Sodium Disorders | Clinical Medicine

what's up Ninja nerds in this video today we're going to be talking about sodium disorders that includes both hypo and hypernia again this is a part of our clinical medicine section if you guys like these videos they make sense they help you please support us you can do that by hitting the like button commenting down in the comment section or subscribing also for your true benefit I really believe that we have some awesome awesome supplemental resources things like notes illustrations quiz Quest questions you can find all of that on our website how do you get

there go down in the description box below there's a link that goes right to our website all right let's start talking about sodium disorders my friends all right let's talk about the first sodium disorder which is hyponatremia so when it's when the sodium level is too low how low well usually we say less than 135 mil equivalence per liter is the roundabout number by which we say Okay below that it is now considered to be too low it's called hyponatremia well then we have to think about the pathophysiology behind hypon netram often times the most

common eological factor is that there's just more water relative to sodium so then you have to think about what hormone really regulates water and that's ADH or vasopressin so ADH really helps to work at the collecting duct to reabsorb water across it into the bloodstream and if we have more water in the extracellular space then there is sodium we dilute down the sodium so then we have to think what are the things that are increasing ADH levels well if they're appropriately increased then we have to have some particular triggers or stimuli right and what are

those triggers so the triggers or the stimuli there's a couple of them but I'd say the most important ones are going to be when the blood volume or the blood pressure is low all right so usually it's when the blood volume is low that's often times a very potent trigger there can be other ones um often times it's kind of related here where it's usually due to your blood pressure is low but both of these you know and often times both of these work kind of in tandem with one another and what happens is that

these circuits help to be able to when your blood volume's low your blood pressure low it activates your juxtaglomerular cells and they produce a hormone which is called renin which leads to the formation of angiotensin 2 and we'll go over that but these are the primary triggers for an appropriate increase in ADH let's understand that for a second so let's say here I look at my circulation right in both of these scenar I here blood is circulating through my vascular system but what I know is that my blood volume is low or my blood pressure

is low when that happens what that does is it tells our cells in the kidney because what happens is our kidneys are very sensitive to profusion so when the JG cells sense that the blood volume is low or the blood pressure is low they pick up on that and these JG cells become activated and they make a hormone or an enzyme if you will called renin and what renin does is it leads to the formation eventually of angiotensin 2 and if you guys know anything about Angiotensin 2 this is a very potent hormone can do

a ton of stuff literally it's a jack of all traits what this guy can do is it can vasoconstrict blood vessels to pump up your blood pressure it can help to increase aldosterone to bring more sodium into the bloodstream but here's another thing it can activate our hypothalamus and stimulate the hypothalamus to send signals down via the poster pituitary and secrete a hormone and very large amount so now I'm going to have a lot of this hormone in the blood stream what is this hormone ADH when ADH is released what it does is it goes

to the kidneys here's a nefron if I take one nefron and I zoom in on it here's my proximal convoluta tubal Loop of Henley distal convol tual collecting duct at the collecting duct there's receptors for ADH these are called V2 receptors another name for ADH is vasal pressent when ADH goes it binds on and stimulates these receptors which triggers an intracellular Cascade this intracellular Cascade leads to the formation of these little subunits these little pores that form within the luminal membrane when they open up water will flood into the bloodstream so water will move from

the Lumen across the cells into the bloodstream so what happens now if I bring more water as a response into my bloodstream I theoretically increase my blood volume and blood pressure which fixes the issue but the downstream consequence which can result here which is what we're talking about is I could dilute down my sodium and Via a dilutional effect I may bring the sodium down to pathological levels to what as we said less than 135 so this is the concept that I want you guys to understand here now another thing that's really important here is

when ADH levels are high if I reabsorb via this pathway tons of water what happens to the amount of water that's present within the urine very little because I'm reabsorbing a lot of that water so as a result here's a really high yield important thing to remember there is very little water that is present in the urine and what that does is that makes the urine appear more concentrated but what that means is when the urine is concentrated the osmolality of the urine is very high so what I want you to remember is that the

urine osmolality as a result here will be very high in high ADH States so one thing important to remember is whether it's appropriately increased ADH or inappropriately increased ADH what happens to the uran osmolality my friends you're going to have a high uranos molality now we'll talk about what that true number is more in the diagnostic section just in case you want to know it it is 300 that is kind of like that number but you'll see these are the same it indicates that ADH is turned on now trigger for this is blood volume and

blood pressure is low we'll talk about some of these causes what about for this one has nothing to do with blood pressure or blood volume that is the big thing has nothing to do with the blood volume or the blood pressure so it has to be due to so no effect from blood pressure and no effect from blood pressure and blood volume the primary trigger for this is usually certain types of things that are very odd peculiar and what we'll talk about a little bit later is this often is due to a disease called s

