Hyponatremia

foreign what's up Ninja nerds in this video today we're going to be talking about hyponatremia before we get started I want you guys to please if you guys do benefit from this video it makes sense it helps you please smash that like button comment down the comment section and please subscribe also I really suggest this I really think it will help if you guys go down in the description box below there's a link it'll take you to our website on our website we have some awesome notes illustrations that I think will really help you guys to kind of follow along with me as we go through this topic together and I hope at the end of this that you truly know and understand hyponatremia like that so let's go ahead and get started when we talk about hyponatremia one of the ways that I like to learn it is I like to learn it in the way that I think is diagnostically helpful there's a lot of different causes of hyponatremia there's a lot of pathophysiology and hyponatremia a lot of tests that you have to run so I like to kind of combine all of that I like to take a lot of the etiology the pathophysiology and the Diagnostics and kind of Clump it together and what I'll do is is we'll go through the diagnostic steps of how to determine someone's cause of hyponatremia in a way that I hope at the end of this will make pathophysiological and etiological sense I hope so so let's start talking about that so oftentimes as a patient generally come in with like features of hyponatremia like hey Doc I got the hyponatremias no no no they don't oftentimes it's asymptomatic it's an incidental lab finding right so you order a patient they get a CMP or a BMP and it comes back and that sodium is low well the question that you have to ask yourself is what is you know a normal sodium well generally it's like 135 to 145 so if it's less than that kind of lower limit of normal then it's abnormal it's a hyponatremia so oftentimes that's kind of how we go about this so if the sodium level in any of these cases we're going to talk about what these mean here in a second but if the sodium is less than 135 and this can vary from Lab to lab but often It's relatively Universal that 135 is the lower end of normal so if it's less than 135 that's considered to be a hyponatremia now the question that comes up here is okay we have a patient maybe they're asymptomatic or they're symptomatic and usually the symptomatics we don't see until they start really dropping down low it's like less than 120 and then you can start seeing things like seizures and cerebral edema risk of herniation headaches nausea vomiting Etc oftentimes when a patient comes in they get the BMP sodium comes back let's say 1 30. mildly low right so there's different levels to the lowneness of the hyponatremia so oftentimes they said 130 to 134 is like mildly low then we say 120 to 129 it's kind of like moderately low and then we say like anything less than 120 is severely low so if we have a sodium that's less than 135 the first thing that we want to figure out is is it real or is it a pseudo hyponatremia so how do I determine that one of the first tests that I like to check for is a serum osmolality and what the serum osmolality is going to do is going to tell me the tonicity of the blood so you know sodium sodium controls a degree of tonicity in the blood so if sodium is low then that would mean that the tonicity of the blood would be low because it's a factor of tonicity so that's that's true right and if that's the case we would want to know okay is it somewhere between like 280 to 295. so if the serum osmolality we're going to say in this case I'm going to put this Arrow here as it's going to be you have different types right so say that you order serum osmolality on a patient as a sodium of 135 it comes back and in this situation let's say that the serum osmolality is really High all right let's see here in this situation the serum osmolality is low and here the serum osmolality is normal okay and that number of osmolality is usually again a normal number is between 280 to 295. so if it's greater than 295 let's actually just write that here greater than 295 but we consider that a hyper osmolar or hypertonic type of solution well that's kind of odd because generally I just told you that if sodium is low hyponatremia that means that there's less tensicity of the blood if there's less tenacity of the blood it wouldn't make sense for it to be hypertonic so what could be a cause of hypertonic hyponatremia that means that there's something else that's present in the blood that's increasing the tonicity of the blood besides sodium but but the sodium is still low what is those things what are those things that are actually sitting here in the blood that's actually represent them in this kind of like black color here there's something else that's in the blood that's actually causing the tonicity to go up so let's see here in this pink color this is sodium here in this blue color is water and then here we have no idea what this solute is what are these things that's a great question so oftentimes it's really really hyperosmolar kind of molecules and the different types of causes for this I want you to think about whenever you have a hypertonic hyponatremious what is this called This is called let's actually write this down this blue color here this is a hyper tonic hyponatremia there's many different etiologies for these the most common ones that I want you guys to remember here is going to be something like whenever the patient has extremely high glucose levels when their glucose levels are super super high what are diseases by which you could see very high glucose levels things such as dka HHS which is hyperglycemic hypo osmolar syndrome those would be very very common causes right another one which may be less common but sometimes the patients are you know having experienced what's called high intracranial pressure they may receive something called Mannitol and Mannitol is a particular molecule that's very hyperosmolar and can definitely increase the tonicity of the blood even though the patient may have a low sodium less than 135 so Mannitol is another one there's other things that patients have received During certain types of procedures so especially look in a patient's history are they status post terp so so a transurethral resection of the prostate sometimes they can use things like Glycine and sorbitol all these other different types of molecules in that type of procedure and it can actually leak into the bloodstream and increase the tendicity of the blood even though the sodium is less than 135 so we don't really call this a true hyponatremia this is not a true hyponatremia in order to be a true hyponatremia you have to have a sodium less than 135 in your serum osmology has to be low because that means that there's no other confounding factor or molecule in the blood that's changing the tonicity and if it is you have to think about these so if I had a for example I get I get a BMP patient sodium comes back less than 135 I throw off a serum osmolality to see if it's real because I want it to be less than 280. if it's greater than 295 that's not a true hypotonic hyponym it's a hypertonic then I got to go looking into their BNP is their glucose really low check a point to care glucose did they receive any Mannitol lately did they just get a Turpin do they have any glycine or sorbitol that they were utilized during that procedure that might be their etiology another really important thing and I really want you guys to not forget this I'm going to add like a little kind of asterisk next to this is especially with glucose I'm not going to give you guys the formula because it's a it's a it's something that you can easily look up going to MD calc and what you can do is whenever a patient has an extremely high glucose which is a very common thing that you will see in practice you need to correct the actual sodium for the high glucose so there is a calculation that you will plug into MD calc and what it'll do is it'll actually take the patient's super high glucose let's say it's like 300 something and then they have a sodium of 132 if you plug it into this calculator they're true sodium after you correct for the hyperglycemia that's causing this tinicity to go up when it should be low it'll actually may give you a normal sodium so make sure you check that always do the sodium correction for hyperglycemia if this is a confounding Factor okay good there we're going to come back to the hypotonic in a second let's see if we go to this one okay truly if a patient has hyponatremia and it's that that's the thing that's actually causing the tendicity of the blood to go down there's nothing else then it should be hypotonic if it's isotonic so this would be what's called a let's do this in blue since we did that one in blue isotonic hyponatremia this is a lab error that's the way I want you to think about this one this is a lab error in other words the sodium in here and the situation which again is the one in pink this is the sodium this is the water the sodium is not really the problem it's not that that's like super low is there's another molecule that's present in the blood that's altering the lab's ability to capture the true tonicity of the blood let's actually represent that here so one of these molecules is lipids if patients have extremely high amounts of lipids or if they have extremely high amounts of proteins so in situations where patients have extremely high levels of proteins in their blood or lipids in their blood it causes a lab air that's what I want you to think about this isotonic hyponatremia lab air artifactual not real so what are the particular causes behind this my friends I want you to think about things like high lipids so if a patient has extremely high lipids in their blood hyperlipidemia that's one particular cause maybe check a lipid panel especially if you get a sodium less than 135 and the serum osmolality of we did that in like this maroon let's keep this in Maroon it's going to be somewhere between 282 295 so it's going to be in that normal range of the tonicity if lipids are a factor check the lipids look at their history also proteins so high amounts of proteins there's so many diseases so think about multiple myeloma oh that's a big one Walden strum's macroglobulinemia oh that's a son of a gun isn't it so waldenstrom's macroglobulinia multiple myeloma there's even another situation here which you can even see if a patient just recently got IVIG IVIG is an antibody it's a protein so look in their history did they recently receive any IV IG therapies and boom you'll list it right from the get-go a patient comes back they have a serum sodium that's less than 135 you say okay they may have hyponatremia what do I do send officeromosomes in a theoretical world perfect kind of world if sodium is the primary problem where it's there and it's low it'll drop the tendency to the blood hypotonic hyponatremia if it's hypertonic so the tendency is high there's something else that's increasing it glucose Mannitol sometimes even urea patients take urea as well as other things such as if they just got a terp like Glycine and sorbitol okay if that's the case that's a hypertonic hyponatremia that's a pseudo that's not real if you check it and the actual tonicity is normal again it shouldn't be normal it shouldn't be high it shouldn't be normal it should be low there's something else there's a lab error there's an artifactual problem here and that is usually due to lots of lipids and lots of protein so check their lipid panel and check for maybe an electrophoresis or diagnose them with multiple myeloma while Insurance macular Global anemia check to see if they got any recent IVIG now if the real situation comes up where the patient actually has a serum osms that's checked and when their Serum osom is checked it's actually between what it's not greater than 295 it's not between 280 and 295 it's less than 280. so this is a hypotonic hyponatremia this is where the money is my friends and this is where we'll be focusing on the most of our lecture so in this point it is hypo tonic hyponatremia and in this point here we're going to move on to many different causes and this is the true causes of hyponatremia so once we get to this point here where we've determined that the patient is a hypotonic hyponatremia I'm going to move on to the next test okay so I hope that part of this kind of like lecture made sense where we start off we check a patient's sodium okay and and also again you're going to find a very important point out of all of this that when patients have again a sodium less than 135 the most common causes of a true hypotonic hyponatremia is where they have a dilutional effect there's lots of water more water these kind of molecules here in their blood than there is sodium do you notice that how in these ones it was pretty normal they were pretty close so there wasn't a true differentiating difference between sodium and water and the hypertonic or isotonic hyponatremia it was the other molecules that were present that were changing the tonicity in true hypotonic hyponatremia do you notice the difference here look at the amount of sodium molecules I have less than the amount of water molecules oftentimes this is the true cause and how do we figure that out well we do something called checking about if the ADH is on or if the ADH is off let's get into talking about that all right my friend so now we gotta talk about hypotonic hyponatremia so we went in we checked the BMP maybe they were symptomatic they were having seizures cerebral edema features or they were asymptomatic and we just ordered some routine lab work sodium came back less than 135 okay and again we have the mild moderate and severe again just to remind you 130 to 134 mild okay 120 to 129. it's like moderate and then if we get all the way down to less than 120 that's pretty severe that's when you start seeing symptoms but either way we got this hyponatremia let me check the serum osmolality to see if it's a true hypotonic hyponatremia meaning that the sodium being low is the problem of changing the tonicity of the blood if it's high that means that there's a lot of some other kind of like tonic molecule in the blood that's increasing the tenicity things like glucose Mannitol or things after a terp like sorbitol and glycine if it's normal tonicity that means that this is a lab or artifactual type of problem and this is such as high lipids High proteins that you see in things like multiple myeloma Walden strums macroglobulinemia and IVIG therapy but if we get it and it's actually less than 280 that means that this is a true hypotonic hyponatremia and that means that there's very little sodium and it may be an increase in the relative amount of water within the body but either way there's going to be more water in the body than there is going to be sodium all right now that leads us to the next thing whenever a patient develops these kind of hyponatremia problems oftentimes the cause the source of it the most common cause is that the ADH levels are pumped up through the roof so oftentimes the most common cause here is that the patient has very high ADH levels and then there's very little causes only a few where the ADH is either we're actually just going to use an X the ADH is off okay so it's either the ADH is on or the ADH is off and if you wanted to just to make it a little bit easier here is that the ADH is like really low we're producing very little 88 just so we keep the arrows kind of the same here all right so that leads to the question then ADH antidiuretic hormone what stimulates it what's causing it to be produced because if I know what's causing ADH to be produced I know what the causes are and I can evaluate those causes right so that's where we got to get into all right so ADH has a couple different stimulatory factors let's use this marker to kind of highlight those factors so first we know that the ADH is produced by what so you have neurons in your hypothalamus and they're kind of extending down to the poster pituitary and they release a particular molecule here called ADH what's another name for ADH just in case different textbooks say this vasopressin just remember that another name is vasopressin so ADH is produced by the poster pituitary but we got to know what's the trigger that makes adhp produce that goes down to the kidneys and produces this type of change that's the important question okay that's the million dollar question the stimulatory factors the stimulatory factors of ADH is what well one of them is going to be hypovolemia now here's the thing when a patient is very volume down hypovolemic there's different ways that we can look at this sometimes when you're very very hypovolemic the amount of water that you have within the body and the amount of sodium within your body gets really low and it changes the plasma osmolality oftentimes we would say that the plasma osmolality in a hypotonic hyponatremia patient is low right so that means that there's more water than there is sodium but we have to figure out how we got to that point how did the patient get to that point where there was maybe a little bit more water than there was sodium it's because of ADH well something had to stimulate ADH to just kind of turn on and one of the reasons is that the patient is volume depleted we'll use down arrows that they're volume down if the patient is volume down or volume depleted that tells ADH hey ADH you better get stimulated and start producing some kind of you know important effect here well the ADH then says don't worry bro I got you and ADH runs down here to the kidneys and it gets to the collecting duct when it gets into the collecting ducts it binds onto these vasopressin receptors you know these are V2 receptors vasopressin receptors and what it does is we're not going to go through the whole mechanism but it stimulates the production of a g protein pathway which activates and stimulates these special blue channels here what are these channels these are aquaporins aquaporin 2 and 4 and get activated now normally what happens is what happens is your body tries to go into this interesting mode so normally when you're hypovolemic your kidneys let's say that they just didn't care about hypovolemia ADH wasn't even present you just continue to pee out a certain amount of volume and you wouldn't try to retain any of that volume and you get more hypovolemic well since ADH is on what happens is all these water molecules that are then flowing through the kidney tubules they're about to get peed out they're like going to the toilet and then all of a sudden it gets to the collecting duct collecting such as he says you ain't going on toilet y'all better not be in that toilet and then what it does is it pulls this water through the aquaporin units and then when it pulls the water through the aquaporin units it pulls this water right into the bloodstream and so you reabsorb a very large amount of water so what's going to happen here you're going to reabsorb a very large amount of water because your problem was that you were volume depleted if I bring a lot of water into the actual bloodstream I'm going to replete my volume status but what it does is it increases the amount of water molecules than it does the sodium molecules and then it starts to deplete this out and then if you get this type of effect what is this called my friends hyponatremia so then the overarching theme out of this is that this may trigger a low sodium we good all right but here's the other thing here's the other Factor then if ADH is on and it works in the kidneys to reabsorb water lots and lots of water that means that the water that was supposed to go into the pp did not go into the pp and that means that you're going to have very little water and instead you're going to have a lot of other things in here so you might have some sodium in here you might have some potassium in here you might have some urea in here lots of other solute molecules that change the osmolality in the urine so we know the serum osmolality in this situation here so if we were to think about this one we already know that the serum osmolality was low why is it low because there's more water than there is sodium there's less tonicity what about here now there's lots of things like sodium water I'm sorry sodium potassium lots of urea a bunch of different metabolites but then what about water very little water so now it's going to happen to the urine osmolality it's going to be very high so isn't that a very interesting thing so that we say here when ADH when ADH is really really high let's actually do it like this one ADH is on if you will or it's very high because there's a volume depletion problem then what does that do to the urine osmolality what does it do to it it increases the urine osmolality because you have less water and lots of salt lots of potassium lots of chloride lots of urea lots of solute molecules here that increase the tonicity to what point greater than 300 is what we usually utilize there's a various various numbers right so sometimes we even just say greater than 100 but oftentimes for it to be truly like high we say greater than 300. now that's that situation okay well before we keep going on we know that that's on one effect of the ADH so one effect of the ADH and the most profound effect on the ADH is that it is going to try to increase the reabsorption of water right you know what else it does it's really cool ADH is a very smart son of a gun it tells the hypothalamus it says Hey hypothalamus I want you to stimulate an increase in thirst I want you to cause the patient to become more thirsty have an increased desire to drink fluids and so then if they drink more fluids what are they going to do so then now here's the second effect the second effect here is that I'm going to increase the consumption of water I'm going to increase my thirst mechanism and if I increase my thirst mechanism I'm going to have more water running through my git if I have more water running through my git I reabsorb more water across the git because if I'm drinking more I'm going to absorb more of that water into my git increase the water amount in my bloodstream to replete my volume but then I dilute out my sodium causing a hyponatremia isn't that a cool concept there so there's two effects of ADH one is it causes reabsorption of water across the kidney so you retain more fluid don't pee it out and the other one is it makes you thirsty so that you drink more water to replete your volume that's so cool all right well that's that's the mechanisms there what you know that's not the only thing another very powerful stimulating factor of ADH is when you have this term can be sometimes like Loosely utilized I like to just use it as a term of blood pressure cardiac output but oftentimes when a patient's effective arterial blood volume you may use hear this term a lot in this situation I like to just think about this as BP their BP is on the lower end they're cardiac output so let's actually put let's put both of those factors there so their cardiac output or their blood pressure is on the lower end they're not circulating as much volume through their blood vessels so the amount of volume in their blood vessels is less they're not truly in a volume depleted state they're actually hypervolemic some of these patients who have a decreased effect of arterial blood volume