 He is Dr. Sathish, our Senior Consultant Department of Nephrology. He is going to educate all of us on how do we receive nephrology emergencies and how do we handle them before we refer them to a tertiary care center. Over to you, sir. So I have given this topic, emergency nephrology. In fact, when it comes to nephrology, you know, if I start talking about all the emergencies, this whole lot, I will just try briefly talk about, I will just, my outline will be few points about acute kidney injury. I am just going to highlight that and I will let it go fast also because I have been asked to finish my talk in 15 to 20 minutes. So hypokillemia, then hyperkalemia, hyponatremia, and acute palmitima. I will just highlight few things about all those things. So when it comes to AKI, we do not call it, there is any more acute kidney failure. We use the word for acute kidney injury because ARF and CRF we no longer use. We use acute kidney injury and chronic kidney disease. So AKI, we just have to know what is AKI? Should we wait for the creatinine to go high like 1.5, 2, 2.5, 3? No, we do not go by that. In any high-su setting or anywhere, we just go by hourly urine output. So we look at, you know, if somebody is passing less than 0.5 ml per kg per hour for 6 to 12 hours, even though the creatinine is around 0.8 or 1, they come under stage 1 of AKI. Stage 2 is around 0.5 ml per kg again for more than 12 hours becomes stage 2 AKI. And stage 3 is, you know, for more than 24 hours or anuria. How long will it take to add on to that? Okay, if there is jump in creatinine, it is fine. More than 0.3 per deciliter from the base or 1.5 to 1.9 times the baseline or 2 to 2.9 times the baseline or more than 3 times. But more than this, don't wait for the creatinine. To diagnose AKI, we don't need the creatinine to go high. We go by hourly urine output. So we measure hourly urine output, but based on that, we'll take a call with the patient as AKI and act accordingly. So it comes with the AKI. So we have, you all know, we have pre-renal intrinsic, what we call as acute tubular necrosis. Tubules gets affected. Nefron has something called as glomerulus, then renal tubules, and then collecting that. So we're talking about pre-renal, where there's dehydration, all those things called as pre-renal. Then intrinsic is something that damages the renal tubules and the post-renal because of obstruction. So pre-renal can be because of hyperbolemia, GI laws, anything, whatever it is across, diarrhea or anything. Decrease cardiac output in cardiac renal syndrome. Decrease in an EF is less. We always have decreased cardiac output because 25% of the cardiac output you need needs to function normally. Anything less than that always, you know, they go for cardiordinal syndrome. Then any decrease effective circulating volume in congestive heart failure, liver failure, or any whatever happens whenever God has given us something called renal auto-regulation. But this auto-regulation can be blocked if you take NASID. So even one dose of NASID can block the prostaglandins because prostaglandins help in auto-regulation. So that's the reason some people may not have any renal failure, but some people can go for renal failure with just one single dose of any painkiller. Even pox2, anything is a painkiller. It's just not a brufan or ibuprofen. A lot of people think pox10-bitters are safe. Pox10-bitters only safe gastric irritation is less. Otherwise, all are painkillers. So try to avoid all these things. And elderly people, you know, the GFR will be very, very less. So we have to take it with a pinch of salt when you give any painkillers. So make sure because though GFR is already low, when you give a painkiller, naturally you're going to block the prostaglandins. Again, they're prone for AK high. When this pre-renal, if you're not treated, if this prolongs certain time, then what happens is the renal tubules get affected. That is called as going to ATN. So yet the glomerules can get affected or the renal tubules can get affected or even the vascular problem. Glomerules is what you call acute glomerulophritis. It can be rapidly progressive glomerulophritis, what you call as RPRF. So vascular disease, anything can cause glomerular injury. Tubules, it can be ischemia. As I told you, prolonged, you know, if you don't treat the pre-renal and prolonged ischemia, low blood pressure, renal hyperperfusion, because water is a cause that can cause ischemia and again cause acute tubular necrosis. Or any sepsis, most common thing in isosutymic is sepsis causing into AKI or prolonged ATN. Then vascular, vascular as I told you, that can cause any malignant hypertension, axillary hypertension, all those things can cause problem and cause acute kidney injury. Or HOS, humanoid economic syndrome or traumatic popular. So these drugs also we have to be worried about the contrast, any aminoglycosides, amphetamine B or any, you know, myeloma, rhabdomylases, all these things can cause AKI. Normally, aminoglycosides, it's not going to happen immediately. So when you give aminoglycosides, what happens is normally go to the lysosomes, stay in the lysosomes for longer times. It takes some time for renal failure to set in. It's not like today I gave, I'm a cast in 500 and tomorrow I'm going to see a creatinine going high. So normally