I ADH syndrome of inappropriate ADH secretion there's so many different things that can trigger this that is very inappropriate very random we'll go over them a little bit later intracranial disease pulmonary diseases drugs and even endocrinopathies okay so we have an understanding here that the primary trigger for appropriately increased is low blood volume low blood pressure for inappropriate has nothing to do with the BL volume of blood pressure it's sadh but the uran osmolality in both of these is high let's compare and contrast to the opposite what if I have a scenario where the ADH

is supressed it may be normal but it's lower than what we would like it to be in these situations that's interesting so now what would be particular triggers that I have to ask myself that would cause the ADH levels to become lower so it's not high well there's really two particular reasons one is that your water intake is way higher than your ability of your kidneys to excrete that water or the second thing is that your solute intake the amount of electrolytes sodium other types of electrolytes that you're taking in is way way lower than

the amount of solvent that you're taking in or water so these are often times the two particular things here is that you have a very high um water intake we'll say water intake or very low solute intake now watch this let's say you have a very high water intake or a low solute intake it's usually a combination combination of these so in this scenario if you have water lots of water or very low solute what happens to your plasma osmolality so now look in my circulation here I'm going to have lots of water and I'll

talk about how you get this water in there eventually but if there's lots of water what does that do that kind of in a way says that my blood volume is appropriate my blood pressure is appropriate right so there's two ways that I could look at this I could say that my blood volume and my blood pressure should be appropriate and if in that scenario that is the case what should that do to the renin Angiotensin aldoshin system it should in theory help to suppress this production of renin Angiotensin aldosterone system activity so this should

be decreased in other words that's not really driving ADH production all right so it's actually not going to lead to ADH production well here's something else that's interesting if your amount of water in your bloodstream is a little bit higher you know what that does to your plasma osmolality it brings your osmolality the concentration of your bloodstream lower because you have more water less solute so now my osmolality is low guess what osmolality when it's low guess what that does to ADH suppresses it so both of these scenarios guess what it's doing to your hypothalamus

it's kind of suppressing your hypothalamus so then your hypothalamus in this response produces less ADH if it produces less ADH what happens then do I have as much ADH present to bind onto the V2 receptors no if I don't have as much of this ADH to bind to the V2 receptors then will it help to stimulate the formation of the aquaporn subunits no will I express these on the membrane no will I bring water across here into the bloodstream no and all of this is what leads to me bringing less water into the bloodstream but

what happens now if I'm not reabsorbing as much water where does this water go right into the urine so now I'm going to have a buttload of water here in my bloodstream I mean in my urine I apologize buttload of water in the on the urine that means that the urine is dilute if the urine is dilute what happens to the osmolality the urine osmolality will drop and if it drops to less than 300 that tells me that ADH is turned off right away I can differentiate between those types of ADH dependent and ADH independent

hyponatremia so now in this scenario urine osmolality is low why is this so important to understand guys because right away when you get a patient who comes in they have a sodium less than 135 guess what you're going to do you're going to go and you're going to send off a uranos molality because it's going to tell you right away is it an ADH dependent or ADH independent process now you're probably thinking okay well if I'm not reabsorbing as much water here how am I diluting down the sodium Zach remember you're taking in lots of

water or you're taking in less solute and so because of that in this effect right here is how you're going to drop the sodium to less than 135 right here via this effect okay now let's take some time and go over thinking about what are the reasons why ADH is so high low blood volume or low blood pressure why is it so high in sadh and then what happens to the causes of hyponatremia and patients who are appropriately suppressed with their ADH because they're taking in too much water or too little solute all right my

friends so now we've covered the path of physiology the next concept here is that we have to then say okay in order to determine the causes of hyponatremia I can really kind of narrow down my diagnosis using the uranos molality to to see if ADH is high or ADH is suppressed in that scenario but the next thing we have to do is we have to look at the volume status of the patient and we'll talk a little bit more about this in the diagnostic section but you're kind of evaluating mucus membrane skin turg you're looking