it's just the amount of volume that's supposed to be in their blood vessels is leaked into other areas it's in their tissue spaces it's in their lungs it's in their legs it's in their abdomen so a lot of these problems is that the fluid is not then they're vessels which actually controls their volume their blood pressure and so their blood pressure gets lower well if that happens ADH gets stimulated increases the reabsorption of water causes you to become thirsty let's actually put this blue arrow over here causes you to become thirsty increase the reabsorption of water across absorption of water across the git and you know what else it does it binds onto it binds onto these vasopressin one receptors so these are V1 receptors and when it acts on the V1 receptors it stimulates these puppies and causes the blood vessel too vasoconstrict some of you guys if you guys have heard of this there is a drug that we give to patients when they are hypotensive and their blood pressure is low guess what that drug is vasopressin guess what vasopressin is ADH so do realize that the ADH at higher concentrations can have a very strong vasoconstrictive effect and so what it can do is it can actually cause Vaso constriction and that will increase your blood pressure because one of the problems that the patient's blood pressure is on the lower end their cardiac outputs on the lower end their effective arterial blood volumes in the lower end I can do a couple things one is I can strict their blood vessels to increase the blood pressure and I can actually pull more water into the bloodstream and if I increase the amount of blood volume I theoretically increase my blood pressure so you understand how these mechanisms are working right there's one more etiology or one more trigger here and the last trigger here is actually What's called the renin Angiotensin aldosterone system is a very powerful stimulator and you can see this in a lot of different triggers sometimes if a patient isn't perfusing their kidneys very well so they're not getting a lot of blood pressure or perfusion to the kidneys that'll trigger the renin angiotensinaldoctrine system sometimes in other situations where their GFR may be affected or they have a lower GFR that may trigger the actual written Angiotensin adoption system if the sympathetic nervous system becomes activated that can trigger the red and angiotense and aldosterone system there's many different things but the random Angiotensin aldosterone system more specifically more specifically Angiotensin II is a very powerful stimulator of ADH and whenever that happens what ADH will do is it'll increase water reabsorption it'll increase the absorption across the git because you're thirsty and it'll increase your blood pressure all of these things are trying to get more volume more circulating volume within the actual bloodstream to perfuse the kidneys better or to increase the patient's blood pressure so oftentimes whenever a patient's volume depleted are their effect of arterial blood volume is low the written angiotens and aldosterone systems also generally activate it but these are the three primary triggers that turn the ADH on so that begs the question then what are causes of volume depletion what are causes of a low effect of arterial blood volume what are causes of like this inactive disactivated reniniotensinaldosterone system well there's many different causes here my friends so I'm not going to go through them all because we're going to talk about them in a little bit but some of the things that I would want you guys to think about is when a patient is extremely volume depleted they're losing volume from the body this could be in situations such as vomiting this could be in situations such as diarrhea this could be if they're I mean theoretically if you really think about it could be bleeding if they're truly bleeding this could be in situations such as um a pancreatitis as well so sometimes pancreatitis can cause a lot of third spacing of fluids into the interstitial spaces this could be things like you're actually giving them medications that cause them to pee a lot so diuretics could definitely be a Cause you can even see this in conditions such as cerebral salt wasting and you know what else another one is basically whenever they have alterations within the amount of aldosterone and so sometimes you can see this in situations such as Addison's disease so whenever they're not producing a lot of aldosterone so there's things like that where their volume down is the problem another issue is that what if it's the low effect of arterial blood volume so what if it's the effective arterial blood volume or the cardiac outputs that it's really low and that's the problem well this could be things like CHF right where a patient isn't circulating a lot of blood because their heart isn't pumping very well or it could be in things like cirrhosis or you can see this in things like nephrotic syndrome and sometimes in these particular diseases what happens is they have a lack of albumin And So It causes a lot of water to actually kind of like leak from their vasculature and so their true amount of volume that's present within their vasculature is lower because they're leaking some of it out because they don't have the albumin to hold that into the vessels which is kind of a cool concept we'll talk a little bit later there is one other trigger for which ADH is turned on but it's not due to a volume depletion it's not due to an effect of arterial blood volume problem it's not to do an alteration of the renangiotensinound system it's actually something where there's an inappropriate production of ADH and we'll talk about that a little bit later okay let's come to the last thing here where ADH is actually off this is the weird ones they're the cool ones but they're the weird ones and so oftentimes the cause is behind someone having less ADH would do what let's think about this if you don't produce ADH are you going to squeeze the blood vessels no so they're not going to have as much of a vasoconstrictive effect their BP won't kind of increase as a result of that are you going to have as much of a thirst mechanism theoretically to drink a lot of water Maybe not maybe not so you might not be absorbing a lot of water across the git okay here's the big thing and this is one of the coolest parts of this to be able to differentiate if it's a patient's hyponatremia ADH dependent meaning it's on or is it ADH independent is it off it ADH is off or it's not being produced a lot will it act on the V2 receptors on the kidney and the collecting duct no will you reabsorb water across the uh you know the collecting duct no if I don't reabsorb water across the collecting of well I have a lot of water present then in my urine yes I will because ADH isn't on it's not pulling a lot of this water across so in this situation here my friends where ADH is off if you will where ADH is off we're going to use the down arrows and we like to say theoretically when the urine osmolality is on the lower end so we like to use the number less than 100. that's why I was saying but technically if it's greater than 100 it's technically you could say that your osmolality is in the higher end but we like to go with the upper end greater than 300. this can vary from textbook to textbook though remember that but in this situation right away I can tell if this is the cause so I checked the serum osmolality to figure out if it's a hypotonic hyponatremia is it real okay that's what I told you before sodium is less than 135 check the serum osmolality if it's high it's not real it's glucose Mannitol things after a terp if it's normal not real it's things like high lipids and high proteins artifactual lab adder if it is less than one uh 280. okay this is a real hypotonic hypnotremia okay well then I need to determine is the ADH on because then this is all the causes of ADH are on that's a lot of them or is the ADH off and that's very little causes and that's actually really easy to differentiate well check the urine osmolality if the urine osmolality is really high I'm I'm resorbing reabsorbing and pulling a lot of water across my kidneys back into the bloodstream and that means ADH is on if I'm not pulling a lot of water across my kidneys into the bloodstream and I'm peeing a lot of that water out that means 80 inches off and if ADH is off there's not a ton of causes thank the Lord for that and the primary things that I want you to remember without getting too complicated because we don't know a ton of the pathophysiology behind this is this could be things like primary polydipsia they used to call this psychogenic polydipsy but I don't think that they liked what we call it our patient psycho so primary polydipsia also is sometimes referred to as psychogenic polydipsia another one is called the T and toast diet the tea and toast diet another one which believe it or not can be sometimes relatively common in our society beer potomania and then one last one is severe end-stage renal disease oftentimes these patients are likely on hemodialysis okay of some type they're likely on dialysis so you'll see these as the particular etiologies if the ADH is low and that would be something that you can kind of sift out from the patient just by history and talking to them a little bit you could sift that out but then again check that you're not you're an awesome it doesn't leave you with as many causes because I didn't even list all the causes here this is a plethora of causes that we're gonna have to investigate so if you get the adh's low and the urine osmolality is very low it leads you to these and this is often history that will elucidate this and that's it all right so we've gone through we've said okay the patient has hyponatremia I checked the serum osmolality to figure out if it's real I checked this urine osmolality to see if ADH is on or ADH is off and that determines the different types of causes now the next thing is is how in the world am I supposed to figure out out of all of these which one it is and if it's all of these you said history Zach I'll go into this through a little bit more detail but Zach can you truly please explain to me in a couple ways the pathophysiology of how these things cause ADH to be produced in high levels how I can differentiate these from one another and is there a volume way that I can determine this and Zach you also didn't mention the inappropriate ADH production can you mention that as well I got you fam let's go talk about that all right my friends so now we've gotten to the point where now we know okay the patient has an ADH dependent hyponatremia meaning ADH is on it's really really highly elevated so something is causing a volume depletion problem something's causing an increased effect over us or a decreased effect of arterial blood volume where they're not having a good cardiac output or blood pressure that's adequate to be able to generate this or there's an you know undesirable activation of the Renaissance system or a desirable one that's causing a lot of this ADH to be produced in high amounts reabsorbing lots of water across the kidneys and if it is it's increasing the amount of water in the bloodstream decreasing the amount of water into the urine so it increase it does what it increases the urine osmolality and decrease the serum osmolality right that's for ADH dependent ones now we have to then go and say okay if the patient is volume depleted what could be the causes behind volume depletion and again is can you explain just a little bit more Zach maybe about how it causes some hyponatremia and other factors so the first one that I want you to think about so let's think about if the patient is volume depleted right so the patient is volume down so whenever the patient is volume down that means that the amount of sodium within their body the amount of water within their body are both depleted okay that's really important to remember so when we talk about this the pink is representing the sodium right so in this situation the amount of sodium within their body is depleted and the amount of water within their body is depleted but which one's depleted more sodium is depleted more okay so when this happens we have to think about the patient is losing volume from their body but they tend to be losing a little bit more sodium in their of their volume losses than they are losing water and then ADH gets turned on because their volume depleted they reabsorb a lot of water and if they reabsorb a lot of water they dilute their sodium even more so here let's think about those causes so the way that I like to think about this is if it's a renal cause or an extra renal cause don't worry you're like why I'll explain a little bit it has to do with another test that we can order called a urine sodium we'll get to that in a second but for renal causes there's a couple different reasons why this can happen so one of these that I want you guys to think about here is if a patient is taking something called a diuretic so if a patient is taking what's called a loop diuretic this could be one potential etiology and let me explain why it's not as common if you're taking this very consistently so Loop Diuretics intrinsically if it's like a couple time usage they don't cause like true hypo they can cause hyponatremia but it's not as severe as the next diuretic that we'll talk about but if a patient is taking a diuretic Loop Diuretics do have the possibility of causing hyponatremia so let's actually put that as like a category here is the first etiology for volume losses from the kidney where you're losing volume sodium and water from the kidneys so this could be due to diuretic usage now when we talk about these diuretics the first one that I want you to remember is the loop diuretic so this is things like furosemide torsomide bumetanide ethocrinic acid what they do is they inhibit the sodium chloride sodium potassium to chloricotransporter you can't reabsorb sodium all right that's inhibited so sodium stays here in the tubules and then you lose lots of sodium into the urine so lots of sodium loss are going to occur here but then what else is going to follow this especially if you're doing this pretty consistently what's going to follow because you didn't reabsorb it here in the descending limit of the loop of henle because that the counter current multiply mechanism when sodium gets pushed out here water likes to leave that won't happen so water stays within the kidney tubules and it also my friends get lost into the urine so you're losing sodium and you're losing water you just happen to lose a little bit more sodium than you do water but you're losing a lot of sodium in your urine so if you're losing the amount of sodium within your urine is very very high what does that do to the urine sodium it increases it so if the urine sodium goes up if the urine sodium is really really high that tells me that that's a renal loss and that's one of the causes Loop Diuretics interesting okay let's go to the next one what if someone is taking uh what's called a thiazide diuretic so a thiazide diuretic is another one and if they're taking a thiazide diuretic that that inhibits this sodium chloride co-transporter in the early distal convoluted tubule and that means that sodium will not be able to be absorbed in this part and then subsequently you won't be able to reabsorb any water as well right so you'll lose sodium and water into the urine and if you lose lots of sodium in your urine what's happening in your urine sodium oh my gosh it's going to go up let's actually just to highlight this again the urine sodium is going to go up well that's interesting that's another test that I could order okay let's see if a lot of other diseases that are within the renal volume loss have this High urine sodium okay the next problem here is we're volume depleted and it's because of diuretics huh what if what if what if I actually didn't produce a lot of aldosterone okay well that's an interesting concept what if the problem here is low aldosterone so it's low aldosterone well if I don't produce a lot of aldosterone very low levels of aldosterone what does aldosterone do oh yeah aldosterone works over here and what aldosterone does is it actually stimulates a lot of different pumps like the sodium the Enoch channels it also stimulates the potassium channels it also stimulates the formation of the sodium potassium ATP aces all of those things and so what it's supposed to do is is it's actually supposed to help you with the reabsorption of sodium that's what it's supposed to do right just like just like the thighs eyes and just like the um Loop Diuretics you're blocking the sodium reabsorption well if I have low aldosterone am I going to be able to stimulate the sodium Transporters to be formed am I going to be able to stimulate the sodium potassium pumps that I can reabsorb the sodium no so because I have low levels of aldosterone low levels of aldosterone I'm not going to be able to stimulate all these channels and so because of that I'm going to inhibit these channels can I absorb sodium no and can I excrete potassium no so then I lose a lot of that sodium in the urine and then some water loss as well so low aldosterone could be due to an actual like Addison's disease that could be one particular problem you know what another one is we we think it actually may be related to this it also may be related to a problem with um the sympathetic nervous system regulation of the kidneys as well but there's one other disease that may be related to low aldosterone because one of the treatments for it is actually aldosterone and this is specifically called cerebral salt wasting it's a very common disease that I see a lot in my patients who have subarachnoid hemorrhages a lot of the times and so there's a large like actual trauma a lot of like problems that actually occur intracranially that may trigger this low aldosterone production and may lead to a lot of sodium wasting into the urine so their urine sodium is going to go through the roof and again with all of these situations you're supposed to be reabsorbing water with the Sodium so you lose sodium and you also lose some degree of water but not as much as the sodium loss and that's why the patient's total sodium is much less than their total water balance okay now these are the theoretical problems that I want you guys to be thinking about with this is there any other kind of renal losses these are the primary ones that I really want you guys to remember so I want you to think about Loop Diuretics thiazide diuretics problems that cause a reduction in aldosterone such as Addison's disease cerebral salt wasting problems these are the big things there is one more um type of problem here where you also could see this generally it's kind of a treatment process so sometimes you can actually see this with a other diseases but we're not going to go through that as much here we're going to talk about primarily these are the primary renal problems that I want you to remember all right so that's the first thing so now we check a urine sodium the urine sodium is high it then tells me that this is a renal loss that's what I want you to associate this with if the urine sodium comes back really high I want you to say okay than it is a renal loss and if it's a renal loss then the next thing I want you to think about here is if it's a renal loss then I want you to think is it due to diuretics or is it due to low aldosterone Okay so we've gone through sodium slow check the serum osms see if that's low check the uranosomes if the uranosomes is high that means ADH is on if ADH is on check the urine sodium if the urine sodium is high that means that the person is losing volume but it's losing it from their kidneys think about diuretic usage and think about a low aldosterone all right so let's say that you kind of go through this you go through the history you're not able to completely elucidate if it's diuretic related or if it's low aldosterone related generally histories should be good enough but if it isn't think about this with diuretics what does it do to your electrolytes it kind of Alters some of your electrolytes yeah so it definitely does alter your electrolytes versus aldosterone that might also alter some of your electrolytes and your acid-base balance as well so here's what I want you to think about I want you to think about two different molecules potassium and then pH with diuretics what does it do to the potassium it causes potassium wasting so really that Loop Diuretics thiazide diuretics and even Carbonic anehydrase Inhibitors diuretics they also cause they all cause potassium wasting well if that's the case then Loop Diuretics and thiazide diuretics are going to cause low potassium within the blood that's going to be low whereas low aldosterone what did aldosterone do it inhibited the actual potassium pumps so remember aldosterone low adashron leads to inhibiting the enact channel so you don't absorb sodium so sodium is lost into the urine urine sodium is high it also inhibits potassium excretion so you don't you don't actually excrete potassium so potassium goes up right so in that situation aldosterone the potassium should go up okay diuretics they actually cause a lot of bicarb loss and proton loss I'm sorry they actually cause proton losses into the urine so since they cause proton loss into the urine what are they due to the actual pH they're causing metabolic alkalosis so they will cause a metabolic alkalosis because they cause proton loss now with the actual low aldosterone they're responsible aldosterone normally stimulates proton excretion if you have less aldosterone can you excrete protons no so the protons build up in the body buildup within the blood and cause metabolic acidosis metabolic acidosis okay my friends all right so the next thing here is we talked about the volume depletion causes from a renal point of view what about the volume depletion causes from an extra renal point of view so in this situation here we now go on to talking about okay it's not the kidneys that are responsible for losing the sodium in the water it's something else that's causing this so what if the patient is losing sodium and water not from their kidneys or losing it from other sources so in other words they're losing blood again not as common but something to consider bleeding that would definitely be one that I want to keep in my list so bleeding would be definitely one okay so let's add that one in what about if they're losing tons of sodium and water from their actual skin burns excessive sweating so that would be another one so if a patient has very very intense Burns or sweating really really bad sweating this can also be potential triggers so lots of burns lots of bleeding that could be one another one what if they're losing lots of sodium from there upper GI tract in their lower GI tract so they're having lots of vomiting or they're having lots of diarrhea these could also be potential triggers and the last one I told you this is an interesting one where the pancreas becomes so inflamed it releases a lot of like systemic mediator molecules that cause inflammation causes vasodilation leakage of fluid out of the actual capillaries and into the interstitial spaces you can see this in pancreatitis so you can also see this in pancreatitis now my next thing that I want you guys to think about is okay this is an extra renal loss