when you give aminoglycosides, normally we should wait for three, four days. Sometimes you see renal failure setting in. So be careful whenever you give aminoglycosides. So one of the frequent causes I told you, ATN is around 45%. Prevent is 21% in hospital setting. Then we have something called Acute Unchronic. A lot of people will have chronic kidney disease. Because of some acute setting, we'll have Acute Unchronic Kidney Disease that amounts to 13%. Then you'd have obstruction because of bladder obstruction. That normally older men with prosthetic diseases. Then we have glomerulophidase of aspirin is around 4%. Acute industrial aphidase is around 2%. Any drugs can cause AIN, antibiotics can cause AIN or any painkillers can cause any drug. Any drug can cause even paracetamol. Any drug can cause acute interstitial nephritis. It's very difficult to prove unless we do renal biopsies. So AIN is one thing, any cause pantoprosal, lot of case reports that have been pantoprosal causing a lot of renal failure, all comes under acute interstitial nephritis. Or any other embolism, any cholesterol embolism, any post angiogram, all those things can cause acute kidney injury. So presenting symptoms you have diminished kidney function. Whenever you have diminished kidney function like edema, hypertension and decreased urena output as usual and any renal failure is prolonged or uremia, then only you will have weakness, reticability, anorexia, vomiting or change in mental status or seizures. Along with that, associated symptoms when you have it helps us in diagnosis, SLE or lupus, like any fever, aphralgia or any pulmonary lesions, any cysts, any vascular disease, all those things will lead to any associated symptoms will lead to vascular disease. People coming with flank pain and oligury, anuria, always reload any obstruction, renal infarction or infection. They should have pain, fever or any decreased urena output. Anuria, if there is bilateral obstruction or severe shock, only then the patient will be, aneurysm, the patient will pass urein at least 100 to 400 mL of urein, that is called oliguria. So treatment, main thing is any AKIF first clinical examination. Clinical assessment is the most important thing. Look for volume status, whether the patient is dehydrated, clinically u-limit or clinically deployed, volume depletion or hyperolimit. That is very important. Look for all the signs, the JVP, all the heart, sound, history, anything else is there. So any go-by clinical examination, that is very, very important. If somebody's clinical volume status is dry, then try to freeze them up. That is the most important part in any AKIF. Just we have to give a lot of fluids and make sure that you hydrate them very, very early. So identify volume status is very, very crucial for us. Then you look at what is the cause. Whatever is the cause I mentioned, look into the cause and then try to look at the cause and try to eliminate the cause for AKIF. Until you look at the cause and eliminate, you are not going to solve the problem. So as I told you fluid resuscitation and urgent imaging, only to root any bladder outlet obstruction. So treatment, whenever the patient is admitted, make sure close monitoring of intake output, hourly urine output chart is very important. Don't delay in getting an effort-concept if the patient remains oliguric for a long time or has any proteinuria or microscopic imagery. So this, when somebody has a proteinuria, microscopic imagery and not passing it, first thing comes as RPGN, rapidly progressive, glominal feathers, or vascularity is the most common. But don't delay in somebody's oliguric ulcer. So relief obstruction in case of bladder audit obstruction, a simple foolish catheter in case of V-page is more than enough. And any early initiation of dialysis in case of persistent oliguria or acidity. So nowadays dialysis we don't wait for creatinine, as I told you, to become urea becoming 150 or 200 or creatinine becoming 5 or 6. We just go by hourly urine output in ICO if the output is lesser. Early initiation of dialysis is a must. The more you delay, you know, the more acidosis patient has, the more complications the patient is going to lack. So early initiation of dialysis based on urine output and ABG is the best thing to do. We should not hesitate for renal biopsy in patients with any unexplained renal failure. Somebody who comes suddenly with 5 or 6 creatinine, then we should not wait to look at. So we do a lot of renal biopsies and in case of unexplained renal failure, we just have to do renal biopsy immediately. There is something, this is a normal kidney, what it looks like. So you can look at the dilatation of the Pelve Euclid system. This is somewhere in moderate adenophoresis. In segar it's a gross dilatation. Whatever is the cause, it's a gross thing. So probably my friend and colleague will talk about more in emergency neurology later on. So let me come to hypokalemia. What is hypokalemia? Potassium being less than 3.5. We tell us hypokalemia. So what happens in hypokalemia? A lot of hypokalemia is very bad. We look at the ECG, we look at the classical, we have lowering and broadening of the T wave happens. Then slightly there will be a, later on there will be a prolonged cutie interval. So this is the ECG changes what we see commonly in