at their blood pressure their heart rate you're looking at their jugular veins you're looking for any visibility of edema in their legs AES you're oscilating the lungs to look for rails upon um oscilation so a lot of evaluation is going into that and then what you can do is you can group these patients into three particular categories are they hypovolemic UIC and then the last one we'll talk about hyper yic the hypothalmic patient often times they are significantly total body volume depletion they've gotten rid of a lot of their water but they've gotten rid of

a ton of sodium from their body and that's really what's causing these patients to have this problem so what we can do is we can categorize these patient in a way of saying that they have a really significant depletion of their total body sodium so I'm going to put total body sodium but they ALS o have a depletion in their total body water so they have more sodium loss though than they have water loss and then in this scenario you make them hypovolemic right so they're already going to be a little bit loss of sodium

more than usual right so they have a little bit more water in general then you increase their ADH production it makes them reabsorb more water you bring in more water on top of the sodium that they already lost you're going to dilute down their sodium even more so that's how this whole thing propagates so let's have an understanding here of the two different ways that we can get rid of sodium and a little bit of water from the body one is you can lose it from the kidneys if I'm losing sodium and water from the

kidneys how could I do this there's a couple different ways one way is I could use diuretics and if I use different types of diuretics what are a couple of these well one could be Loop Diuretics and the other one could be thigh iide diuretics so what are your Loop Diuretics this is going to be feride torside bumetanide all of those guys right what are they blocking we'll represent it right here it's in the ascending limb of loop of Henley you block the sodium potassium 2 chloride Co transporter can you reabsorb sodium potassium chloride and

water no where do you lose it you lose it in the urine so what do they lose they lose a lot of sodium and water in their urine but more so sodium than water so they're going to have lots of sodium loss and their urine but they will have some water what's another diuretic thides and believe it or not these actually cause more hyponatremia than Loop Diuretics would how do they do this they block the sodium chloride sorter present in the distal convoluted tubal can you reabsorb sodium here so I can't reabsorb sodium here I

can't reabsorb sodium here so where do you lose it you lose it into the urine and what else do you lose water so again in both of these scenarios you're losing water but you're losing more so sodium all right what else another scenario is you could have low aldosterone you're like low aldosterone how how is this coming into play Zach what the heck you know there's a renal tubular acidosis we call for this one it's called RTA Type 4 there's a lot of different reasons why this happens right one is honestly could be to to

adrenal damage so right so you could have adrenal insufficient efficiency that truly could be one reason we'll represent that as AI another one is you could be using drugs ACE inhibitors arbs all of these suppress aldosterone in indirectly right and what happens in these particular scenarios is if you have low aldosterone are you going to be able to reabsorb sodium here at the distal convoluted tubal no and so I can't reabsorb sodium here and so what happens is I lose a lot of the sodium and the water and the urine so this could be a

couple different reasons there is another one it's important to remember this it's believed to be kind of linked here and it's called cerebral salt wasting so it's called cerebral it's believed to be maybe due to a low aldosterone cerebral salt wasting and so this is different in the other scenarios adrenal insufficiency ACE inhibitors arbs this one usually see patients with heavy polyurea so you'll see two things one is it's often times they have a subarachnoid hemorrhage and the other time the other situation here is that they have very very very heavy urine output excessive polyera

so again thinking about these patients who have renal causes of hypovolemic hyponatremia they're peeing out tons of sodium Rich fluid whether it be diuretics or low aldosterone related States Okay cool so high urine sodium would tell me that this is a renal cause so what I want you to start thinking of in this particular scenario is if the urine sodium is really high that means that I'm probably peeing out a lot of the sodium Rich fluid there's some type of tubular dysfunction going on here whether it be diuretics or low aldosterone the other concept that's

really kind of important here to think about is that these patients are often times their blood volume is going to be low right we know this because they're depleting it from their kidney you're getting rid of a lot of it in that scenario what that should do is do what to the kidneys activate the renin Angiotensin aldosterone system renin Angiotensin aldosterone system and this will help to increase ADH and it will also help to increase your aldosterone levels problem is is that in this scenario your tubules this will help to propagate more water reabsorption which