well Zach said that the renal losses cause urine sodium loss okay well in this situation you're not going to see a lot of urine sodium lost in theoretically right absolutely there's one exception that's vomiting I'll briefly explain it but for the most part in all of these you're going to see primarily no excessive loss of urine sodium so how do I determine that okay in this situation here the kidneys are working okay no Transporters in the ascending limit Loop of Henley the early distal convoluted tubule none of the problems with aldosterone are present so the kidneys are intact in other words they're reabsorbing sodium here there's no Loop diuretic inhibiting this right so sodium is being reabsorbed here sodium is being reabsorbed here sodium is being reabsorbed here there's no defects within Loop Diuretics or low aldosterone that's the problem here okay and so because of that you're not losing a ton of sodium in the actual urine that's one particular thing but here's here's another thought process is that all of these things such as bleeding Burns sweating vomiting pancreatitis they cause volume depletion when you cause volume depletion what does that do to the ADH what is it an ADH it increases the ADH presence and ADH will then stimulate water reabsorption right so the problem here is that you're not really going to be having a lot of sodium loss that's actually going to be present within the urine because you're reabsorbing sodium perfectly and all of these places that you weren't when it came to diuretics or low aldosterone so in this situation what happens to the urine sodium the urine sodium is going to be watch my friends it should be on the lower end it should be on the lower end and again these numbers can vary from textbook to textbook sometimes they say like a urine sodium greater than like 20 sometimes they'll say 40 urine sodium less than 20. so it obviously varies from textbook to textbook I'll just say from the textbook that I got usually we say urine sodium greater than 20 and then a urine sodium less than 20 would be considered that lower end oftentimes we may go a little bit higher for this one to go up to 40. but that's the concept that I want you guys to understand here is that in these particular etiologies they're not altering the effect of the reabsorption of sodium the kidneys are intact they're working they're reabsorbing sodium fine and they're even reabsorbing some of the water so again this affects the dilutional effect of the blood right so then if you look at the bloodstream out of this you're going to have again the problem here is that you're losing sodium from all of these other sources your kidneys are doing the best they can to reabsorb some sodium but they're reabsorbing a lot of water and so then again when you look at this you're losing lots of sodium from bleeding Burns sweating pancreatitis diarrhea vomiting but then your kidneys are on trying their best to reabsorb some sodium but it's not going to be enough but they are reabsorbing a lot of water and then again what is the effect here hyponatremia now another thing that obviously you could do here is if a patient's bleeding figure out their bleeding source so obviously scan them look for them do a fast exam try to find out where the bleeding is coming from if they're sweating that's obviously pretty obvious if they have burns on their body that's pretty obvious vomiting again history but if you really want to go the route that sometimes they may ask in the exam potentially is that vomiting causes a lot of proton losses so what would that do to the pH of the body it would cause a metabolic alkalosis so again think about that think about checking for a metabolic alkalosis whereas with diarrhea you're losing a lot of bicarbonate in the actual poo and if you're losing a lot of bicarbonate what does that do to the pH it drops the peach and causes a metabolic acidosis and so check for a metabolic acidosis so these are the things that I really want you guys to think about when it comes to the source of again why is the ADH on is it on because you're losing volume from the body and that excessive loss of volume is causing 80s to be turned on and to reabsorb a lot of water across the kidneys the git and to get your water volume to come up in the body depleting the sodium causing hyponatremia if that is the case what's the cause of the actual volume loss is it because your kidneys are peeing out tons of sodium and water if it is think about diuretics and low aldosterone check the urine sodium because they're peeing out a lot of sodium if the kidneys are intact there's no kind of drugs or low aldosterone that's causing a problem here and it's an extra renal sodium water loss then think about bleeding Burns excessive amount of sweating from fevers or also losses from the git vomiting excessive NG tube suction as well as diarrhea and then the other one pancreatitis now I did mention really quickly that vomiting has a little slight exception to it I'll put a little asterisk next to it that vomiting causes a metabolic alkalosis as compared to diarrhea which causes a metabolic acidosis when patients develop a metabolic alkalosis one of the ways that their body tries to compensate is their kidneys try their best to excrete what to excrete bicarbonate and so one of the things that happens here is of the actual vomiting will try to cause it'll try to stimulate the kidneys to pee out bicarbonate but you know what happens when you try to pee out bicarb to try to improve so you're trying to pee out a lot of bicarb and if you try to pee a lot of bicarb that'll try to actually help to bring the pH back down because if you're losing base then you're actually going to cause the pH to come down but you know what else happens whenever you actually have this process whenever you scrape bicarb guess what unfortunately you excrete it with sodium and so sometimes as a result the sodium may be a little bit elevated because it's a compensation mechanism to the metabolic alkalosis so do be careful with this one on the exam yes vomiting is an extra renal loss you lose a lot of sodium and you lose a lot of water from vomiting that's the source but their urine sodium is one of the few exceptions where it may not be low and the reason why is they have a metabolic alkalosis their kidneys compensate by causing them to excrete bicarb when they excrete bicarb they also excrete sodium so this is the only exception to the extra renal ones that you could potentially see in the exam that I don't want you to forget okay that covers the volume down problem now we go to the next situation which is what if the patient is volume up all right my friend so the next situation is if the patient's volume is super up all right and now this may seem a little odd so the patient is volume up Zach I thought that you know the patient has to be volume depleted and that's one of the stimulators of ADH production if ADH is produced it'll you know that'll cause one of the factors of hypernatremia we talked about that yeah well here's the weird thing I use the term low effective arterial blood volume right I use that terminal another way here's what I want you to think about when you hear of a patient who is hypervolemic this is often the patient population of a low effective arterial blood volume so that's the other way that I want you to remember that so I'm going to write that down here like on the side here is I also want you to associate this as being the low effective arterial blood volume or that low cardiac output kind of low blood pressure state right really really important now when a patient is hypervolemic okay we'll talk about what that looks like and we'll even talk about like a volume depleted or volume down patient will look like like on the physical exam things that they could ask you to also help you to point to which one of these it may be which can be a very challenging thing uh in in the actual true reality but I'll give you guys some tips but in a patient too is volume up or hypervolemic it's a very interesting patient population so in this situation they're total like sodium believe it or not they're total body sodium may actually be just a little bit elevated so in this patient population and you're like wait wait wait wait wait is that what yeah I know just go hang with me for a second their total body sodium may be a little bit elevated in the normal patient but their total body water is through the roof now that includes what now remember when I talk about this like I'm not just talking about it within the vasculature I'm talking about this within the actual interstitial space because you're saying Zach there's a lot of water in there their their their actual vessels it could be but oftentimes the effect of arterial blood volume their cardiac output their blood pressures on the lower end some of this water may not only be in the blood vessel some of this water may be in the interstitial spaces some of this water may be in the cells so when we talk about total body water I'm talking about the water in there extracellular fluid which means they're vascular space and then the interstitial space as well as in the intracellular compartment these patients tend to have a lot of like water in all of these compartments and their sodium may even be a little bit all of it because they have a little bit of sodium here some sodium here and some sodium there okay that's an important concept to remember but again we first said if it's ADH dependent it's volume down or it's a low effect of arterial blood volume these are also the patients who tend to be hypervolemic appearing and I'll explain what that means because this is usually referring to volume status and that's a way that we can examine them if we think that this patient is volume hypervolemic meaning that they have a low effective arterial blood volume or cardiac output or blood pressure then what are the potential cause I told you it could be CHF it could be something called cirrhosis or it could be something called nephrotic syndrome let's explain that for a second now and the patient who has CHF right so they have congestive heart failure this is usually seen you can see this in diastolic heart failure you can see this in systolic heart effects whether ejection fraction is low or it's actually like normal their problem is they're having a difficulty getting blood out of the heart right so their cardiac output is low so what I say they have a low cardiac output a low cardiac output is another way of saying it's a low effective arterial blood volume right the effect of arterial blood volume is low what does that do stimulates ADH if ADH is produced what does it go and do it increases the water reabsorption and if you increase the water reabsorption you're going to cause the patient to have more water in their body than they will have sodium and so what that does is that increases the total body water relative to the amount of sodium and that's why the patient looks hypervolemic they look like the Michelin Man right they got edema all over their arms and legs they got fluid in their lungs oftentimes because their venous pressures are very high and the back flows so if the left-sided pressures are high it may backflow into the lungs causing pulmonary edema if their right-sided pressures are high it may plump up their jugular vein or cause their legs to become very swollen their abdomen become may be more distended because of ascites so those are the things that I want you guys to think about here so again you can see that with CHF now that's one the second thing here is really interesting so when a patient has cirrhosis there's two particular ways that it may cause hyponatremia oftentimes cirrhosis is a very poor prognostic sign sorry if a patient is hyponatremia and they have cirrhosis a very poor prognostic sign and should push them up the transplant list if they're kind of a true candidate for it but let's say that the patient has cirrhosis right so they have a lot of this kind of like fibro connective tissue kind of like accumulation and what it does is it actually causes that lot to form on these actual hepatic portal veins and what does that do to the hepatic portal vessels it increases the pressures so oftentimes these patients will develop who have cirrhosis what's called portal hypertension right that's the result of the high blood pressure Within These portal veins due to cirrhosis so the pressure trying to flow through here is very low that means very little volume will kind of get through the actual liver right and so what happens is the liver tries to release these molecules to try to be able to cause the portal vein to dilate things like nitric oxide unfortunately some of these nitric oxide molecules get into your actual systemic circulation and if these nitric oxide molecules get into your systemic circulation guess what the nitric oxide does to your blood vessels it actually caused them to vasodilate so then you're going to get a lot of nitric oxide causing this systemic vasodilation effect especially of the splanchnic vessels which some of those Supply the kidney if you cause this splantic vasodilation so what this may cause is splanchnic Vaso dilation when you dilate these vessels what you do is you lower their effective arterial blood volume believe it or not because now the amount of volume within the vessel is actually lower with respect to the size of the vessel because you've got a big old plump vessel and very little fluid in it now the effective arterial blood volume is now reduced if you have a low effect of arterial blood volume you're actually not going to perfuse the kidneys as well and so what happens is the kidneys start to undesirably activate what they stimulate the renin Angiotensin aldosterone system and guess what this son of a gun does he goes and tries to stimulate ADH production and increase your total body water which causes what hyponatremia that'll drop down your sodium and again we know this mechanism why because again if you think about this concept here if ADH is actually going to be present then ADH will do what buying onto these tubular cells and the collecting duct and increase the reabsorption of water and if you increase the reabsorption relative to the actual amount of sodium what's going to happen you're going to cause a dilutional effect on the actual sodium and cause hyponatremia so that's some of the ways that this can actually happen plus the low effect of arterial blood volume will also do what it may indirectly stimulate ADH via this pathway but it also can directly stimulate ADH as well so you're going to see this type of effect here and again it's whole it's all often due to to what this kind of disease here cirrhosis so you can see this in cirrhosis because in these patients they have portal hypertension causes vasodilator chemicals to actually cause the portal vessels to try to dilate but they get into the systemic circulation causing splinting vasodilation that causes a decrease in the effect of our tier blood volume which indirect and directly activates the range intense and aldosterone system and increases ADH but it also directly increases ADH production if you increase ADH production you increase your total body water and then you increase your amount of water in the blood vessels relative to sodium it will drop the patient's sodium I hope that makes sense so you can see this in CHF you can see this in cirrhosis one more thing cirrhosis actually can cause another effect here which is really interesting that's why if you do see hyponatremia in a patient with cirrhosis this is a very poor prognostic sign so the patient has something called cirrhosis or they have something called nephrotic syndrome here's another way that we can see a drop in the effect of bacterial blood volume um nephrotic syndrome in these diseases either your liver loses the ability to produce a protein called albumin or your kidneys pee out a lot of the albumin so either way the amount of albumin that they're contributing to the bloodstream drops all right so let's say here's going to be some albumin molecules here so here's some album molecules there's very little of them now why because in cirrhosis you can't produce albumin because it's a protein-producing factory and a nephrotic syndrome you're peeing out all the albumin and so there's very little albumin within the blood albumin generates an osmotic gradient so it helps to be able to keep water present in the bloodstream so it helps to keep the water molecules present within the bloodstream but if you don't have that osmotic gradient can you pull the water into the bloodstream no and so if you can't pull the water into the bloodstream you don't get a lot of these water molecules to stay in the bloodstream and so what happens to the amount of water then theoretically in the bloodstream it drops if you drop the amount of water technically you drop the blood volume and if you drop the blood volume you theoretically drop the effective arterial blood volume and that will stimulate ADH production and we already know what if you stimulate ADH production does it causes the reabsorption of water across the kidneys to be able to bring more water into the bloodstream cause you to drink more and try to reabsorb more across the git and again dilutes down your sodium so that's why these patients will have lots of fluid not in their vessels sometimes but where if the water can't go keep in their vessels sometimes it leaks into the interstitial spaces and into the cellular components so it's a very important concept to remember now one more thing here is in these patients their kidneys should be functioning properly when it comes to reabsorbing sodium so again there's no problem with these patients being able to reabsorb sodium in this the ascending limit Loop of henle reabsorb sodium in the early distal convoluted tubule and reabsorb sodium and the aldosterone dependent portions so the amount of sodium that's present within their urine shouldn't be very high it should be on the lower end of the normal end so generally the urine sodium should be what on the lower end lower to normal end right so we shouldn't have tons and tons and tons of sodium present in the urine in this patient population and again we say less than 20. why because their kidneys are intact they're good at being able to reabsorb sodium and reabsorb water okay so that's an important concept to remember here so again if I have a patient population who I'm not I'm not sure what's their ADH dependent cause of hyponatremia what can I do okay think is a volume depletion if it's volume depletion they're either losing it from the kidneys they're losing it from another source so then how do I go about determine that urine sodium the urine sodium is high they're losing it from the kidneys think about diuretics low aldosterone causes if their urine sodium is low that means that their kidneys are the source they're either losing that volume from their skin from their pancreas from their blood system or from their git and then if the urine sodium is also low and they look puffy and they're effective arterial blood volume is maybe on the lower end because of CHF cirrhosis or nephrotic syndrome then go thinking about these as the potential cause and sometimes looking at volume status can be a very tricky thing but I will teach you guys some tricks in a second so you guys are probably at the point where we talked about okay I guess that's all the ADH dependent causes no there's one more and it's the one where it has nothing to do with volume not no volume depletion uh no low effect of arterial blood volume and the patient looks puffy or hypervolemic this is the patient population where the volume status looks almost completely normal there is no true issues with volume status like they don't have a low effect of arterial blood volume they don't have a low volume depletion they don't have an undesirable activation of the Renaissance system that's excessive or anything like that this is a weird thing where patients are producing ADH inappropriately without a true strong stimulus what are those things let's talk about that all right my friend so the next one is a little bit funky so this is basically where a patient does not have any volume depletion right they don't have any decreased effect of our terrible at volume and there's no true excessive you know activation of the renin angiotensinal adoption system there's a lot of things that can activate the red Angiotensin aldosterone system but it's it's not excessive okay to the point where we talked about in situations like you know cirrhosis that's causing that splanchnic vasodilation and you know decrease perfusion to the kidneys things like that we're not seeing excessive amounts so I think the first thing to think about is okay if the patient does not have a volume depletion if they don't have a decreased effect of arterial blood volume they're not truly volume down from the volume depletion aspect they're not hypervolemic meaning that they don't have an increased total body water um like in excessive situations like they don't look at the Michelin Man all right that's exterior case scenario so they're not hypervolemic or a low effective arterial blood volume and there's no you know undesirable or excessive activation of the range intensity system what's what's their volume status then it's normal so oftentimes these patients are euvolemic so that's sometimes the terms that you may hear I'm going to write that here on the side just because I want you guys to remember it another terminology for this where it's this straight arrow here is you volemic their volume status is normal that means that there is no issue with their volume depletion and there's no issue with effective arterial blood volume and there's no issue with the renonia tense and aldosterone system that's not their problem that means that the posterior pituitaries producing ADH or another part of the body is producing ADH from some for some other reason and it's a really interesting concept so let's talk about that the first one that I want you to remember is actually in situations where the patient maybe has adrenal insufficiency so they produce very little cortisol and this is the primary problem so there is other kind of hormones that your adrenal gland actually makes right but this is the primary one so it's whenever a patient is producing very little cortisol now you're like okay what the heck I know cortisol does have some effect on reabsorption of sodium right so I know that cortisol does actually play a role in the proximal convoluted tubule it actually does help to reabsorb sodium at this point so if you have low cortisol then what's going to happen then okay then I won't absorb this sodium and I'll lose some of the sodium in the urine right so some of the sodium may end up in the urine as a result of that okay so that's that's one effect absolutely that's one effect but that doesn't explain the ADH problem well you know what's really interesting ADH so here we said that there's neurons right there's these neurons in the hypothalamus they come down to the poster pituitary and they pump out this hormone called ADH you know some of these neurons there's other neurons that may produce a little bit of ADH so when patients have low cortisol so let's say that they're adrenal cortex is pumping out low levels of cortisol the natural responses is to tell the actual hypothalamus