[Music] hello and welcome to nursing emergencies renal failure this is part of the nursing emergencies program my name is David Woodruff I am the editor of critical care nursing met incredibly easy I hope to make this incredibly easy for you too so let's talk a little bit about renal failure and starting off with our acute renal failure so before we get into that we need to talk a little bit about the risks for renal dysfunction in order to identify renal failure in our patients especially with acute renal failure we want to be looking for those risks so these are the things that are gonna make this patient at higher risk for developing this dysfunction age the very young and the very old have less control over their immune response and inflammation and they can tend to develop more renal dysfunction shock obviously it could cause damage to the nephron the glomerulus there and we can end up with renal dysfunction vasopressors we cause vasoconstriction we're not only decreasing the perfusion to some of the other organs in the body but we're also decreasing the perfusion of the kidneys volume depletion and nephrotoxic drugs both of those things can cause damage directly to the nephron and then we have diabetes and hypertension we've long heard about how the long-term effects of uncontrolled diabetes and hypertension can scar the tissue in the kidney and cause renal dysfunction and renal failure renal failure can be of one of three different varieties whether this is acute or chronic and in most cases chronic renal failure is the result of untreated or poorly treated acute renal failure intra renal type glomerular dysfunction or damage means that we have damage occurring directly to the nephron itself so it's deep inside the kidney and into that functional unit of the nephron pre renal dysfunction means we have a mean arterial pressure for some reason that has been decreased now this could be due to a lack of fluid so the patient has hypovolemic shock it could also be due to some renal artery constriction or maybe some renal artery stenosis that is decreasing the blood flow going to the kidney and then we have decreased flow getting to the nephron and we're not perfusing not only we are we perfusing and housing filtration occur but we're also not perfusing the kidney itself post renal means we have urinary obstruction so we're obstructing the ear etre you're in backs up into the kidney causes pressure on and unfortunately it causes a bad pressure on the kidney reverse pressures on the filter so we're not getting the filtration that we should normally have so as we work our way through this nephron here and we take a look at these again we have our pre rino which means not enough blood flow so now you can see the blood is coming in here to our nephron this is the filtration area number one there this is where filtration occurs if we don't have enough blood flow coming into the nephron there won't be enough force favoring filtration and there won't be enough perfusion occurring in order to maintain homeostasis at the same time we're not getting enough blood flow going into the kidney to perfuse the kidney itself and we could have damage that's occurring so and I don't need we have decrease in our filtration but we also have damage directly occurring to the nephron in torino means that we have damage that's occurring to that filtration device so now we're having damage that is occurring inside here in the glomerulus we're actually scarring the filter so think about it like having a coffee filter if you punch a bunch of holes in the coffee filter it's not gonna filter very well thirdly we have posterino which is obstruction a urine flow you're in backs up into that glomerulus up there now there's too much pressure for the filter to have to filter against and we don't have adequate filtration renal failure will first go into this Ola Jurek phase where we have decreased urine output so we normally associate this by having the decrease your an output but you notice there's all of these other symptoms here and this is just the top ten nausea and vomiting and that's occurring because those electrolytes are building up in ways they shouldn't be decreased level of consciousness related to our decrease in our sodium level GI bleeding asterixis as we're starting to build up those proteins in the blood those proteins are irritating and they cause asterixis which is also called liver flap have the patient hold their arm out straight in front of you and pull the fingers back so that the palm is up and showing and what will happen is that the hand will flap this is the result of neuromuscular irritability as a result of having too much protein in the fluid that's not being filtered out so we're building up those ammonia's and other results of protein metabolism an increase in potassium as potassium increases and as we're starting to build up fluid and we're not able to filter it out the kidneys are gonna dump off sodium so they try to dump off sodium in an attempt to try to dump off that potassium and the extra water it doesn't help a whole lot obviously or we wouldn't have the increase of potassium but the end result is a low sodium and that's what causes our decrease in level of consciousness acidosis also occurs so we're gonna see cardiac dysrhythmias coos moles respirations which are fast rapid respirations in an attempt to try to blow off some of that co2 and correct that metabolic acidosis hypervolemia is the result of hanging out of all this fluid which then results in edema and hypertension so our treatment will be dialysis fluid restrictions and renal diet the next phase is the diuretic phase and in the diuretic phase this is a good sign because it indicates that the kidneys are starting to heal however during the diuretic