will lead to hyponatremia this will try go and reabsorb more sodium but because all the tubules are being blocked by diuretics or a low aldosterone State this won't properly work in renal causes and that's why the UR in sodium will be really really high in these scenarios okay let's come over the extra renal causes what's another way that we can lose fluid from the body sodium Rich fluid that's not coming from the kidneys well you could be losing it from the git so we can have gi losses what are a couple different ways that we

can lose sodium or fluid well vomiting Di diarrhea and even I would say to some degree poor intake so I would say vomiting diarrhea and decreased po intake so oral intake these could be a couple different reasons why you're losing sodium Rich fluid from the body another one is you could be losing it from the skin believe it or not so this one's interesting so skin losses this actually could be due to a lot of sodium Rich loss from the cells or from your sweat glands so what if I destroy some of the cells and

I release a lot of the sodium Rich water from my cells what could do that burns so severe burns you know another one another one is diaphoresis so excessive dieresis what the heck is that Zach sweating so you're sweating like a banshee often times you see this in patients with severe fevers so if you have uncontrolled fevers you can really lose a lot of sodium mer fluid via sweating okay via these mechanisms I'm depleting my blood volume right I'm getting rid of sodium fluid from my body so as a response my blood volume will drop

all right if my blood volume drops what does that do to the kidneys helps to activate the renin Angiotensin aldosterone system so now this puppy is going off and what is it going to do increase ADH which will do what we already know increase water reabsorption precip itate hypon nmia but the other thing is that it's going to activate that aldosterone when you increase aldosterone what does that do to the kidney tub if they are not being dysfunctional meaning there's no diuretics on board there's no low aldosterone states that are occurring well if it's the

kidneys are functional it'll go to the kidneys and it'll help to reabsorb a lot of sodium if it reabsorbs a lot of sodium it's doing that to try to replenish your blood volume and the sodium Rich fluid loss that's occurring but what happens to the urine sodium the amount of sodium that's present within the urine drops now do you see how we could have a test that if the urine sodium is high it's coming from the kidneys if the urine sodium is low it's coming somewhere else Isn't that cool all right that tells us about

the hypovolemic patient so in these patients they're going to be volume depleted look for decreased skin turer look for dry mucus membranes look for low blood pressure tachicardia and even potentially in these patients you have no evidence of any edema all right uvalic hyponatremia in a uvalic patient it means normal so in other words when you look at their total body water and their total body sodium they have just a teensy teensy bit more total body water relative to the total body sodium so they're just going to have just a Teensy bit more water than

they will sodium within the body so in these particular situations really the only thing that's happening here is that the body is inappropriately producing ADH that was an appropriate production of ad because it was low blood volume low blood pressure in this situation the patients are usually uvalic their blood volume's normal their blood pressure is normal so they're not producing ADH for that reason what would be a reason we would produce ADH well the pituitary is either pumping out a lot of ADH without any blood volume or blood pressure stimulus or I have a tumor

a malignancy of sorts that is pumping out high levels of ADH and then when this is happening we already know that high levels of ADH is going to do what it's going to come down here act on the V2 receptors and increase water reabsorption and as a result I'm going to bring in more water than I will have relative to sodium not losing sodium technically in in this particular situation so I'm bringing in more water which is going to dilute down my sodium okay question is is what in the heck is causing this inappropriate ADH

production because this is really how we would Define this this is Si ADH it's the inappropriate production of ADH without a prop stimulus so then we have to start thinking what are some causes what are some s a DH causes and there is a plethora of them and that's what kind of makes this challenging when you think about it one is it could be you have some type of CNS injury so some type of CNS injury so what are some CNS injuries or dysfunction that I would really think you guys I urge you guys to

consider well one is have they had a a recent stroke right so you know in this particular situation have they had a CVA a cerebrovascular accident whether it be es schic or hemorrhagic has there been any type of traumatic brain injury right another thing is you want to think about pulmonary diseases so hypoxia is a very very weird stimulus of ADH production and so things that cause hypoxia so pneumonia ards maybe severe COPD so pneumonia COPD ards these things also have a very stimulus for ADH production drugs tend to be very profound stimuli as well