the hypothalamus will then say okay if that's the key I'm going to take this reaction I'm going to bring it out over here to the right so you guys see it so I'm going to take this reaction here I'm going to zoom it out over here there's neurons that will release something called crh so it should stimulate this process called the production of crh crh should then go and stimulate other neurons to produce what ACTH and then ACTH should then go to the actual adrenal cortex and try to stimulate them to produce more cortisol that's the natural kind of like negative feedback system right that low cortisol tells the hypothalamus to make crh crh tells the pituitary to make ACTH ACTH then tells the actual adrenal gland to pump up the cortisol but you know what else happens it also pumps out ADH there is the pathology there so there is your pathology my friend so that in the situation you're low cortisol is stimulating an increase in crh which is trying to stimulate an increase in act production but it's also causing ADH production to be undesirably increased that means ADH will then come down here to your actual kidneys it'll act on the what receptor here let's actually bring that receptor here the vasopressin 2 receptor stimulate this receptor and start reabsorbing tons of water across the kidneys it'll bring lots of water across the actual collecting duct and into the bloodstream and then by that default what happens then what happens to the amount of water then then you're going to technically just slightly increase your total body water but your sodium should be Rock Solid normal so you're not you shouldn't be technically losing very much sodium you may lose a little bit of sodium from cortisol kind of in the kidneys there may be a little bit of sodium loss but it's not going to be excessive but the amount of water that you reabsorb your total body water is just a slightly increased so it's normal to just slightly increase because I'm reabsorbing more water across the collecting duct because ADH is inappropriately produced via this mechanism I think that's pretty cool and I hope that makes sense but this leads to the next question and if I'm losing so is there another way that I can say Okay Zach you said urine sodium was low in situations of CHF cirrhosis nephrotic syndrome you said it was low in extra renal losses that cause volume depletion such as you know vomiting was the exception remember that one but diarrhea pancreatitis bleeding Burns excessive sweating from fevers things like that that that that made sense okay what about this one is urine sodium a little bit effective well think about it what what happened to the sodium I I inhibited it's reabsorption here's the proximal convolut tubule so the urine sodium will be a little elevated so that's an important thing to remember here so yes the urine sodium it's actually just right right here the urine sodium theoretically and patients who have low cortisol could be what slightly elevated meaning greater than 20. you're in sodium greater than 20. okay very cool very interesting concept then okay but at least to the next concept then okay we talked about low cortisol there's another situation here and this one's probably I'm not gonna lie probably one of the more common causes of hyponatremia let's talk about the very feared siadh my friends all right saadh now in true reality this could deserve its own like lecture but I think it's really kind of like it's fear because it's kind of complicated and when it comes to like the Diagnostics of it but oftentimes whenever when in doubt if you can't figure out the reason why the patient has hyponatremia it's likely sa ADH it's just you got to be really careful because saadh truly is one of those diagonal Diagnostics of exclusion but it happens to be sometimes the most common cause and there's a lot of different reasons for it so we know that yes the hypothalamus has neurons that come down to the posterior pituitary triggers that puppy to make ADH and then we know that ADH will then go and work on the kidney tubules work on The Thirst mechanisms work on our blood vessels all of those things but again there has to be a true stimulus as to why you want to reabsorb more water why you want to increase your effective arterial blood volume replete your volume increase your cardiac output and blood pressure all of those things but in this situation there is no true appropriate stimulus it's inappropriate and sometimes what I've seen is a lot of the times this can be drug related so sometimes I can see this a lot with particular types of medications or drugs so you can see this believe it or not with things like ssris so you know things like of that nature antidepressants selective serotonin reuptake Inhibitors you can see this to some degree as well with a lot of like medications for seizures so some of the things like carbamazepine is a very very common one and we could we could keep going on there's lots and lots and lots of drugs I'm just going to put here Etc to go through every single drug I think is excessive but some of the more common ones that may come up on your exam tend to be ssris carbamazepine other anti-epileptics of sorts but drugs are definitely one and they may by some particular mechanism stimulate this inappropriate production of ADH that causes ADH levels to just increase undesirably and this is due to a medication effect there's another reason there could be a malignancy so sometimes um you know you could see this sometimes in certain types of intracranial pathology so let's actually say that so let's say that there's some type of intracranial pathology whatever this may be you can see this in things like Strokes bleeds subarachnoid hemorrhages so think about that as well as a potential etiology so one could be drugs that could trigger an inappropriate production of ADH a second one that I really want you to remember is any kind of intra cranial pathology these are really really important a lot of the patients that I tend to see who may have large Strokes large hemispheric Strokes large bleed subarachnoid hemorrhages tumors things to that effect they may actually trigger this ADH production and then again cause an inappropriate production of ADH another thing is actually pulmonary pathologies so pulmonary pathologies is a huge ones so if I see a lot of like patients who may have a very mild kind of like sodium drop think about things like COPD think about pneumonia I know this sounds crazy but even positive pressure ventilation so them being intubated is actually a trigger for hyponatremia so these are some of the things so I like to think about is there a pulmonary pathology oh ards ards is a really big one as well don't forget that one but there's a lot of different diseases TB I'm not even kidding there's so many pulmonary pathologies but my thing is is there a lung problem is there a brain problem is there a drug problem and there's one more etiology that I want you guys to think about here and this third one here is malignancy some malignancy oftentimes you'll see this with intracranial or you'll see this with pulmonary pathologies you may at times see this with colon so any type of colorectal cancer any type of malignancy there could be two potential thoughts behind this one is that it could be the tumor oftentimes I'm not going to lie to you the most common one is lung where the lung actually has the ability to pump out ADH or this tumor here has the ability to pump out ADH or this tumor here has the ability to pump out ADH but that could be the potential etiology is that the patient is producing an inappropriate amount of ADH due to an ectopic or malignant Source or there's drugs intracranial or pulmonary pathologies that are causing a stimulus of the pituitary and causing it to produce ADH and it has nothing at all to do with volume depletion effective arterial blood volume or the rain and angiotensinaldoctrine system which is very interesting but out of all of these things if ADH is inappropriately produced due to an ectopic Source or a stimulus from these particular etiologies what's the overarching kind of effect here and I think it did three twice this is actually Four this would be the fourth trigger I apologize so the fourth trigger would be malignancy but if ADH is produced we know that again kidneys are intact right for the most part in this Theory theoretical situation you could be reabsorbing sodium reabsorbing sodium reabsorbing sodium within all of these thoughts here but here's the big thing ADH is really working at a high level here it's really working at a high level and it's really really trying to reabsorb as much water across the git as I'm sorry across the kidneys as it possibly can and so it is really trying to pull lots of water across the kidneys so that very little water is present in the urine if that's the case even though you are reabsorbing some of this sodium because the kidney tubules may be intact you're still going to lose some of the sodium in the urine you're always going to lose some of the sodium in the urine so there's always going to be some degree of sodium loss into the urine but you're reabsorbing so much water that the amount of sodium that could be present in the urine could still be pretty dang High because you reabsorb so much water and so in this situation this is one of the few kind of situations here where I want you to again remember that the urine sodium will actually be high and I know that may seem like slightly confusing here because there's no true loss of sodium somewhere it's just you're reabsorbing so much water that the amount of sodium in the urine and could in comparison to the water is just so high there's so much more sodium in the actual urine than there is water so the urine sodium will be on the higher end because you're reabsorbing tons of water and also the urine osmolality will be very high so that's the big thing that I want you guys to remember for this so this would be again what is this situation here called this disease is called s i a d h really want you to remember that so it's an inappropriate of inappropriate ADH production due to a pulmonary pathology an intracranial pathology such as again a tumor a stroke a bleed a mass some type of drugs such as ssris carbmazepine pulmonary pathologies such as COPD pneumonia pneumothorax positive pressure ventilation ards or it could be an ectopic source of ADH production from a malignancy most commonly lung cancer okay but it could be for me intracranial pathology or sometimes colorectal renal carcinomas as well all right my friends we come to the last cause the last cause here the this last one here is in a patient who has hypothyroidism and I'm not going to lie to you there there was a lot of like literature um that could be written about hyponatremia but not a ton that explained the true pathophysiology so I'm going to kind of dumb it down a little bit for you guys so in this situation the patient is not producing an adequate amount of T3 and T4 so this is called hypothyroidism so hypothyroidism so hypothyroidism is an interesting kind of situation here so T3 and T4 control your heart rate your cardiac output and even to some degree it even controls the glomerular filtration rate and so what the literature has shown from this is that whenever the T3 and T4 are on the low end it affects the heart and it affects the kidneys and what it may do is it may drop your cardiac output because it actually you know thyroid hormone controls the sensitivity of the beta receptors the beta 1 and The beta2 receptors so it'll drop effectively it'll drop your heart rate so you won't have as many conductions that are moving through the heart right sort of drop the heart rate and it'll also drop the contractility controls the beta1 receptors and the contractile portion of the heart if you drop the heart rate and you drop the stroke volume stroke volume what are you going to do your cardiac output you drop your cardiac output what is cardiac output again this is one of those weird situations what does it do to the actual uh poster pituitary hypothalamic area it triggers the production of ADH it triggers the production of ADH and so that's a weird concept because exactly you were saying that this was actually one of those situations where it's an inappropriate production of ADH it doesn't have to do with volume depletion it doesn't have to do with uh a low effect of arterial blood volume well truly this patient is not actually volume depleted and they're effective arterial blood volume it may be on the lower end but again it's due to an endocrinopathy and again this is why it's kind of a slightly weirder situation here the other thing is it may actually reduce the glomerular filtration rate and again a weird concept here but if you lower your glomerular filtration rate what do you do to your written angiotensinaldoctrine system you activate your renin Angiotensin ondosterone system which does what stimulates ADH production and an ADH production increases what does that do it then goes acts on the kidneys and if it acts on the kidneys what is it going to do to the kidneys it's actually going to stimulate them to reabsorb water and if you reabsorb your water you're going to increase your total body of water just a little bit even though your serum sodium should be your actual total body sodium should be normal your total body water will just go up a little bit and it'll drop your sodium now the next question is what about the urine sodium well the urine sodium be high will it be low well oftentimes in this situation here because of again reabsorbing a little bit more water than you are and with respect to the sodium again you're going to lose some sodium into the actual urine it's going to be similar to the saadh so it's a similar effect if you're reabsorbing a lot of water but you're going to have again very little water that's present in the urine so with respect to this your water is actually going to be very low but your sodium because you reabsorb a lot of this water very little sodium is actually going to be getting reabsorbed in comparison to that the actual urine sodium in this situation should be High again this is one of the only few uvulimic hyponatremias that truly has a lot of pathology to explain it so I hate to say this but unfortunately just try your best to remember that hypothyroidism can cause a drop in the cardiac output because it decreased the sensitivity of the beta receptors in the heart and it also reduces your GFR because of maybe even a decrease in cardiac output and because of this this leads to what the overarching effect here is that you'll activate ADH production which will cause reabsorption of water increasing the total body water with respect to the normal total sodium and that'll cause your hypo hyponatremia to occur but the volume status in these patients should be relatively normal the one thing else here is that because you're causing a lot more water reabsorption and very little sodium reabsorption in comparison to that the sodium will be a little bit more elevated again greater than 20. so this is the things that we think about with uh you know the uvulimic hyponatremias is sidh low cortisol and hypothyroidism so so far up to this point we have said patient is hyponatremia check the serum osms is it real so in other words it's a hypotonic hypernatremia or is it pseudo is it a hypertonic isotonic determine the proteins the lipids determine the glucose the Mannitol the status post terp medications okay we determine that it's hypotonic is ADH on or off how do I determine that you're an osmolality if you're an osmolality is high I'm reabsorbing a lot of water very little water present in my my actual urine so ADH is on if the actual urine osmolality is very low that means ADH is off that means I'm losing a lot of water into my kidneys if that's the situation I could say is it ADH dependent or ADH independent we've gone through all the ADH dependent causes and the way that I can look at that is I can say okay are they volume down so then I look at are they volume depleted have they lost things from their kidneys is it diuretics low aldosterone causes or is it extra renal losses are they vomiting diarrhea is there any situation where their pancreatitis bleeding Burns excessive amounts of sweating from fevers okay I can go through this and think about that and then how do I determine if it's a true extra renal versus renal look at the kidneys look at the urine sodium if I'm dumping a lot of sodium in my urine then it's because the kidneys are responsible for that that's your diuretic your low abdosterone cause if it's if it's normal or if it's high sorry if it's a lower end I apologize lower end that means that the kidneys are not the problem for the loss of sodium it's the skin it's the pancreas it's the bleeding or it's the git causes then you go here's the patient hypervolemic do they look puffy do they have a lot of fluid in their lungs they look at the Michelin Man they're hypervolemic but they're effective arterial bloodline the amount of volume circulating through the bloodstream is in the lower end their critic output's low this could be CHF cirrhosis or nephrotic syndrome and again in all these situations their kidney tubules are intact reabsorbing sodium and then again they're actually going to be reabsorbing water their urine sodium should again be on the lower end the last situation here is where a patient is again inappropriately producing ADH the two ones that make the most sense are going to be hypocortisolism they're producing very little cortisol that's triggering the production of ACTH and then inadvertently ADH levels and then again you're losing a lot of sodium into the urine because cortisol actually causes sodium reabsorption and again you're also causing lots of water reabsorption from the kidney so there's going to be more water that's actually going to be taken out of the urine and again more sodium is going to get lost sadh there's a pulmonary intracranial or drug pathology causing this inappropriate age production or there's a malignancy that's pumping it out adhes being producing large amounts which is causing massive reabsorptions of water and again very little sodium to actually be reabsorbed in comparison to the water so the urine sodium is going to be on the higher end and then the last one which is the little funky one is the hypothyroidism which drops your cardiac output drops your GFR causes ADH production reabsorbs lots of water but again your urine sodium will be high these are the weird ones and I know the urine sodium part may be a little bit more complicated but just do your best to remember that uvulimic hyponatremias are usually going to have high urine sodiums that's low cortisol saadh and hypothyroidism all right my friends now the question that you probably need to ask in is okay I used my urine sodium I use my history to determine what's ADH dependent type well the next thing is I don't really know how to determine the volume status of the patient not only determine if they're volume down how do I determine if they're volume up how do they determine if their volume is normal because obviously that's one of the features that you were looking at here Zach is you were trying to tell me if the volume is depleted they look volume depleted think about these if they're volume up if they look hypervolemic think about these and if they're you bulimic think about these well how do I really determine that Zach I got you let me teach you a little bit about volume status all right my friends so we talked about all of the ADH dependent hyponatremias again the beginning that I'll go through the Diagnostics again I'll give you guys a little kind of recap of everything in a quicker succinct kind of way but it's important to remember that when we talk about volume depleted the easiest way to differentiate those is obviously urine sodium right when we talk about the hyperbole make it obviously one of the easiest ways to determine that is their exam when it comes to the you bulimic patient we really look at that urine osmolality and we try to use our volume exam again urine sodium could sometimes be beneficial and again I think one of the important things that it may have seemed confusing especially with the uh saadh and hypothyroidism that urine sodium was a little bit elevated that seems like maybe a little bit confusing a lot of textbooks actually have contradictions against that some say that the urine sodium can be appropriately normal and some say that they could be increased but again I think one of the big things that you may see is a question on your exam may be something to help you point to that and I find that sometimes the difficult thing is determine if the patient is euvolemic or hypervolemic oftentimes volume of depletion sometimes is a little bit easy but volume status is a very challenging thing there was um I think a study once where they took like a bunch of nephrologists and tried to determine a patient population if they were uh volume depleted hypervolemic or euvolemic I think like 47 or 49 of the actual nephrologists were able to identify correctly the patient's volume status and so it just goes to show that it's a very difficult thing to determine a patient's volume status so use a lot of different things history physical exam are very crucial other kind of tools and kits I'll show you guys to use as well one of the things I like to use as vitals it's not always helpful but oftentimes if I look in the patient's heart rate is like through the roof so if I see that they're extremely tachycardic and their BP maybe is a little bit on the softer it that maybe is a little bit helpful especially for patients who are hypovolemic so if I see a patient who has a very high heart rate and a low blood pressure especially their systolic blood pressure right there their shock index may be on the higher end now that right there could tell me okay could it be potentially in this patient population could it maybe be something like a hypovolemia cause absolutely it could and the other thing is could it be a hypervolemic cause absolutely it could and so you got to think about these things and we'll talk about other tools but oftentimes I like to think about is this a volume depletion cause are they super super volume depleted to the point where they're almost in hypovolemic shock so sometimes you can see that to the point where they're in what's called a shock State because oftentimes we can utilize what's called heart rate and systolic blood pressure to determine the patient's shock index another thing is could it actually be due to a very low effect of arterial blood volume and if the effect of arterial blood volume is low this could actually produce a shock State as well absolutely it could in situations where patients maybe are losing blood or they're losing massive amounts of volume this could be something like a hypovolemic shock this may be hypovolemic shock so sometimes you may see this and the other thing is if their blood pressure and heart rate are going to be like this this could also be maybe a cardio genic shocks what if the patient's cardiac output is so poor that they're not able to generate a proper blood pressure and so they develop a tachycardia as a compensatory mechanism this is definitely the case so you see how sometimes vitals May sometimes be helpful if it's really on the lower end think about hypovolemia look