hypokalemia. You don't see commonly in all mild hypokalemia. So if you have hypokalemia only, we can see easy changes unless you look for it. Because otherwise you just miss around lowering and broadening of T waves and the prolonged cutie interval. So what happens in hypokalemia if you are not treated? So you will have severe cardiac arrhythmia, respiratory failure and apathetic encephalopathy. So people with older patients or patients with heart diseases, patients on deoxyne and patients on arrhythmic drugs, they are all prone for arrhythmia. So what is potassium loss? When you talk about potassium, you know it's around 3.5 to 5 is a normal range. When somebody is potassium, you know it's around 3.5, it is not normal. So how much you think is a potassium loss? It's just not around 10 or 12, 20 or 30 milliquarets. When somebody's potassium is around 3, there's a potassium deficit around 125 to 250 milliquarets in a 70 kg. So this is a replacement, you have to do it. So in case of potassium is around 3, the loss is around 150 to 400 milliquarets. In case it is around 2.5, it is around 300 to 600. With 2 potassium, it is around 500 to 750. So these are the losses we have to replace when you look at the number here. So we are just not giving the number of 10 ml three times a day or 20 ml three times a day. We're not going to help you in any way. So we have to look at the replacing the losses over the potassium losses that are happening. So first step in what we do is identify again, stop ongoing losses of potassium. If somebody is using diuretics or lagerative, please stop that. Use in case you still need a diuretic, use a potassium sparing diuretic like spinal lactone. If diuretic therapy is required, treat diuretics or vomiting if somebody has, and use H2 blocker to decrease any, if somebody has a nasogastric suction loss, try to use these drugs, or control hyperglazinga if glucosuria is present. So second step, then you have to replace either orally or IV. Oral potassium, we know it comes as potcloth. So every 15 ml, 15 ml comes as 20 ml equivalent. So as I told you, you can get 20 ml three times a day or six hourly, but normally this potcloth, when you give IDOS, they cause severe GI irritation. You can mix it with fruit juices. If patient is okay, you can mix it with fruit juices and then they can drink. Tablets are not available in India, but otherwise, you know, ADK is available, it gives us a 90 ml equivalent per 750 ml of tablet. But stick on to potcloth, but make sure that how you keep potcloth depends on the losses, how much of losses has happened. So it's very readily absorbed, large doses can be given safely. Only thing is, a lot of GI effect. That's the reason we ask them to take it at fruit juices and it may feel better. If somebody has renal tubular acidosis, also they replace it with potassium citrate. Liberally, always, this is the only time we tell them to eat a lot of fruit. Otherwise, you always stick on to don't take tender coconut, don't have a lot of fruits. So otherwise, this is the time, liberally you can have a lot of fruits. So IV, how do we give IV? You know, when you have a life-threatening condition, we need to give IV. As I told you, you know, take an ampoule of potassium. So normally, if you're having a peripheral line, don't give potassium very fast. Don't use peripheral line for a longer time. It's always dangerous. So but if you have a peripheral line, what you do is in case you want to give, if you think somebody's potassium is around 3, you want to give IV potassium. Try adding, you know, around 40 ml equivalents. You can add it in 100 ml saline or 500 ml bottle. But now what I do is what I recommend is you add around 40 ml equivalents in 100 ml normal saline and you give it around 5 to 6 hours. Because if you told in peripheral line, don't make sure you don't give potassium IV more than 6 to 8 ml equivalents per hour. That means if you add 40 ml equivalents in 100 ml, so you give it over 5 hours. So 100 divided by 5, it's 8 ml equivalents per hour. So giving 8 ml equivalents per hour, that is quite safe in a peripheral line. Okay, so that is very simple. I have concentration if you use, you know, around 60 ml equivalents also what happens is sygmy of phlebitis, sygmy of phlebitis. So make sure you, when you're using a peripheral line, use a burrata cannula and also make sure you don't add more than 40 ml equivalents in 100 ml saline and give it over 5 hours a very safe way of giving. And please avoid glucose containing fluid because again, they'll be shipped again. You can have apocalymia. So in emerges as it will be, same thing, take 100 ml bag, use 40 ml equivalents, ideal in potassium of 3 or something like that, 5 to 6. But whereas you need potassium is around 2, 2.5 where we need to give lot of IV potassium, better to give central line. In central, you can give up to 10 to 15 ml equivalents. Like same thing you can give, if you're doing, if you add 80 ml equivalents or you can give up to 20 ml or 25 ml per hour. So up to 10 to 15 ml equivalents per hour you can give only a central line. But stick on to 6 to 8 ml equivalents in 30 for a line. Infuse always with a larger central line. I've written as femoral because an emergency is very easy to insert a femoral. Juggler also femoral, whatever central line is quite okay.