and so a couple different drugs that are usually worth remembering here is going to be particularly in the vicinity of uh SSRI so selective serotonin reuptake Inhibitors that we use for depression and anxiety as well as another very important one would be carbamazapine which is an U anti-epileptic carbamazapine the other thing that I would want you guys to remember is malignancy so malignancy is a very very profound stimulator as well usually it's via A paraneoplastic syndrome so the tumor itself gains the capacity to produce ADH not the pituitary these things are all stimulating the pituitary

so here I'm going to put this as stimulating the pituitary stimulating the pituitary stimulating the pituitary this one is not necessarily stimulating the pituitary it's the mass itself right that's producing the cancer you know what the most common cancer is that we usually see associated with this it's usually small cell lung cancer and this is the tumor that's actually gaining the capacity to produce ADH the last thing is we actually sometimes group it into siadh believe it or not and it's endocrinopathies so endocrinopathies of some sort that can kind of mimic s ADH but you

have to rule these out before you can make any of these other assumptions and the two that are worth remembering here is going to be adrenal insufficiency so adrenal insufficiency so you have to check their cortisol levels and the other one is hypo thyroidism so truly before you can make the true definition of these related causes of sadh you have to rule out adrenal insufficiency low cortisol or hypothyroidism low thyroid hormone these are the triggers for sadh sadh leads to increased water reabsorption now I put it in in the renal causes category and I want

you to understand why it's very interesting because they're reabsorbing water and there's no volume loss in these patients their blood volume is what do we say normal and if you really want to think about it you could say normal to slightly elevated just slightly as a result what is that going to do to the renin production by the kidneys and it's going to suppress it because and it's going to appropriately suppress it so in this particular scenario what would happen to the renin Angiotensin aldosterone system it would be appropriately suppressed so the aldosterone levels will

be appropriately low if the aldosterone levels are appropriately low what will that do to the kidneys will it reabsorb sodium no and so as a result what happens to the sodium so we'll kind of represent it like this what happens to the sodium will I reabsorb it no and so the urine sodium will be high and that's why we say that the sodium will be a little bit higher in the urine and that's why we classify this as a renal cause of uvalic hyponatremia so again for this one I want you to remember that if

the urine sodium is high then this is likely a renal cause think about sadh and what of the reasons CNS p pulmonary drugs malignancy but you have to rule out endocrinopathies first if the urine sodium is normal all right let's let say it's not in this per situation uh high it's normal then we have to think about extr renal causes this is the weird one all right in this situation there is a couple different reasons why this can occur but the two big ones is that the solute intake is low or that this the actual

water intake is extremely high whoopsie this should be up upwards so it solute intake is really really low or the water intake is crazy high so if I have a crazy crazy low solute intake means I'm not taking in enough uh the electrolytes within my diet and my water intake as a response here is really really high what am I doing to my circulatory system I'm filling it with tons of hypotonic fluid so now my volume is pretty good all right so now here I can say that my blood volume is pretty good it's pretty

normal if anything it might even be a little bit pumped up in kind of the scenario but I'm filled with water right there is a lot of like hypotonic fluid inside of my circulation as a response what is my kidney going to try to do it's going to do its best to try to dump a lot of that water out into the urine and so it will kind of produce a very very very dilute urine all right so I'll have a lot of water a lot of water that's going to be present in the urine

right and so what does that mean that means the urine osmolality is going to be very low right that was those um ADH independent causes so I'm going to do my best but no matter how much water I try to be able to excrete out of the vi the kidneys there's too much high water intake or very little solute intake that no matter what the the blood that's actually leaving the Glarus and coming out I'm still going to have too much water in my system so no matter what there's still going to be too much

water remaining in my circulatory system and as a result this will drive down my sodium so then you have to ask yourself the question okay what are the things that are I'm either taking in so much water that my kidneys can't excrete enough of it or what are things that causes a very low solute intake where now I just have more water in my circulation with respect to low solute there's two reasons one is this can be due to what we referred to as a tea and toast diet so the tea and toast diet or

another one is it could be beer potomania where patients are just drinking very large amounts of beer or they're just drinking a lot of fluid and not getting a lot of solute within their diet the other one is excessively high water intake and this is usually in the disease that we refer to as primary polydipsia we see this in schizophrenic patients who drink tons of water or fraternity hazings another really common one that we see in the hospital a lot of the times is the patients are just getting too much hypotonic fluid so half normal