at their history have they been taking a lot of like have they had a lot of vomiting a lot of diarrhea poor po intake that's an important thing to think about or does the patient have a heart failure do they just have an MI to what put them into cardiogenic shock the next thing I like to look at is I like to I haven't found these to be very helpful but they do mention it on your exams so mucous membranes so checking those mucous membranes May sometimes be somewhat beneficial looking at the eyes do they look sunk in so do the eyes sink in look at the tongue and the oral the buccal membranes so do they look dry or do they look moist I think those are important things to kind of figure out because if a patient has dry mucous membranes that means that they may be on the hypovolemia end if they're moist if their eyes kind of don't look very sunken in they may actually be more on the normal volume kind of end right so that's an important thing to think about the other thing I actually can would consider potentially again for the exams is skin turgor so you kind of pinch the patient's skin and see how long or how if it returns back quickly to its normal kind of elasticity so patients who are super super dehydrated it'll let go and it'll take a long time for them to be able to get that turgor to go back and so I like to think about that as well so sometimes this can be very helpful so patients who have a very kind of delayed skin turgor that may be very helpful so if they have a very delayed kind of skin Target where it takes a long time for that skin to kind of go back into place this may be somewhat indicative of like a hypovolemia type of cause so that's something else to potentially think about okay now that would cover I think some of the first beginning steps so one of the first things I do when I go into the room is I look at the patient's vitals on the monitor I like to look at their heart rate are they super tachycardic and is there blood pressure on the softer end that tachycardia may be a compensatory response especially if it's a sinus tachycardia are they losing volume are they not pumping enough volume out of their heart that's the first thing I like to think about and that can kind of help me to risk stratify then I try to take a look at their mucous membrane see their eyes look sunken in do their oral mucous membranes and nose look super dry to look moist and clear good color skin trigger is it taking a long time for the skin to go back to the normal kind of position that could be indicative of a hypovolemia just again remember you have a lot of elderly people who might not have as good elasticity in their skin so again I've been found to be super useful but it's something to think about what are some other things that I like to utilize let's go down here okay so the next thing here that I actually find very useful is to go and listen to their you know lungs so take a listen so what I auscultate do I hear any kind of like uh crackles uh rails uh that's a really helpful sign because that could be potentially indicative um of pulmonary edema so what I like to also do is sometimes getting a chest x-ray or doing a bedside ultrasound are very very helpful so utilize these in addition so use things like a chest x-ray use a bedside ultrasound and again these things may lead you to a very overarching theme that if I see a lot of pulmonary edema if I see a lot of pulmonary edema this tells me that this is a lot of increased in total body water relative to the sodium and so this could tell me there's a lot of like you know a hypervolemic type of state so that's a really really important thing to think about is to think about that hypervolemia as a potential cause in other words this is the patient with a low effect of arterial blood volume they may be having something such as CHF or there's less sided pressures are backing up or high and backing up into the lungs when we talked about that so very very important thing to think about whereas if they're dry I don't hear any crackles no rails their chest x-ray ultrasound shows no pulmonary edema this could be a euvolemic patient or a hypovolemic patient so you see how sometimes volume size can be really tricky but that's one thing I like to look at I also like to look are the right-sided pressures really high or do they have a serotic you know type of problem so do they have any type of generalized edema because if they have a big old fat legs this could be indicative of high right-sided pressures and high right-sided pressures could be potentially indicative of what could be indicative of a hypervolemic Cause and again just as an example here I.E CHF I also like to think okay maybe it's not just generalized edema from CHF maybe they also have something going on with their liver too so what if they have again that problem where they have cirrhosis or and that's causing that splength vasodilation problem or what if they have nephrotic syndrome and they're not producing an added they're peeing out a ton of albumin into their actual urine and so because they have very little albumin in their blood and so because they have very little albumin in their blood they can't keep fluid what in the actual blood vessel so it causes it to leak into different spaces such as the legs or into the abdomen causing a lot of ascites and so the other thing I like to look at is is there any ascites or hepatomegaly this could be helpful because again you can see this in both a hypervolemia cause so I could see this in what else if I saw both of these I could see this in situations such as cirrhosis or nephrotic syndrome so again it leads me to kind of like a hyper bulimia type of cause and you can see this in a lot of them you can see this again and which ones I could see all of these really and CHF cirrhosis and nephrotic syndrome so this is one of the parts of the exams that I find sometimes to be beneficial so look at their vitals look at their skin look at their mucous membranes evaluate their lungs do they have a lot of pulmonary edema deliver crackles and rails that are evident there could be a hypervolemic cause do they also have generalized edema and ascites could be high right sided pressures or cirrhosis nephrotic syndrome problems where there's very little albumin and low effect of arterial blood volume and in these situations what's happening it's causing a hypervolemic type of presentation would generalize the ascites or apatomegaly so these are things to be considerate of the last thing that I also like to utilize here as I like to look at the jugular vein so not only could right side pressures cause these but if the jugular vein is super distended look for any evidence of jugular venous distension because if the jugular venous distension is actually really high this could be indicative of what a hypervolemic cause potentially meaning that the right side of pressures could be very elevated so it could possibly be indicative of what a hyper bulimia possibly I also like to use my ultrasound and check the IVC diameter so what's the IVC diameter now this isn't always perfect but if the IVC is very very collapsed very very collapsed it's very very very very very very small versus if it's plethoric and big as a son of a gun then what could it mean well Big Country it could mean a lot of different things so sometimes this hasn't been perfect but it may be if it's super collapsed it could be indicative of a hypovolemia type of State whereas if it's super plethoric and big it could be indicative of high right-sided pressures or a very hypervolemic type of state so these are things to potentially consider and so that's something else I like to do another thing I like to do is while I'm here if I'm doing the ultrasound check their heart ultrasound they're left ventricular side and see if they have any decrease left ventricular ejection fraction if they have any diastolic dysfunction so this could be another thing to utilize there because again it will point right towards your source of the patient's hyponatremia so these are some of the things that I like to utilize again I like to look at the the vitals I like to look at again not only that but the skin turgor the mucous membranes to a smaller degree I like to listen to the lungs use my ultrasound look at the chest x-ray evaluate their extremities look at the belly see if they have any hepatomegalierscities and again also use my ultrasound to look to see if there's any IVC collapsibility or the jugular vein if that looks nice distended and plephoric as well and again also use your ultrasound and take a look at your um your heart to look to see what's the ejection fraction is there any diastolic dysfunction these are helpful things as well why you're there but there's a lot of different tools to utilize other things is I'm not kidding a really good history ask the patient have they been vomiting have they had any diarrhea have they not been eating very much have they had any blood loss that they're aware of that they didn't tell you or something sometimes they will not tell you have they been taking a little bit too much of their diuretic you know I think it's really important to get a good history from these patients in combination with their volume status the objective of Zam exam to help in determining the actual true etiology but sometimes volume status may be somewhat beneficial if it's in a perfect world okay my friends let's now talk about the last part here which is we've gone through hyponatremia Serum osms is on the what truly to be true low end check the urine Awesomes uranosoms will tell me if the patient's ADH is on or off the ear in Osmos is high very little water in the urine ADH is on we went through all the causes we went through volume depletion hypervolemic with low effective arterial blood volume and a normal volume status we went over what the volume status would actually look like if we could try to evaluate that on an exam on top of that we said if the actual urine osomes are on the what lower end that means that ADH is off and lots of water is being lost into the urine and that's causing their urine to be dilute and that situation it was primary polydipsia it was tea and toast it was also things that we talked about such as end-stage renal disease or beer podomania that's the ADH independent hyponatremias let's briefly talk about those armor friends let's now talk about the ADH independent hyponatremias with this particular cause of hyponatremia it's really interesting so we've talked about how whenever ADH is on WE reabsorb lots and lots of water across the collecting duct into the bloodstream water increases relative to the amount of sodium the tonicity then drops and then it causes again a dilutional type of effect of hyponatremia instead of all the causes volume depletion low effect of arterial blood volume and inappropriate production of ADH like in low cortisol or low thyroid hormone or saadh which is a diagnosis of exclusion we'll talk about that a little bit later but what if it's not due to ADH that's kind of weird then right so that means that we have to in some way shape or form if it's not ADH that's reabsorbing you know lots and lots of water across our kidneys are making a strength more so that we actually pull a lot across our git what could be the cause I want you to think of three causes the three clauses I want you to think about is water intake problem solute intake problem or an inability to excrete free water and so we're going to use arrows here in this patient population the first one I want you to think about is that the water intake is exceedingly high or the solute intake is extremely extremely low now in order for the water intake to be high you gotta you gotta you got to consume at least I'm not even kidding greater than or equal to 12 liters per day to actually accomplish this and so we see this in the disease called primary polydipsia and sometimes you can see this in patients that very commonly schizophrenics so you can see this in schizophrenic patients who just have this ex UNC controllable desire to drink very large volumes of water throughout the day when this happens if you think about this theoretically right how would this work if a patient is consuming very large volumes of water that means that they are taking in a lot of water across their git into the bloodstream that means a lot of water is going into the bloodstream that means we have a ton of water into the bloodstream now ADH wants to reabsorb water would you want ADH to be on or off in this situation you wouldn't want to be on because they're going to reabsorb more water so what happens in this situation is this will shut the ADH off because I don't want ADH to be produced because if ADH is produced theoretically if ADH is produced what's going to happen it's going to bind onto the actual collecting duct reabsorb more water and increase the amount of water and worse in the patient's hyponatremia I don't want to do that so what happens is ADH gets turned off if ADH is turned off then what happens is ADH will not be as present as usual to bind onto the V2 receptors and if ADH isn't as present then it will not be able to reabsorb as much water into the bloodstream very very little so that means tons and tons and tons of water are going to be peeped out and you're going to try to make a super super dilute urine this is going to have massive amounts of water present within the urine because you're drinking so much water you have to dilute your urine as much as you possibly can so ADH has to be off so if ADH is off this will do what to the actual urine osmolality well this is Uranus morality you're going to have tons of water so the urine osmolality should be very very low and that was one of the things that we talked about the ADH independent causes now that right there would help you to determine that if you have a patient with schizophrenic who is drinking massive amounts of water greater than 12 liters per day right there you have your diagnosis you don't need to do any other kind of additional tests or anything like that oftentimes it is truly history that'll lead you to the answer here okay so I hope that part makes sense the next thing is what if the patient's solute intake is so low so you see this a lot in the geriatric elderly population patients who don't have a lot of money and aren't really drinking a lot eating a lot of like true substance in their food in other words they're not getting a lot of proteins they're not getting a lot of fat they're not getting a lot of electrolytes in their diet they're just eating things like primarily carbohydrates really and and fluids teas Waters things like that beer and so there's two etiologies that I want you guys to remember here one is called the tea and toast diet so that's that tea toast diet or syndrome now this doesn't mean that you have to only eat tea and toast it's just trying to give you an idea that primarily the patient's drinking fluids right and their primary diet is a carbohydrate Source you can see this with toast you can see there's crackers things like that and what happens is the basic I don't want to get too crazy down into the Nephrology kind of Lane and utilizing a lot of osmolality and stuff like that but here's what I want you to remember solute intake the amount of solute that you intake determines your urine output that's that's I'm not even kidding I want you to think about it the simplest way as possible so here's the way I want you to think about it if you have a very low solute intake this controls your osmolality gradients which helps to determine urine production what would happen to your urine output your urine output will decrease so if your solute intake is low your urine output will decrease so you won't make as much urine as general okay now here's what happens another concept here is whenever a patient is again not getting a lot of solute into their diet what it does is is if you're getting very little solute in your diet it means that your plasma osmolality is what Supply you know osmolality within a diet again is very important so if you're not getting a lot of like solute in your diet then you're not having a lot of things that can affect your tonicity of the blood and so that what happens is the plasma osmolality in these patients tend to be on the lower end so if they have a low solute very little I'm going to put black dots here very little solute this decreases the plasma osmolality and what that does is that means that this is not a very strong stimulus for ADH this inhibits ADH production if the plasma osmolality again is on the lower end what that tells me is that there can be very little solute in the blood and maybe enough water in the blood and so I don't want to produce a lot of ADH so I want ADH to be off in this situation here I don't want ADH to be on okay now here's another thing when you're an output is really really low again this is another important concept low solute intake not only does it cause low urine output it turns off ADH and the reason why is because the urine output is low if ADH is on what would it do reabsorb water and lower the urine output even more oh well I want to turn ADH off so I can actually lose produce some type of urine so if ADH is off that means that it's not going to bind to these V2 receptors as much if ADH isn't binding to these V2 receptors as much it's not going to do what what is it going to do is going to reabsorb tons of water no and so what happens then it doesn't reabsorb water just like it doesn't in this situation so what happens to the water in the urine they have lots of water in their urine tons and tons and tons of water in their urine but even though they don't produce a lot of urine output because of the low soil you didn't take the primary urine that they're producing is very dilute urine so the urine osmolality in the situation will be very low but here's the key thing if the solute intake is low the urine output's low let's let's just give an example let's just give an example as an example and as you can see this not only the tea and toast diet but you can also see this in another disease called beer podomania beer potomania this is when patients are just primarily the diets just beer all they do is they just chug and beers every day Budweiser all day if that's the case where their primary diet is very pretty much beer or again toast crackers things of that nature what happens is that's very little proteins electrolytes true nutrients in the diet you're pretty much just getting carbohydrates and carbohydrates primarily just gets converted into CO2 I mean that's really what it is and water but what happens is in this situation here your solute intake is very very low all right so you're a lot of very little nutrients that affects the plasma osmolality that turns ADH off ADH off means that you actually will not reabsorb a lot of the water and you'll lose that water into your urine because your urine output is going to be on the lower end and we don't want to try to do anything to the plasma osmolality okay so if that's the case then if let's say the cellular intake is so low that the urine output let's just give an example I.E urine output in this patient due to they have low solute intake so let's say whatever the solute is that they get with beer potominium or tea and toast diet the urine output is only we're just going to say throughout the day throughout the day let's say one liter per day that's all they produce throughout the day one liter is it out of this world to the things that if a patient is pounding beers all day or drinking tea and water whatever they are in their diet that it's theoretically not out of this world for them to drink two liters per day no so then the problem comes when they decide to drink beer or have lots of tea in their diet and absorb lots of water into their diet and then if they're water intake so now let's say that they've increased their amount of water and their water intake is two liters per day the amount of water that I'm peeing out is what less than the amount of water that I'm taking in that's enough to dilute the actual sodium and drop the sodium so that's the theoretical effect with the actual low solute intake so low solute intake causes such as a teen toast diet or beer podomania you take in less solute less solute intake does two things one it lowers your plasma osmolality because you don't have as much solute to be able to bring the plasma osmology up if plasma osmolality is down it turns off ADH also low solute intake means that you have a lower urine output just keep it simple low urine output if that's the case then the amount of urine that I do want to make I want it to have primarily be dilute urine so ADH is turned off so the primary urine that I'm producing is dilute so the urine osmolality is very low the thought behind this is that if the solute intake is low your urine output is low theoretically if the sodium intake is very very low the max amount of urine the patient can try to make that's dilute is one liter per day if the patient drinks more fluid via beer tea water whatever it is then they actually output per day theoretically their water intake outstrips their solute intake and then the amount that they're able to produce what will happen they will cause a hyponatremia I hope that makes sense so again primarily history here my friends use the Uranus molality to lead you to these causes and then use your history to determine which one of these it is let's come to the last one really quickly and blow through that one I'm a friend so the last situation here is we have a patient who is taking in way too much water more water than they actually their kidneys can produce right 12 plus leaders that's a lot all right the other one is that the solute intake is really low the last one here is that what if the kidney loses the ability to excrete free water so in other words if I can't excrete free water from my kidneys that's interesting that means I retain a lot of water theoretically right so in other words the patient has damaged kidneys super super damaged kidneys so I'm talking like end-stage renal disease I'm talking like a GFR of like two so less than 15. if that is the case here's what happens kidneys don't have the ability to excrete free water so the amount of water that there actually can be able to excrete is very very limited so this is one of those weird situations they have a very decreased ability to excrete free water if that's the case then a lot of this water that's actually moving through the kidney so you have a lot of plasma coming through the kidneys it's supposed to excrete the free of water and then what happens is you know whatever is remaining will get returned back into the bloodstream well I'm having a decreased ability to excrete this free water so the amount of water within the bloodstream goes up if the amount of water that's present within the bloodstream goes up that means what happens that means that the patient's volume is pretty adequate that means that the plasma osmolality is really low what would that do that would shut the ADH off I wouldn't want the actual poster pituitary to produce ADH so if ADH is off well there you go now I'm actually going to do what try my best what to get rid of free water but the kidneys aren't able to do that very well so that's the problem here is that the ADH is low right so ADH tries to come and bind here but these kidney tubules are damaged