pressure drops. Surge is an acronym for systemic inflammatory response syndrome. It's the body's attempt to help compensate, but it actually ends up hurting in the long run. So when surge turns into septic shock, then we send patients to the ICU where we can watch what the body's doing and titrate our volume resuscitation and vasopressor administration based on those advanced hemodynamic parameters that I had talked about earlier. All right, I'm getting off on a sepsis tangent. If you want to learn more at sepsis, check out episode eight with my buddy Yasha. We break down the pathophysicist sepsis way more in that episode. Back to acute kidney injury. So a lot of patients develop acute kidney injury from something that impairs flow to the kidneys, be it some sort of shock that drops the blood pressure like septic shock or cardiac shock or hemorrhagic shock, or even some surgeries. It's common for blood pressure to drop from the anesthetics. If fluid recitation fixes the renal function, then it was just a pure pre-renal acute kidney injury. But when the kidneys continue to struggle to filter out toxins and produce urine, then we have acute tubular necrosis, which is only sometimes reversible. If you can't fix the underlying cause, the kidneys will not improve. As an ICU nurse, that was such a huge win when I received a patient from the emergency room or the operating room with an AKI, and I was able to turn their AKI around. I didn't know in nursing school how excited I would be to see a patient make urine, but when you know what a difference it makes in the patient's outcome, you would be excited too. Okay, so let's get to the nursing pearls from this case. First, remember the patient was hypovolemic and the nurse had the IV fluids on the pump at 999 mls per hour. I get it. We were all taught that the only safe way to infuse medications is on the pump, but the guardrails on. But at 999 mls per hour, it would take an entire hour for a leader of fluids to infuse, and this patient was too hypotensive to wait an hour. Now, if your patient's hypotensive and awake and talking to you or pink, warm, dry, normal breathing, normal heart rate, sure. 999 mls per hour on the pump is probably just fine, but this patient had some concerning symptoms of not enough cardiac output. He was pale, cool, clammy, red flag number one, and he was lethargic and difficult to arouse, which tells me there isn't enough flow going north to his brain, and it's affecting his mental status. My point is, symptomatic hypotension gets a fluid bolus on a pressure bag. Next, the kidneys rely on adequate volume and pressure to function. If either of these drop, it can cause a pre-renal acute kidney injury, which is often reversible with fluid resuscitation. But if lack of flow or volume or pressure or oxygen continues long enough, the cells themselves become damaged. Medications that are nephrotoxic can also damage the filtering cells of the kidneys. Then we refer to it as an intra-renal acute kidney injury. This can also be reversible, but it's more difficult to reverse. And finally, obstructions south of the kidney can cause things to back up in the kidneys, which can cause a post-renal acute kidney injury. In summary, AKIs are serious as they greatly affect your patient's chance of survival. So stay on top of those eyes and nose, and don't be afraid to be your patient's voice, and let someone know if you notice a trend in the wrong direction. Before you go, I just wanted to let you know that if you liked this episode, you would probably like my course too. My one-hour rapid response and rescue course is an introduction to how I approach emergencies. If you would like to learn to think, assess, and respond quickly when your patient is crashing, then you can check out my website, rapidresponseandrescue.com. And if you message me the word "podcast" on Instagram, I will send you a coupon code for $10 off the cost of the course. Oh, and did I mention that the course is approved by the AACN and worth one continuing education contact hour? So if you want to level up your emergency response skills and get one CE in the process, then this course is what you want. I put the link in the show notes for you. Well, thanks for listening. I hope you learned something that will save a life. Remember, nursing is a team sport, so trust your intuition and don't give up advocating until you are confident you've done what's right by your patient. The views and opinions expressed on this show are that of Sarah Lorenzini and hers alone. They are not intended as medical advice and should not take the place of your institution's policies or procedures. Evidence-based practice is ever changing, and your patient care should reflect the current best practice. If you want to get in contact with Sarah, you can find her at rapidresponseandrescue.com or on social media platforms as the Rapid Response RN.