saline uh lots of water things like that that could actually also dilute down their sodium all right that covers in this particular scenario here all of the hypovolemic and UIC causes of hyponatremia let's now talk about the last one which is hyperemic all let's talk about the last type of hyponatremia which is hyperic hyponatremia so in this particular scenario these patients are very volume overloaded and so often times what we say for this is that they're going to have a very very large amount of total body water right so there's a lot of fluid that's

leaking in between their interstitial spaces in their cells and so usually they have a very heavy total body water but they also when you look at them they have a little bit more sodium within their body than other people usually do and it's usually leaking into their interstitial spaces or into their cells and so what happens is they also have a very slightly increased total body sodium now in this particular scenario if we have a very high amount of total body water and again a little bit more total body sodium this is what we would

see in these patients they're usually very emitus so they have maybe a lot of peripheral edema in their legs they also may have aites they may have pulmonary edema so when you osculate you may hear rails on oscilation they may even have a a very distended or plethoric jugular vein and on top of that usually these patients they gain a little bit more weight easily so they're a little bit more fluid overloaded their blood pressure might be a little bit more elevated as well all right often times though they have good mucous membranes good skin

turer so we talk about these patients because they're adius right what are the things that we want to think about you want to think about diseases that retain fluid right and often times that CHF curosis and CKD so let's talk about the extrenal causes which includes CHF and curosis how do these really cause this well in patients who have CHF they have some type of dysfunction of their myocardium which impairs their cardiac output so what happens to their cardiac output the amount of blood that they're pushing out of their ventricles into the aorta or into

the p ponary trunk is reduced so either way in these particular scenarios they have a very very low cardiac output so this would be the primary pathophysiological process here in CHF so in patients who have CHF they have a reduced cardiac output why is that a problem why is the reduced cardiac output a problem well if you think about it reduced cardiac output leads to a reduced amount of blood that is circulating within our arterior IAL circulation so what we say is they have a reduced effective arterial blood volume that is what's reduced so if

that's reduced then then what we can say is the amount of blood circulating through their bloodstream is technically low so they have a low effective arterial blood volume what would the JG cells sense they would sense a low blood volume a low perfusion to their kidneys as a response to that what will they release renin renin will lead to the increased formation of angiotensin 2 as well as odstone ADH so as a response here what are we going to get we're going to get a hyperactive renin angens and ostrin system and then you're going to

get a high ADH as a response here what is that going to do go to the kidneys reabsorb water what else is going to happen well the other thing that's going to happen is is I'm going to lead to more aldosterone and if I lead to more aldosterone what does that do that goes to the kidneys and helps to reabsorb sodium so if I go to the kidneys and I reabsorb more water via ADH and I reabsorb more sodium via aldosterone what happens to the sodium that's present in the urine it's going to be low

because I reabsorbed it so I'm stimulating these processes and now my amount of sodium that is present within the urine is going to be low that's how we remember extrenal causes usually they have a low urine sodium the ADH brings more water and then what happens is in these patients they're going to have more water in their circulation they also have lots of water and sodium sitting in their interstitial spaces so when you look at these patients they have lots of sodium sitting here very little sodium in their circulation and then they have lots more

water in their circulation and lots of water in their interstitial spaces and that's what makes these patients what we refer to as hyperemic they have more volume in their interstitial spaces not as much volume in their circulating circulatory system their arteries and veins now with that being said we understand how this leads to increased water reabsorption diluting the sodium and we cause increased reabsorption of sodium while the urine sodium is low how does therosis do this therosis is a kind of interesting one so therosis in patients who have very very severe therosis they undergo lots

of fibrosis of their liver and this fibrosis leads to reduction in hepatic synthesis but it also leads to compression of the hepatic portal veins and then the pressure builds up in this portal vein what do we call that we call this portal hypertension so they start developing something called portal hypertension where the presses is in their portal circulation are high what happens is the liver releases some chemicals the little vasod dilators and what these vasod dilators try to do is is dilate the actual splank niic the circulation that goes to our git so it tries

to undergo something called splank Nik Vaso dilation what this does is now watch this here's our circulatory system it goes here and it causes these vessels let's say that are going to your git this is going to your Git it dilates them and now what I do is I pull lots of blood to my git which leaves very little blood to go where through my the systemic circulation other than my git especially to my kidneys my kidneys sense a low effective arterial blood volume what do they do as a response to that they release renin