right so you'll have low ADH if there's low ADH right you normally again ADH would try to bind onto kidney tubules and try to reabsorb water again ADH is not present it's turned off so again what am I going to do here if ADH is off am I actually going to reabsorb water in this situation no but again the problem is is that I the kidneys have such a difficult ability of being able to excrete free water and so that's generally the problem here but generally again you're going to try to shut off the water absorption because you don't want to reabsorb any more water so they do their best they do their absolute best to lose some of this water into the urine that free water it's just not enough and so what happens is and these patients they have a lot more fluid kind of within their actual bloodstream right so they're more on that hypervolemic end so this is technically what you can consider a hypervolemic hyponatremia but it's ADH independent in this patient population if they aren't making a lot of urine because their kidneys are so damaged so if their kidneys are super damaged they have a really really challenging time of being able to make urine so even though their urine will try to have a little bit of water in it it's going to be very little urine so the urine output is extremely extremely extremely low so it's not enough dilute urine that it's able to excrete so ADH is off so yes they will not reabsorb as much water and so it'll try its best to actually excrete free water into the urine but the urine output is so low that it won't even be able to make much urine that's like actually diluted in general so because of the urine output is really really low let's say let's say that the urine output for them per day is 400 MLS per day that's all they're able to produce and they decide to consume via their daily intake of water they try to have a water intake their intake is one liter per day well now their intake is greater than their output and what happens they again get this hypoinatremia that develops because the amount of water that develops within their bloodstream is higher than the amount of sodium that's present within their bloodstream and so that's a really important concept here so again usually with this patient population it's not very common we see this when the patient is in stage renal disease and pretty much at the point of being on hemodialysis oftentimes when I see these patients they come into the hospital because they're getting ready to have hemodialysis and then you check their sodium like the day before they have hemodialysis and it's a little low and the reason why is is because again the urine output's so low they haven't been dialyzed yet so they're a little bit hypervolemic because maybe their intake has just been a little bit higher than their ability to put out and so once you dialyze them their sodium kind of comes back up so it's a really important cause so again with the situations where ADH is off is again very high water intake primary polydipsia very low solute intake tea and toast diet or beer podomania or an inability to excrete free water decrease free water excretion because the kidneys are damaged ADH is off and it's trying its best to cause the kidneys to dump water and it will dump some water but these patients are almost to the point of a neric they barely produce any urine the water that they actually urine that they do produce the kidneys will do the best job they can to put free water in that urine but it's such a low urine output and if their intake outstrips their output boom you end up with more water in the blood and therefore diluting down the sodium causing hyponatremia all right my friends we've gone through at this point every cause every pathophysiological process and believe it or not the Diagnostics of hyponatremia so what I want to do is in a very succinct kind of way since we've gone through this now is test your knowledge and say okay we have a patient coming in with hyponatremia what's the test that I order and then what are the causes that are associated with that and we're going to blast through this and then what we'll do is we'll talk about a patient who comes in with hyponatremia how do we treat the one that's acute severe symptomatic and then how do we treat the underlying cause let's get into that all right my friends so now what we got to do is we got to talk about a diagnostic approach type on the treatment so a patient comes in again this is really a recap of everything we talked about it should really be super easy now patient comes in they have a serum sodium of less than 135. so yeah let's put that kind of like under here so their serum sodium is less than 135. if that's the case we want to figure out is this true hyponatremia in order to check to see if it's true hyponatremia what's the next test that we'll order come on guys think about it what is it serum osmolality so that's the next thing that we're going to do so I want to check my serum osmolality now remember the norm was between 282 295. so if I go through and I see that my serum osmolality in this particular scenario is one of three particular serum atoms in other words and this arm here it's less than let's say two I'm sorry let's actually say it's 280 to 295 over here so let's say that the serum osms is normal serum osms so it's a normal serum osomes which we said which was what that's between 282 295. if that's the case then which one is this which one is this my friends this is the isotonic hyponatremia this is otonic hyponatremia isotonic hyponatremia to quickly go back what is the particular causes of isotonic hybrid treatment not going to write them all down what is it it is situations where there is lots of lipids such as hyperlipidemia or lots of proteins multiple myeloma waldenstrom's macroglobulinemia or IVIG in the other situation the serum osmolality is super super high you have a high serum osmolality if you have a high serum osmolality in this particular scenario my next question to you my friends is again in that particular situation what is the number that means that this is greater than 295. again I'm not going to write down all of the causes but again I want you to think about it in this situation what is this called when the serum osmolality is too high this is called hypertonic hyponatremia and I want you to think about things like glucose things like Mannitol things like urea things like sorbitol or glycine that they use after Terps all right good the last one here as you check the serum osmolality and it's low so in other words it's less than 280 million this is hypotonic hyponatremia this is a hypotonic hyponatremia and there is like a plethora of causes this is the true hyponatremia if the serum osmolality is actually low meaning that it is again less than 280 and we figured out that it's a true hyponatremia what do we do next to determine the cause of it well then I got to know is the ADH on or is the ADH off how do I determine that come on the urinal osmolality so then I check my urine osmolality if I check my urine osmolality and in this situation I get a two arm approach here now one of these the urine osmolality is really what low very low you're an osmolality and the other one the urine osmolality is super high if that is the case if the urine osmolality is very low I want you to think about this with respect to water so I want you to think about it guys and we use this terminology here for Uranus molality we used greater than 300 or less than 100. so the urinal osmolality is low meaning that it is less than 100 that means in that situation that there is a ton of what water ton of water in the urine so what does that mean for the ADH that means in this particular situation the ADH is off it's suppressed and if ADH is off or suppressed that leads to three potential etiologies my friend off of this off of this this leaves what one is there is a very high water intake this is psychogenic or primary polydipsia it's a very low solute intake such as tea and toast diet or beer podomania or there's a very decreased water excretion such as in end-stage renal disease like less than 15 GFR on hemodialysis okay then was there anything else that we could do with these these were those ADH independent hyponatremias it's all history baby all history in this situation though Uranus morality is high the Iran osmolality is high greater than what 300. that means there's a lot of solute very little water there's very little water and I mean ADH was on ADHD ohm are you trying to reabsorb all that water if ADH is on we said the first thing that we want to do is check volume status so we said that this is really kind of first dependent upon volume status so you want to check and see what's their volume status and we used all those different like ways of being able to describe the patient's volume status is it hypervolemic hypovolemic is it euvolemic there's lots of different ways there so that's where it's going to kind of lead us into this kind of discussion to this point here which is what is the volume status my friends so is the volume really low is the volume high or is the patient uvulimic you will use a lot of those terms right so in a patient who is volume down we went through all of those different causes how do we kind of differentiate which one it is remember I told you that there was a renal and extra read loss so what do I do so the next thing I want to do is I want to check my urine sodium and the reason why I want to check the urine sodium is the urine sodium is going to tell me am I losing sodium and water from the kidneys or am I losing it from extra renal sources so check that urine sodium if the urine sodium when we check this puppy here if the urine sodium comes back high or low this automatically lends us to some degree of a diagnosis and we can use our history to be able to discern that so if the urine sodium comes back and the patient is dumping tons of sodium into their urine what would that tell you oh that'll tell me that that's a renal source of their loss so that means that they have a high urine sodium in comparison to this being a low urine sodium so we're going to put una now for the urine sodium so the urine sodium is high and the urine sodium is low this is Arena loss my friends so they're losing their sodium from their kidneys and in this situation they're losing the sodium from some other source their skin from their bloodstream they're also losing it for maybe things like their git vomiting diarrhea or the third spacing from pancreatitis or very poor mpo intake so in this particular situation this would be a renal loss so then you got to start looking are they taking any diuretics are they taking Loops thiazides have they also have any issues with aldosterone maybe checking out the ostero level see if they have any kind of problems with aldosterone production or do they have a subarachnoid hemorrhage that would suggest cerebral salt wasting urine sodium is really important as well for this one because this would tell me this is an extra renal loss there was one and I don't want you guys to forget this though there is one out of all of these extra renal losses that did actually cause some mild degree of sodium loss and I don't want you guys to forget that one so I'm going to put it in this Source but I'm going to put a little asterisk next to it that you guys don't forget it it was the only one that actually did cause urine sodium to actually increase to compensate for the metabolic alkalosis do you guys remember which that was vomiting so please don't forget that that's the only one the only one of the extra renal sources of volume loss of sodium loss that actually can cause a little bit of renal sodium to actually increase a little bit so again and this is because we'll put vomiting because they develop a high pH because they're vomiting out all their protons and so they try to trigger their kidneys to do what again just so that you guys don't forget this it's a little quick little one to remember it tries to tell their kidneys to pee out lots of bicarb but when you pee out lots of bicarb to bring the actual pH what back down you also excrete what other molecules so you excrete the bicarb but you also excrete sodium so that's why their sodium will actually be just a little bit elevated okay so that covers the volume depletion once now what if the volume is actually the patient appears hypervolemic and this is that one that I told you where it's a little bit kind of confusing they use that terminology what was that terminology I told you guys they have a low effective arterial blood volume in this patient population right so in this situation believe it or not it's all kind of like history and utilizing other tests in other words does the patient have a history of heart failure do they have a history of cirrhosis is there a lot of albumin in their urine a lot of the times you can check those things but also check their urine sodium what do you think their urine sodium would be well they're renin Angiotensin aldosterone system is what it's on and so it's reabsorbing lots of sodium so because of that in this situation here their urine sodium should be very low okay but again use other tests I'm going to put these kind of like in an asterisk so use your other ancillary test to determine the other etiology of that so for example considering things such as what considering things like an echo to determine CHF considering things such as you know lfts considering things such as a urine albumin for nephrotic syndrome Etc okay the next thing here is to check the patient okay what if their volume status appears normal so they are you bulimic if they are euvolemic this is a really difficult one to determine right so here's how we go about this we try to figure out these first we check the urine sodium this will help us out a little bit to these degrees here's the next thing I do I don't worry about the urine sodium just yet you can check the urine sodium and the urine sodium theoretically again it can vary from textbook to textbook in a perfect world the urine sodium should be on the higher end for these patients but that's not the soup for help super helpful tip what I like to do is I like to rule out the endocrinopathies first and then come to the last exclusionary diagnosis which is sidh so what I like to do is if the volume appears normal and all these other things have kind of gone through then what I do is I go to the next test and I checked two things I check my thyroid function test and I check my cortisol level and the reason why is from here I can get a two arm thing if the tfts are abnormal okay so let's say that this is the problem so the patient has tfts that are consistent with low T3 and low T4 I have my diagnosis hypothyroidism if my cortisol comes back super low very very low cortisol level boom I have my diagnosis cortisol insufficiency but if the tfts come back normal and the cortisol comes back normal normal and the cortisol comes back normal and I've ruled out that it's not a hypervolemic cause it's not a volume depletion cause then what I can do is I can go ahead and I can see if it's s i-80h so then I think okay okay maybe this is siadh is it s-i-80h well then I got to figure out what's the cause of the SI ADH and so oftentimes it's looking through their medication history but oftentimes we have to do like a CT scan we have to do a CT of the head see if there's not an intracranial pathology CT of the chest make sure there's not a lung pathology CT of the actual abdomen and pelvis to make sure that there's not kind of any kind of like uh colorectal cancer renal cell carcinoma anything that could be a malignancy source of this inappropriate ADH production and that's how we would go through this and then use their history obviously but I think that's the really really big things to think about here and once you've gotten to the point of oh this is Si 80h this is supposed to be blue then you can kind of say okay this is a diagnosis of exclusion I just got to figure out what's the source of the inappropriate ADH production and then again look for meds look for intracranial pathologies look for pulmonary pathologies look for malignancies that's the big thing to go about here but again if you really wanted to you could also add an additional test here that in all of these circumstances if you checked a urine sodium in this patient population what would you get the urine sodium theoretically should be high and again this can vary from textbooks to textbooks it's just the last thing that you check urine sodium is way more helpful just remember it's way more helpful for determining the hypovolemic cause of hyponatremia not as helpful in hypervolemia and not as helpful in the uvulimic seeds the last thing that I want to talk about is sometimes this will come up which is there is a specific type of renal loss which is very interesting which can kind of look like siadh so there's a specific one here I think it's important remember it's called cerebral salt wasting and then you have s-i-adh one of the big things I think that's also kind of beneficial because sometimes these can come up and they're not sure which one it is in cerebral salt wasting what I like to do is I like to check what's called a fractional excretion of uric acid and then I like to check in si 80h another test here which is a fractional excretion of uric acid because oftentimes these patients will kind of their volumes as may be slightly difficult to determine but you know that they have hyponatremia their urine osmolality is high and then their urine sodiums are high but you're not sure which one it is sidh or cerebral salt wasting because they both can have an intracranial pathology as a cause if you track the fractional excretion of uric acid and patients who are super super volume depleted their fractional excretion of uric acid is very high so their bun goes up whereas in patients have siadh their bun often tends to be on the lower end they're not as volume depleted they're relatively normal volume and so they tend to be on the lower end and that's an important kind of thing to add here to kind of help you to differentiate saadh from cerebral salt wasting okay my friends we have gone through the Diagnostics the pathophysiology the etiology all of these things the last situation here is how do we treat them and what are the complications watch out for all right my friends so now we have a patient they come in right let's see that we don't even know the cause of the hyponatremia but they come in they have potentially a low sodium and again I want you to remember those numbers mild hyponatremia 130 to 134 right moderate 120 to 129 and then less than 120 is a very severe hyponatremia when a patient comes in with hyponatremia sometimes if it's like a mild hyponatremia sometimes even a moderate hyponatremia they may have no symptoms that's really really important to be able to differentiate when you have a patient who comes in who is symptomatic and they also have a hyponatremia associated with it that's an emergent type of thing that you need to think about so what we need to talk about when it comes to how we emergently treat hyponatremia is three factors that are really determining the treatment of hyponatremia one is the timing one is if they're symptomatic and one is the degree of hyponatremia with the most important factor being the timing and the symptoms so let's say the patient comes in they have hyponatremia the first things you need to be able to discern is the timing is this acute or is it chronic that's extremely important my friends so the reason why I think that's important is and we'll talk about a little bit later is that patients who have chronic hyponatremia they're at high risk of something called osmotic demyelination syndrome which we'll talk about but we want to determine is it acute or is it chronic so how do we determine that time frame so acute hyponatremia means that it has occurred in less than 48 hours therefore patients with chronic hyponatremia meaning that if we look through their history they've had hyponatremia for more than 48 hours they live with this this is their daily life that's a really really important point and I will explain why a little bit later but that's the first thing so whenever a patient needs emergent hyponatremia therapy oftentimes we prefer that it is an acute hyponatremia it's developed within less than forty dollars I'll explain why later patients who have chronic hyponatremia that maybe live with this daily they already have compensated they've developed a compensatory mechanism in their brain to actually compensate for that and if you try to treat them and push their sodium up too quickly you can cause something called osmotic demyelination syndrome so preferably we want the patient to have acute hyponatremia sodium dropped to a particular level in less than 48 hours the next thing is symptoms and we'll talk about this one a little bit later but the the pathophysiological process by which symptomatology occurs is very interesting let's actually just hit it now so here we have sodium molecules right so we'll have some sodium molecules here and then over here we're going to have some water molecules when a patient develops hyponatremium you know there's water in two components you're going to have water in your extra intracellular component and you're going to have water and the extracellular component right let's say that you have very little sodium so the sodium level in the blood is very low sodium has the ability to control the movement of water it controls osmotic gradients but if the sodium is very very low is the water going to want to stay near the areas of low sodium or would it want to move into the cells where maybe there's lots of glucose or maybe there's higher amounts of sodium here or maybe there's higher amounts of potassium here things of that nature things that actually can generate an osmotic gradient there's more of these solutes that are present here in comparison to the amount of solutes in the blood well where would water want to move if we use this kind of concept here where the solute concentration is lower in this compartment and the solute concentration is higher in this compartment we know via the process of osmosis Which Way water would want to move it's going to want to move to things of higher solute concentration so the water will start flushing out of the blood and into the interstitial fluid inside of the compartment and what's going to happen to these dang cells they're going to swell like a moss like a they're going to swell and so you develop cells swelling and this is super super critical because this happens in very specific areas of the body where sometimes whenever cells start to swell there's a lot of bone around that particular tissue that doesn't allow for it to swell very much and this causes problems one of these things is let's say inside of the skull you know something called the Monroe Kelly Doctrine the monorail Kelly Doctrine says that you have a the cranium kind of inside here that it's in a fixed space you have this bone and then inside there's blood there's brain tissue and then there's cerebrospinal fluid if you increase the amount of brain tissue it's going to swell and it's in a fixed space it's not going to be able to move and so the pressure inside of the skull cavity is going to increase and that's one of the fearful complications so one of the fearful