phase even though we see lots of urine output the kidneys still aren't filtering we have damage to that filter remember again like punching holes in a coffee filter we can see lots of fluid coming through but we're not filtering the way that we normally should so the patient may be unable to concentrate the urine or be able to filter out the wastes in a way that they should unfortunately though we can have an excess excretion of potassium and the patient can actually end up with a low potassium level at this point so our symptoms could be hypovolemia hypotension and electrolyte imbalances and we're still doing dialysis because the patient can't get those waste products out but we may have to do volume replacement and may actually have to replace some of these electrolytes like potassium so here's what the course looks like we have the initiation phase there with a sudden increase in bu any creatinine and then we get into this maintenance phase where the bu any cratan end is severely high as the patient goes into the recovery phase so the first part of this is diuretic and you can see that really steep drop-off in the BU N and creatinine but then slowly over weeks to months during that recovery phase to be you at in creatin and come back down to normal another thing to keep in mind about the bu n and creatinine elevation is that when we look at this in relationship to creatinine clearance so b-1 and creatinine start to elevate when we've lost about 75% of our renal function so we're all the way down there to the 25 mark 25% of renal function left and that's where the bu and incretins start to rise notice though that the creatinine clearance and our estimated creatinine clearance and GFR are going to start to change as the renal function starts to change so even when we're starting to lose renal function out there at the 175 50 mark way before bu and creatinine rise we're gonna see changes in creatinine clearance and see changes in our GFR those are the early warning signs and in fact we don't really get high elevations in BO and cratan until the patient has lost 90 percent of the renal function so we're down to 10% renal function left here when that bu and cratan and actually get really high well if our acute renal failure does not resolve then it's going to become chronic renal failure at this point we're gonna see it go through these different phases here the first of which is called decreased renal reserve so in the process we're seeing a decrease in the number of functioning nephrons and we're starting to see that v1 and creatinine rise at this point in time the patient may not have symptoms or just starting to see an asymptomatic increase in v1 and creatinine and probably the patient won't need to have any further intervention and laz they have some kind of a stressor some other hit on the kidney and maybe sepsis for example that stresses the kidney and now that decreased number of functioning nephrons is not enough to maintain normal renal function so then we move into renal insufficiency this is an in a systemic increase in BO and in cratan so now we're seeing those go up as asymptomatic which means the patient may not even know about it so they're not running off to the doctor saying hey wait a minute it might be you and a cratan or hi they may not even know it until they get to a physician and for some reason the physician does a full workup and says hey you're being cratan or high this is now the renal insufficiency stage this is where the patient may have some lifestyle changes etc to try to maintain their renal function now we move into renal failure and we have a symptomatic increase in BU and incontinent at this point the patient may need to have some intervention maybe we have some intermittent dialysis or while they're patients in the hospital they may even have continuous renal replacement therapy CRR T when the patient reaches the stage of end-stage renal disease this is the patient that needs chronic hemodialysis so hemodialysis allows for the rapid removal of our waste products and fluids however it requires vascular access so and it also requires some systemic heparin ization even though we try to keep it in the tubing as much as possible that blood is going back into the patient's body so some side effects could include bleeding cardiovascular instability as we're moving lots of electrolytes and fluids around hypotension and dysrhythmias a more gentle approach is to use continuous renal replacement therapy and this is like a long-term dialysis so rather than pulling off a whole bunch of fluid over a period of a couple hours now continuous renal replacement therapy is done for maybe 12 hours 16 hours a day it's a continuous therapy this is typically done in the intensive care unit still requires systemic heparin ization side effects could include clotting of the filter blood loss in the system potential for hypovolemia if we pull off too much fluid however this does allow for a varied rate of removal which may be better tolerated by our critical care patients so some of our takeaways include acute renal failure must damage about 75% of the nephrons prior to symptoms occurring so don't count on symptoms first let's be looking for that change in GFR watch for the risk factors and the subtle changes in renal function dialysis and cv VHD that's continuous veno-venous hemodialysis are used to protect the kidney from additional harm and remove the waste products healthy nephrons will hypertrophy in order to be able to maintain renal function and this is why oftentimes we don't see that there has been damage occurring until almost all of the renal function has decreased well thank you for joining me for a nursing emergencies renal failure my name is David Walker FN until next time [Music] you