so then we pump up the renin Angiotensin aldosterone system and we get the same thing that we just talked about here increase water absorption bring more water in the circulatory system dute down the sodium and then aldosterone goes and tries to reabsorb some of the sodium and bring it into your bloodstream which makes your urine sodium low now there's one other mechanism and this helps to explain the edema Factor where your liver struggles to produce an adequate amount of a very specific protein called alumin when it gets destroyed if albumin is low albumin is supposed

to be a very potent osmotic agent so imagine here is these black dots are alumin they're supposed to keep water into the bloodstream what do they do if you don't have enough abuin are you going to be able to keep the water or pull it into the bloodstream no and so all of this is inhibited and guess where the water stays out here in the interstitial space what happens now to the amount of volume in your bloodstream it goes down so what does that do to your effective arterial blood volume it drops it so there's

a twofold process in sorosis and how this causes hyponatremia splenic visitation and hypo ABIA woo all right now obviously this could be elucidated via history the last one is also elucid via history but if you really needed to you could check a urine sodium urine sodium and these are going to be low the urine sodium in this one should be high again this last cause would be chronic kidney disease at least at the point of where these patients are like stage four five or they're on hemodialysis so we get to the point where we're calling

them almost instage renal disease usually what has to happen is these patients usually need a GFR at least near less than or equal to 15 milliliters per minute so as their GFR is really really significantly low what happens is let's say here I have some water right so here's some water patients are drinking water their kidney can only excrete so much water because they're they have very little nephrons we've destroyed tons and tons and tons of nephrons so they have very little nephrons available this water is supposed to move through the circulatory system it's supposed

to be filtered out and then eventually we're supposed to pee this water out but the problem is is that the kidney stinks at doing its job and it's not able to properly excrete the water so what happens to the amount of water that we excrete it is very very low so we bring in lots of water for this patient but their kidneys aren't able to excrete the water because they have very little nephrons available what happens to the amount of water that's leaving the glami then unfortunately they're going to have way more water so if

I have increased water that's present in my circulatory system what's that going to do to my sodium that is going to bring down my sodium but here's what's really interesting if I have lots of water what is that going to do to ADH it's going to suppress ADH so remember this suppresses ADH production so ADH suppressed States could be what disease is it could be due to beeram Mania it could be to the te and Toes diet primary poly dipsia or patients with in stage renal disease One More Concept so if I have low or

let's say suppress let's actually just for the Simplicity sake let's say low ADH the reason why they have hyponatremia is because they aren't able to excrete enough water from their kidneys what happens to this situation here well if they have lots of water then we say that their blood volume should be appropriate then if anything so their blood volume should be appropriate if it's appropriate right because if we think about this they have a lot of like water in their circulation and it's diluting down the sodium what happens now if their blood volume's low normal

what's that going to do to the kidneys it's going to tell the kidneys hey don't release renin as much don't lead to the formation of angiotensin and aldosterone as much so now the RAS system should be suppressed so what happens to aldosterone it should be low if aldosterone is low is it going to be able to reabsorb the sodium across the actual DCT no and since aldosterone struggles at this area to try to be able to reabsorb sodium it won't do that the sodium will get lost into the urine so what happens to the sodium

and their urine it goes up and so the sodium in their urine is up and so that's why you have high sodium in their urine so again renal causes you have to remember they will have a high urine sodium all right I know this was a lot hang in there with me and let's now move into the next step which is hypernatremia all right my friends so now we're going to move on to hypernia so it's the other end of the sodium disorders when the sodium is way too high greater than 145 is generally the

what we kind of Define that as now when a patient develops hypernut treia the pathophysiological mechanisms are listed over here it's usually the exact opposite so in hyp nmia usually the patient is just pumping out tons of ADH reabsorbing a lot of water diluting down their sodium and the opposite situation here is is one of the most important ones to remember we can see that there's a decreased ADH release so usually we Define this as something called Central or nephrogenic di so let me explain these two in central di diabetes incipits the problem is that

the poster pituitary area the hypothalamus in some way shape or form is not adequately producing enough ADH so the ADH levels are usually deficient right and we'll go over this a little bit more later when we get into the subcategories of hypernia hypo uvalic and Hyper but if the ADH is low what happens well then it doesn't hit the V2 receptors appropriately right and if I don't hit these V2 receptors appropriately am I going to increase the expression of aquaporn sub units no no am I going to be able to reabsorb water across the uh