complications here is that as you have a lot of this cell swelling it causes an increase and the intracranial pressure so lots of swelling means that this actual area let's kind of represent this here let's say that a patient has lots of swelling now in their brain lots of fluid within the brain that is going to cause the brain to swell now the pressure inside of the cranium is going to increase patients with high endocrine depression can develop a lot of problems they may kind of manifest with headaches they may manifest with nausea vomiting they may manifest with an altered mental status they may start developing kind of like focal deficits or they can progress to the point of herniation and herniation syndromes are beyond the scope of this lecture but obviously with herniations they maybe start having pupillary changes maybe weaknesses maybe they start having respiratory irregularities a lot of different problems so this is a scary scary one with the most fearful one being herniation syndromes okay but again one of the more common features here is the patients can develop Headache nausea vomiting alter mental status focal deficits or herniation so look for that okay now that's one particular etiology the other one here is sometimes when you cause cellular swelling right when you cause cellular swelling it can actually cause dysfunction of some of these cortical neurons and so what happens is you may develop kind of this irritable Focus so now if you're causing all this cellular swelling here let's say you're causing swelling in the brain all this cellular swelling it may become a focus of irritability within the brain and then this irritable part of the brain starts developing electrical excitability and this electrical excitability leads to increased firing of neurons and this increases the risk of seizures these are the things that I actually completely fear of and you know what else is really important here High intracranial pressure is actually more concerning so let's say that a patient has this cerebral edema it's actually more concerning even more fearful if a patient is and I don't mean to be rude I'm not I'm not this is literally evidence pre-menopausal women they're more at risk because their brain is actually going to be more likely to swell so if you're pre menopausal women or another potential thing is you have some type of brain substrate and what do I mean so you already have a stroke you already have a bleed you already have an aneurysm you already have a tumor so there's something there and then you increase the actual intracranial pressure by causing more edema because again it's going to cause it's going to cause cerebral edema and the edema that you generate is what actually increases the intracranial pressure which can cause these problems if a patient already has a pre-menopausal or they have a brain substrate in other words they have a CVA they have an intracranial hemorrhage they have a mass and then on top of the you had cereal edema oh my gosh they're likely going to herniate in the same situation here because the cerebral edema can occur cerebral edema can cause seizures and the seizures are at higher you have patients who are higher risk because what happens is if you have a history of epilepsy and you drop the patient's sodium that will increase the risk of seizures so on top of that if the patient has a history of epilepsy and they have cerebral edema boom they're at risk for seizures so what I like you guys to think about is what's the development the timing is it a cute hyponatremia oh okay if it is that's really scary second thing symptoms are they having any features of cell swelling or cerebral edema in other words they have any Headache nausea vomiting any types of alter mental status or any herniation syndromes that are developing and even more worrisome that would actually urge therapy is are they premenopausal do they have something in their brain that's already increasing the pressure even more second they start seizing if they start seizing and they have a history of epilepsy that's a really scary situation because hyponatremia will increase actually cause more seizures actually lowers the seizure threshold okay so that's the big things to think about symptomatology so acute symptomatic with the most worrisome symptoms if I wanted to add this here is going to be increased intracranial pressure or seizures the second thing is how low is the sodium how low is the sodium so in other words is this this is going to go back to that son of a gun that's going to go back to this discussion here which is is it mild is it moderate or is it severe oftentimes if a patient has a mild hyponatremia so in other words mild moderate severe we can determine this based upon numbers is it 130 to 134 that's pretty mild I'm not going to really be too aggressive about treating that one so I wouldn't really treat that one moderate if it's 120 to 129 I would consider that one but the most concerning one that I need to act on is severe especially if it's less than 120 because usually the point where the patients get a sodium of less than 120 is when they start seeing this cell swelling effect and especially if it's acute you need to get on that all right so I think the really really important thing here is that patients who have hyponatremia that come in less than 48 hours with symptoms of high intracranial pressure like herniation or symptoms of seizures and this is again a sodium that's very low less than 120 I need to emergently administer particular therapy so the question is is what is that therapy let's talk about that all right so patient comes in right just less than 40 hours ago they started seizing right come in get their sodium it's less than 120. it says 118. right when that happens they now fulfilled at least three criteria they're cute they're symptomatic and their sodium is very severe if that's the case how do I start treating these patients emergently well here's the thing my cells are swollen here's my cells you see how swollen these suckers are looking big and swole like you know just big old suckers so if that's the case what I want to do is I want to try to generate a pool of water because before the water got sucked into the cells because there wasn't enough tonicity enough sodium within the bloodstream to keep the water in the bloodstream well what if I increase the tendicity of the blood so one of the ways that I can do this is I'm going to increase the tonicity and the way that I can do that is I can give the patient salt if I give the patient salt how I'm going to do this I'm going to administer something called three percent hypertonic saline and oftentimes we do this as boluses and so what I'll do is if a patient comes in with acute symptomatic severe hyponatremia what I'm going to do is and I'm going to start off by giving them what's called three percent hypertonic saline and I'm going to do it as a bolus therapy meaning I'm I'm going to push this you don't slam the whole thing in no no no you push it into like maybe over five ten minutes and so what you'll do is you'll start off with a hundred milliliters and you'll give them that bolus and see if they improve if they stop seizing if they stop kind of developing headaches nausea vomiting alter mental status or risk of herniation if that doesn't work you can do that three times with a Max of obviously 300 milliliters okay of hypertonic Saline now when I increase the tonicity what am I doing I'm using this hypertonic saline to increase the amount of sodium that's present in the bloodstream and if I increase the amount of sodium into the bloodstream what am I going to do I'm going to increase my sodium so my sodium will increase but also I'm going to yank all of the water molecules or some of the water molecules that's present in these cells out and get some of the water to come out of these cells back into the bloodstream and if I decrease the swelling I decrease the symptoms in other words I lower the intracranial pressure or I decrease the seizures or cease the seizures you guys get that that's pretty cool concept right so that's how we would generally do this is we would give the patient hypertonic saline to increase the tonicity of the blood and pull some of the water out of the cells at the same time we're improving the sodium so we're fixing two things we're increasing the sodium back to a normal level and we're also reducing the cellular swelling and that's the pretty much the big thing that's why symptomatology is actually the most concerning feature if they have symptoms that's the most concerning feature now after we've done this here's the problem sometimes sometimes you'll do the bolus therapy and then you may plus or minus do what's called a hypertonic saline infusion so you may continue to administer you may continue to administer hypertonics or three percent hypertonic saline for a while so that's again going to do what that's going to increase the patient's sodium there's something called over correction and again what happens with is whenever you increase the sodium too quickly over a 24 hour period if you increase it too quickly and how quickly generally we say if you get greater than eight Milli equivalents in 24 hours it increase the risk of something called osmotic demyelination Centrum I will talk about this a little bit later I just want you to understand this for right now so yes I want to increase the sodium acutely because the patient is seizing I got to get their sodium up so oftentimes what I like to do and what the most evidence supports is when you do this hypertonic saline you're giving them the three percent hypertonic saline and you're trying to increase their sodium at least six mil equivalents per liter in six hours and then what I do is I have like maybe two more Mill equivalents I can bump up with an infusion if I need to but I don't want to go over eight in a 24 hour period sometimes what may happen and you don't mean to do this but you give them the hypertonic saline and you push their sodium up let's say 16 mil equivalents and you're like oh my gosh if I go over eight I can develop this concerning thing called osmotic demonation syndrome how do I prevent that from happening I got to stop the patient from seizing or stop them from herniating by giving them hypertonic therapy but I don't want to go too fast because if I go too fast over a 24-hour period I'm going to demyelinate their neurons in the pons well how do I prevent myself from over correcting over a 24-hour period that's where we use something too and decrease over correction and there's two therapies I um tend to be very fond of one but there's another one that you can utilize so here's the thing you're giving them a lot of sodium right what do we know about ADH it turns on water reabsorption across the kidneys well what if I what if I had them or it caused you to become thirsty and drink more water what if I just push a lot of water down their git because often these patients are altered they're herniated and they're seizing they can't drink water so sometimes you have to put an NG tube in and then give them water so I can actually give them water well that's one thing I'll do because if I increase the amount of water I will dilute down their sodium so one of the things I can do here is I can try to increase their water so I'm gonna so in order to over prevent over correction I need to increase the water I need to try to get more water in to bring the sodium down a little bit so what I'm going to do is the way that I'm going to do this is I'm actually going to do this in two ways one is I can actually give them free water you can do this two ways you can do it po so I'm literally pushing free water down their gut or I can do it IV so D5 W oftentimes is the way we can do this so we're giving them free water whether it be via IV or whether it be them drinking that but I'm trying to get more water to move across their git into the bloodstream or through this bag of free water into their bloodstream to increase their water and the reason why is if I increase their water I will help to decrease their sodium a little bit now you're like Zach wait I was trying to increase my sodium because the hyponatremium was causing them to have high icps and seizures yes but I just want to get the sodium down to where I don't go greater than eight and 24 hours I don't want to break that eight mil equivalent range in 24 hours because there's risk of negative outcome such as osmotic demandation system so I'm using water to help to prevent the over correction so in other words I give them I give them hypertonic saline I push it up to 16 mil equivalents well I got maybe a little bit less than 24 hours to give them free water whether it be po or free water within IV to get that down eight mil equivalent so that I don't go over eight in a 24 hour period I hope that makes sense okay so again an example is I give them hypertonic saline I push it up to 16. so I increased at 16. so the sodium went up 16. well now I got to give free water to decrease the actual sodium eight amount so in other words let's say I came in with um I don't know 120 all right or let's say one yeah 120 just to be easy and I bumped it up 16 all right so I went to from 120 to 136 that's way too much I got to bring it down a little bit so I'm going to drop it down eight and that'll bring me to like 128 and that's appropriate over a 24-hour period because that won't cause osmology demonation Center but if I went from 120 to 136 within a 24-hour period high risk of osmotic demyelination syndrome okay that's one way so one way I can do this is I can give them free water I'm gonna put like a little thing here next to it so one way I can do this I can give them free water whether it be po or D5W there's another way that's a little bit easier okay another way that I find a little bit easier and I find to be a little bit cleaner and the second way is I can give them something that will actually cause ADH to be reabsorbed across their kidneys and that is ADH and ADH we give a very specific drug so again this drug is actually called desmopressin so desmo present I want you guys to be aware that there's also the common abbreviation d d a v p so we call this a ddavp clamp so you're giving them hypertonic saline okay if you give them the bowl of therapy first try to get it up six within at least the first six hours so they stop sneezing and they don't herniate then keep checking their sodium levels you got to check this thing almost like every two to four hours because you don't want it to break eight in a 24-hour period because they have a risk of osmotic demonication syndrome so while you're checking your sodium every two to four hours you're giving them free water po or D5W and an IV to bring their actual water amount up and bring their sodium down so that you don't over correct another way that you can do this is you can continue to monitor bmps so again it's really really important guys please remember this bmps sometimes we're doing like every four hours because if you you push all this hypertonic ceiling you check ah check the next day you're going to cause a lot of problems so check their bmps to check their sodium very frequently to prevent over correction one way that you can do that is free water the other way you can do that is desmopressin you ddfp I find this to be a little bit more elegant and the reason why is this is ADH right ADH is going to bind onto the V2 receptor if it binds onto the V2 receptor what is it going to do it's going to cause more water reabsorption if I increase the amount of water reabsorption what do I do to the amount of water within the bloodstream I increase the amount of water within the bloodstream if I increase the amount of water in the bloodstream what am I going to do to my serum sodium I'm going to bring the serum sodium down so I'm going to bring the serum sodium down and that's going to prevent over correction so I want you to understand that you're often utilizing these two things in tandem you're giving them a hypertonic saline bolus to get their sodium up you can go up to 6 ml equivalents in six hours just for the love of goodness don't go above eight in the 24 hour period if you do you risk this I'll explain it a little bit how do I prevent them from going over that in 24 hours at this after you give them the hypertonic ceiling to get them to stop seizing or herniating check a BMP every four hours make sure that if that sodium is going up above the eight mil equivalent range you give them free water or you give them desmopressin to bring it back down bring it back down just a little bit so that I can prevent them from going over the eight mil equivalent range in a 24-hour period okay so the whole concept is as this example here I give the patient hypertonic saline I pump their sodium from 120 to 136. if I leave that go and I do a BMP the next morning and they're 136 get ready for a lawsuit okay because you're going to cause osmology demolition syndrome so what I got to do is keep monitoring their BNP oh dang I push up 16. I got to start giving them free water or decimal pressure and get that down to what well the max I can go is eight so I got to try to get that down eight mil equivalents from that point so that's where free water or decimal pressure comes into play You're utilizing these in tandem all right now that we've beaten this like a dead horse let's now talk about what is osmology demomination syndrome and how do I prevent that all right guys let's now talk about something called osmada demomination syndrome this is really really important just I want to quickly go through this and I want to spend a ton of time on it because it's again it's a small piece it's a complication of treating hyponatremia but it's something that you may experience on your exam so whenever a patient comes in who has hyponatremia and you correct them too quickly again here's the thing there's so many different numbers out there there is a lot of numbers some I think at one point time it used to be don't go over 12 mil equivalents within a 24 hour period and then there was a lot of cases where they're saying oh well we we did and we we were in the 10 to 12 range and we still caused an Osmond denomination syndrome and they said okay let's go less than 10. and then again there were still cases between 8 to 10. so I think there's been a lot of like support and a lot of like just logistical support and evidence and safety for the patient to stay within at least no more than eight mil equivalents per liter over 24 hour period of that sodium increase if you want to go to eight to ten again there has been some case reports that show that you do get osmology syndrome but oftentimes it's safe and some literature will actually support again an eight mil equivalent don't go greater than that so at least to this kind of discussion what is osmotic demonination syndrome how does it happen and what are some things that I really have to be careful for besides over correcting them greater than a ml equivalents within a 24-hour period well first thing osmology demonization syndrome is this really interesting kind of concept here so let's say that a patient has hyponatremia right they have the hyponatremia so they have very little sodium within their bloodstream and then let's say whatever the cause of it is it doesn't really matter let's just say that they have hyponatremia right what we said is as a result of this they have less tenacity less osmotic control to keep water inside the bloodstream water moves into the cells and they swell then what you do is you give them hypertonic Saline when you give them hypertonic saline what you do is is you pump up their amount of sodium within the bloodstream and now it's two bras molar there so what does that do if these are swollen cells these cells are swollen what is it going to do it's going to pull water out of the cells and then what happens is the cells will shrink and this can cause cell death and particularly this can actually cause maybe some of the oligodendrocytes within the pons to die and then they demyelinate the axons within the pons and so what you actually start to experience here is in the ponds you start to develop this demyelination syndrome so they also used to call the central Ponte myelinolysis I think now it's kind of supported as osmotic demyelination syndrome so as modic demyelination syndrome is you demyelinate the pontine neurons and the reason why is is that you push the sodium up way too fast or maybe not necessarily too fast but you over corrected the sodium over a 24 hour period so you increase the sodium what greater than eight mil equivalents over a 24-hour period and that caused so much water to be yanked out of the cells that they shrunk and again as they shrink some of the cells may die especially the oligodendrocytes around the actual pontine neurons now if that happens there's so many different things that run through the ponds this is not an anatomy course but I want you guys to understand there's obviously the cortico spinal tracts so they can actually develop you know paralysis there is the cortico bull bar tract so they can develop different types of speech problems so they can actually develop like dysarthria and they can even develop what else maybe dysphagia so dysarthria dysphagia it can even hit the media longitudinal fasciculus maybe or the sixth nerve nucleus and so this can even hit like maybe the medial longitudinal fasciculus or the sixth nerve and this may even lead to some type of diplopia so there's a lot of different things and one of the worst case scenarios if they hit the reticular formation if you hit the reticular formation within the pons so you demyelinate some of the particular formation neurons let's actually write that one down if you hit the reticular formation this could lead to decreasing level of consciousness sometimes this can even put a patient to a locked in state I'm kidding so you want to be really really careful of this kind of disease so the whole concept with those Moda demyelination syndrome is that the patient has demyelination of the neurons within the pods that can cause destruction of the corticospinal tracts causing paraplegia quadriplegic it can cause a critical bulbar track fibers to be effective so maybe they have dysphagia dysphonia dysarthria or it can hit some of the actual ocular fiber motor neurons I'm sorry so the sixth nerve nucleus movie the medial longitudinal fascicles causing diplopia and another thing is that you actually can hit the reticular formation causing like a decreasing level of consciousness so it's really important to be able to understand these things and usually the most common cause is an over correction of sodium greater than eight mil equivalents over a 24-hour period but what are some other risk factors so we know that it's over correction but what are the people who are at highest risk because sometimes you can actually bump that sodium up and they may be okay you don't want to play around with that but what are the patient population that you really really have to be cautious of because they can over correct really easy and I'll explain why and they're at higher risk for this than other patients one of them is patients who have chronic hyponatremia so chronic hyponatremia is a very important risk factor for osmotic demyelination syndrome so greater than 48 hours of hyponatremia they live with this and oftentimes this patient population is this patient population which I'm going to mention patients who are serotic who are malnourished and also Google alcoholics so increase alcohol intake oftentimes these patients all have chronic hyponatremia they're very common patient population now I want to explain really quick why these particular etiologies here can increase the risk of osmotic denalination syndrome I'll see this last one for a second here here's why okay here's a patient who is a serotic malnourished alcoholic who has chronic hyponatremia okay if they have chronic hyponatremia let's say that they develop hyponatremia so here's their sodium molecules here's their water molecules and here's their cells all right what happens is when they develop let's say hyponatremia so this is their first kind of inciting event of hyponatremia they develop hyponatremia what do we say it happens to the water molecules they can't stay here because there's not enough sodium so where does the water molecules go well they go into the cells and they cause the cells to swell right what happens is this is cool these cells will then start pushing out molecules so they you you cause these cells to swell so they're they're swollen they're all big so these cells swell because of the initial hyponatremia water gets pulled into the cells right when the water is in the cells now and they're swollen the cells start to compensate and they secrete out let's see let's put here this one this blue molecule they start to secrete something called little Osmos this could be glutamine this could be glucose they could pump out potassium they could pump up a lot of different molecules but these molecules that they pump out are osmotically active that's cool right now these I'm going to call osmoles so they pump out Osmos this is the cell's own way of compensating when they pump out Osmos guess who likes to go out with the Osmos the water so they're like oh wait there's Osmos out here I'm going to move out of the cell and so what happens is this has got a compensation mechanism so now look at what happens as these cells compensate this is a Auto compensation now come here the cell's Auto competency so they shrink a little bit because why well there was some water molecules in here that were there from the swelling right but now the water molecules got pulled out here why because the cell had pushed out these things called Osmos little idiogenic Osmos and it pulled some of the water out of the cells and so they shrunk right so now they shrink this is a way that they can protect themselves because this happens in the brain so a patient who has a serotic malnourished alcoholic who has chronic hyponatremia they end up having hyponatremia their brain swells when their brain swells a little bit their brain cells produce Osmos that yank water out of those cells so that they shrink so that they don't suffer from herniation or seizures Isn't that cool it sucks for the for the patient because then their brain atrophies but that's the effect now you take this patient who's already this is they're compensated they are compensated now hit them with the Sodium you increase their sodium with a hypertonic Saline you know over you over correct them big time now look at this you increase their amount of sodium now drastically they have some water in here they have some water here in these cells right and then you pumped all these like little idiogenic Osmos out here that were already out here that helped to pull some of the water in this point now you increase the sodium even more what are you going to do to these poor cells here oh poor cells are going to yank more water more water and they're going to shrink even more than this one where they were compensated so they were compensated here you push their sodium up even more their cells shrink and shrink and shrink and so it increases the shrinkage funny increase the shrinkage and then what happens is the cells will start to die and then you end up with osmotic demyelination syndrome so the whole concept here is you have a patient Who develops hyponatremia they compensate by producing Osmos yank water out of their own cells now they're compensated you give them tons of sodium and You Yank even more water out of those compensated cells you cause the cells to die oligodendrocytes in The Ponds no longer demyelinate them you end up with ODS okay very important concept and again what is this sodium correction factor greater than eight mil equivalents per 24 hours I can't say that enough my friends Please be aware that this number can can actually change from textbook to textbook though this is the one that I found to be the most beneficial the one that I use in my Critical Care kind of experience last one hypokalemia hypokalemia like hypokalemia if a patient has low potassium and you also again they have a high risk of osmotic demyelination syndrome so I'm just going to add this there high risk of osmotic immunization syndrome why it doesn't have anything to do with this it leads to this indirectly now watch this it's really cool you have a patient who's hypokalemic oftentimes patients who are serotic malnourished alcoholic chronic hypothermia often have a hypoglymia as well but now when you have hypokalemia what's the thing you got to treat it you're going to treat that and the treatment is to give them potassium you got to give them potassium so you should have given potassium supplements or potassium IV and then what happens is you push the potassium into the bloodstream when you push the potassium into the blood sugar there's these things called sodium potassium ATP Aces these sodium potassium atpses pump potassium into the cell because right now your cells are just screaming they're very hypokalemic you're going to pump tons and tons and tons of potassium in if you pump tons and tons of potassium in what are you going to pump out sodium and now the sodium in the bloodstream goes up so when a patient has hypokalemia and it's actually right like this when they get hypokalemia and then you try to replete their potassium so you give them potassium you stimulate the hack out of the sodium potassium ATP Aces and that causes a massive shift of sodium out of the cell as potassium is shifted into the cell to try to replete the low potassium now sodium goes up so now take this example here where you're giving you have a patient who has hyponatremia chronically they compensate it so now they're at this you give them hypertonic saline and you give them potassium you're going to push their sodium up even more shrink their cells give modes and they're going to be a lawsuit you're going to be living on the side of the road so you don't want that right so how do we prevent that we take into consideration these factors that this patient population tends to be the most at risk for hyponatremia so be careful giving them hypertonic saline don't go greater than eight within a 24-hour period so use your things like free water and decimal pressure to prevent over correction but again these are the patient populations where you give them sodium they will over correct they're at high risk for ODS and again this patient population if you're correcting them and they have hypokalemia very scary population all right my friends that covers ODS the last thing that I got to talk about to finish this whole office you have a patient comes in hyponatremia you found out that they were actually symptomatic right you treated their emerging symptomatic hypnotremia you didn't give them ODS but then you got to prevent them from continually developing hyponatremia see if the treat the underlying cause how do we do that all right my friend so I think the really important thing to think about is if we have an emergent therapy of hyponatremia we know what's the patient population they're acute they're symptomatic and they have a sodium that's really really low less than 120. we already talked about the therapies without the three percent hypertonic saline preventing over correction with free water and desmopressin watching out for ODS we know that if a patient doesn't qualify for maybe emergent therapy or maybe they were treated with emergent therapy and we haven't had the chance to actually kind of like maybe send off some tests and figure out what was the cause of their hyponatremia well once we figure out the cause of their hyponatremia the most important thing is actually treating the cause so if a patient has hyponatremia the first thing is to think about is their hypovolemic hypervolemic or euvolemic because at this point we would have gone through let's say we went through everything we used the Sierra Muslims we use the Uranus we use the urine sodium and again we delineated if it was hypovolemic from renal extra randomly determine if they are hypervolemic we determine if they're at sidh whatever it's important to be able to know how we would treat that and this is very simple this is all I want you guys I want to bake this too hard if the patient is volume down they're hypovolemic give them back the volume they were losing what and hypovolemia what were you losing a lot of salt and water so in this patient population they were lost they had a lot of sodium greater than water loss so I want to give them back sodium and water because right now their total body water is low and their total body sodium is even lower how do I do that I'm going to give them a solution of this is really the only time I like to use this dang fluid but normal saline so 0.9 percent sodium chloride solution normal saline may be a potentially beneficial fluid in this particular scenario so maybe consider giving them some IV fluids so IV fluids sometimes likely the more commonly utilized one is zero percent uh normal saline sodium chloride okay now once you do that you're going to be giving them sodium you're going to be doing what at this point they were depleted of sodium and they were depleted of water you're going to be giving them back sodium and you're going to be giving them back water so you're trying to replete the problem and then obviously treat the underlying issue it was a diuretic discontinue the diuretics or decrease the dose it was cerebral salt wasting this is the only other one that I got to add in here if it was a low aldosterone cause in other words it was due to cerebral salt wasting or it was due to Addison's disease how do we treat that in these we give them a particular drug that is going to replace that what's that drug fluidrocortisone fluidro cortisone so you can give this in situations such as cerebral salt wasting or what else what else Addison's because it's basically going to give them back the aldosterone and help to retain more sodium excrete some type of potassium and then help to be able to keep in some water so generally we'll give them IV fluids 0.9 sodium chloride treat the underlying cause of its diuretics discontinue them if it's low aldosterone give them fluger cortisone if it's vomiting get them to stop vomiting if it's diarrhea get them to stop you know Hershey squirts treat all of those particular issues and then after you've done that again that should help to resolve the hyponatremia that's very very important oftentimes IV fluids is going to be the answer that you want to remember on the exam if you get a little bit of a tricky question add on with a little aldosterone fluger cortisone that's usually going to be the way that they'll actually ask you on the test again same thing I can't stress this enough if you're giving them some type of sodium please monitor these patients continuously though with bmps to make sure that they don't develop greater than eight mil equivalent per 24 hour increase in sodium that causes osmotic demyelination syndrome you still monitor for it all right in this patient population their volume up so they're hypervolemic this is your CHF patient this is your cirrhosis patient this is your nephrotic syndrome patient most common one out of all those CHF and these patients their problem is is their total body sodium is elevated but what's even more elevated their total body water so I do not need to give these guys any IV fluids I do not need to give them any sodium because they already have high sodium they already have lots of free water well what if I got rid of the free water or I actually restricted them from taking any free water in that may be beneficial I'm going to try that so one of the first things I'm going to do is I'm going to fluid restrict my patient that could be really challenging because sometimes you got to keep that to like less than or like 1.5 liters per day could you imagine drinking like less than that every single day it could be super super difficult to do that but oftentimes that what that's what we'll actually try first because if I actually restrict the amount of water intake that this patient is getting in then I can actually reduce the amount of free water that's actually in the blood that's causing their hyponatremia now oftentimes fluid restriction won't work okay and if they fail or if their sodium is really bad it's really low and there's no way that you're able to get that sodium to come up enough with fluid restriction we may try something else and this is what I like to do what I like to do is I like to cause the kidney to maybe excrete free water it's excrete a lot of free water into the urine and maybe even some sodium because I got a lot of sodium here so what I'm going to do is I'm going to cause the excretion I'm going to try to excrete free water to the best of my ability well how do I do that well there's three drugs one is I can give something called a loop diuretic do not give a thiazide diuretic you'll actually drop their sodium even more but a loop diuretic will do what it'll inhibit the sodium potassium II chlorideco Transporters and I will not reabsorb sodium but on top of that I won't pull water via the counter current multiplier mechanism so we know that what I'm going to get a lot of in here is I'm going to get a lot of I'll get some degree of sodium but I'm going to get rid of a lot of water Loop Diuretics cause way more water loss than sodium loss way more so if you look at Lou diuretics they're going to cause more water loss than they will sodium loss thiazidaritis cause more sodium loss than water loss so it's really important to remember that so that's one way I can get rid of a lot of the free water if I decrease the amount of free water that will help to again allow for my sodium to start coming up because again I'm getting rid of some of the free water so I'm going to fluid restrict them maybe even consider giving them a loop diuretic there's another one another one that I could do so that's one the second thing I could do is I could give them what's called an ADH antagonist an ADH antagonist and this is something like tolvapton I'm not a big fan of the VAP Tans but they're decent if you have no other option or if they're refractory so when you do this what you you know ADH loves to bind here and increase water reabsorption right increase water reabsorption but that would actually make things worse because you increase your free water what if I give a drug that actually blocks ADH from binding here and then inhibits water reabsorption and instead causes water to be lost in the urine so you excrete a massive amount of free water I'll decrease my free water if I decrease my free water then my total body water will come down and my actual total cell body sodium is a little bit higher boom my sodium will come up so that's another mechanism that I could utilize so again Loop Diuretics ADH antagonist will cause you to excrete free water primarily free water and then if you fluid restrict them you prevent the amount of water that they're getting in that'll also decrease your total body water so the whole goal in this patient is to decrease the amount of total body water they have and a hypovolemic patient you want to give them back sodium and water a solution that has a little bit more sodium than water would be potentially beneficial and then treat the underlying disease and if it's a low aldosterone problem give them aldoster in the form of fluger cortisone there is another drug that you can use in here but it's not super common to utilize I'll talk about down here with SI ADH but that's called urea but let's actually come down to the last one here which is sidh all my friends the last one here is siadh so saadh in this patient population where no hypovolemic is they have very low total body sodium and then low total body water but less total body sodium so we want to give them back sodium and water so sodium chloride Solutions are going to be the best and then also fluticortisone up there low aldosterone patients with hypervolemic hyponatremia they're having an excessive amount of total body water and an increase in the total body sodium I want to get rid of a lot of free water or restrict the amount of free water that's coming into the body oftentimes free water restriction isn't enough I have to excrete free water via Loop Diuretics or ADH antagonists in refractory cases for sidh it's very similar to the hypovolemic patient what we want to do is in this patient here is when you look at their sodium intake in comparison to their sodium amount versus their water amount they have a little bit of an increase in their total body water and oftentimes their sodium tends to be pretty much like normal to slightly elevated but I like to think about it just to make it easy it's usually pretty much almost normal so there's just maybe a little bit more water than there is sodium so one of the things I can do is I can do the same thing like a hypervolemic patient if it's too much total body water I can have them restrict the amount of fluid intake and that's the first thing that I'll do so the first thing I'm going to do is is I'm going to try to restrict there free water intake so restrict fluid intake and I'll get that to like less than like you know 1 to 1.5 liters per day sometimes it's really difficult to meet this goal but you can try it if I do that I decrease the amount of water that they're in taking and I kind of decrease their total body water and that may help to be able to bring their sodium up sales then what I'm going to do is is I'm going to do two other things oftentimes in these patients they sometimes need a combo of two particular drugs I need to give them more sodium because if I'm restricting their fluid intake and it's not working then the second thing that I need to do is I need to increase their salt intake and you can do this in two ways one is you can literally I'm not even kidding you can give them sodium chloride tablets but oftentimes and these patients have a very low sodium we will use hypertonic saline infusions oftentimes the more common one is three percent hypertonic saline infusions and what we're doing is is we're going to infuse in sodium and that's going to help too increase the sodium because their sodium is kind of like normal so I'm going to try to increase the amount of sodium that I'm giving them via salt tablets or hypertonic saline infusions what that's going to do is is it's going to take the actual sodium and increase the sodium a little bit and that may help to help the patient out but maybe it's not enough I'm increasing their salt intake but they still have a high water intake their total body water is still high well I want to get my sodium to go up and I want my total body water maybe to come down a little bit so how do I do that that's where I can attack the Nephron so the third thing that I can do often in tandem with the salt intake the third thing I can do is I can excrete free water and how would I do that my friends one is I could give a Loop diuretic and this is often in combination with a hypertonic saline infusion and so what you'll do is you'll give the loop diuretic and it'll inhibit the sodium potassium to clerical transporter you don't reabsorb sodium therefore you don't pull water out of the descending limb all the water gets lost lots of water gets lost into the urine you're losing tons and tons of water in the urine and what am I doing to my actual total body water I'm decreasing my total body water and by giving them salt tablets or hypertonic saline infusions I'm increasing the sodium at the same time I'm excreting free water with a loop diuretic right so that's a pretty cool concept now oftentimes if the patient is refractory to restriction of fluid intake increased sodium intake with salt tablets or hypertonic saline infusions with the lube diuretic usually has a combo between these two then the last thing is for the refractory for the refractory SI 80h that's when we'll do the ADH antagonist same thing for the hypervolemic patient here often they usually respond to a loop diuretic and then again like less fluid restriction more fluid restriction but a refractory saadh patient sometimes they may require an ADH antagonist and again that's going to massively cause a lot of free water excretion I just think it's really really important to remember that if you're giving an ADH antagonist or you're giving a Lube diuretic in a hypertonic saline infusion really monitor that sodium okay bmps every like four hours I think are kind of beneficial to make sure that you don't over correct them over at 24 hour period as well but that's the things I would utilize so restrict fluid intake increase salt intake and again cause excretion of free water there's one last thing that can excrete free water it's kind of like a plus or minus I'm just going to add it in I actually kind of just recently started using it I really like it it's oral urea and so what I use this instead of is I find it to be a little bit elegant so it's an alternative to the loop diuretic and hypertonic saline combo I feel I find it to be very cool so what urea is is it's a it's a solute molecule it's an osmolar kind of molecule so you take it orally gets across the git and what it does is it gets filtered across the kidney tubules and as it gets filtered across the kidney tubules what it does it creates an osmotic gradient that pulls water with it so it'll get peed out into the urine right and what it'll do with it is it'll pull lots of water along with it so to yank water along with it into the urine and so it'll really cause a lot of free water intake I mean for free water excretion I apologize so sometimes oil urea is a good alternative to a Lube diuretic and a hypertonic saline infusion combo these are usually very commonly utilized in tandem very commonly utilized I just find them to be sometimes a little bit difficult to manage so I like to give the oil urea usually a 15 or 30 gram oral urea and find that it's really beneficial and just easier to be able to cause excretion of free water so it's excrete free water because it'll act like an osmolar molecule and yank water out into the urine and so that's kind of nice alternative I don't have to kind of do a combo between these two drugs but my friends that would cover hyponatremia we've talked about a massive amount in this adventures level movie I really hope that it made sense I hope that you guys enjoyed it love you thank you and as always until next time [Music]

Channel: Ninja Nerd

Views: 819,618

Keywords: Ninja Nerd Lectures, Ninja Nerd, Ninja Nerd Science, education, whiteboard lectures, medicine, science

Id: Jd6HoA3ZSPU

Length: 189min 53sec (11393 seconds)

Published: Fri Dec 02 2022