Lumin cells and into the blood no so I lose a lot of water into the urine another thing is for nephrogenic diabetes and citus these receptors are the problem so in nephrogenic di these receptors are not appropriately responding to the ADH so the ADH could be present it could be in high amounts it won't matter it's not going to respond so there's no response are you gonna be able to express these aquaporn subus no as a response are you going to be able to reabsorb water no so as a response I get decreased water reabsorption

into the bloodstream if I get decreased water reabsorption what happens to the relative concentration of sodium it'll start to go up because it'll start concentrating my blood as I lose more water from the vascular system right it's straightforward and again the concept here is is because we are inhibiting the expression of oorn sub and as a response I lose tons and tons of water into the urine what is that Doe to the osmolality of the urine well it's super dilute now so the osmolality of the urine is going to be very low and this is

usually pretty much indicative of a patient who has something called diabetes and citus now with that being said if I see a patient who has a very very dilute urine I send it off to the lab and when I check it I see a very very low urine osmolality generally we say like less than 600 all right usually 300 to 600 it's pretty low in that situation I could definitely think about diabetes and citus the other scenario that I want you guys to think about is what if the aldosterone levels are too high if aldosterone

levels are too high there's a couple different reasons why that could happen but the biggest thing here is when your uh adrenal cortex for whatever reason is pumping out tons of aldosterone maybe it's because there's a a stimulus a secondary stimulus or maybe there's a tumor of the ad cortex that's pumping a lot of aldosterone out either way there's a lot of aldosterone when I have a lot of aldosterone what is the problem with that why is that a significant issue well let's imagine here let's say I have high amounts of Ostrum will'll represent this

with kind of this blue Air this blue dot here it gets into the cell right it's a steroid so what it's going to do is when it gets into the cell it activates a receptor increases the expression of these guys so it increases the expression of these enac channels if I increase the expression of the enac channels what am I going to do what am I going to reabsorb across this cell I'm going to pull tons of sodium across the cell so I'm going to increase the expression of the enac channels which is going to

increase sodium reabsorption but it'll also bring a little bit of water often times in aldosterone release States when it's high alone you're going to increase your sodium and water reabsorption which is going to pump up your blood volume which is going to pump up your blood pressure and so that's one really really important thing to remember is that often times these patients are slightly hyperemic and hypertensive and it's a very common cause of secondary hypertension so please think about that so in a patient coming with excessive polyurea think about di in a patient coming in

who is hypertensive hyperemic admit is slightly appearing start thinking about hyperaldosteronism there is another one that you want to think about we'll talk about a little bit later but I want you to start having a differential diagnosis and the differential diagnosis that you have to start Cons considering in these states is sodium chloride containing Solutions so as a patient getting a lot of sodium chloride Solutions are they in the hospital and in the hospital are they getting a lot of isotonic saline hypertonic saline bicarbonate tpn all of these things can also create a hyperemic hypertensive

and Hyper nitrc State all right last scenario here is when a patient is losing a lot of water from their body and they're not just drinking enough water back in they're not bringing it back in so let's say I have a patient who's peeing out a ton of water so they have lots of renal losses right tons and tons of water that they are losing here or they got a punami going on they're dropping turds and it's just filling up the bowl the bowl with water or they're vomiting out a lot of water right so

in these particular scenarios what am I doing I'm losing water from a renal Source or I'm losing water from an extra renal Source maybe from the git maybe from the skin so we're going to call this extra renal losses and we'll get into the different types A little bit later but in this scenario I'm getting rid of a lot of water it's not from you know it's from either the git the skin or the kidneys so as a result and am I reabsorbing enough water from the kidneys am I absorbing enough water across the git

am I retaining fluid inside of my skin cells well in this particular situation no and so what starts happening to the water inside of the bloodstream it starts going down because I'm not absorbing or reabsorbing things appropriately so as water starts getting lower what happens to the sodium concentration inside of the bloodstream it resultingly goes up so now I have a patient who is hypernatremic what would this do well generally when you're water goes down and your sodium goes up what it's supposed to do is activate your thirst centers so it's supposed to activate your

hypothalamic thirst centers and make you drink water if I drink more water what will then happen hopefully I'll bring up my water concentration and dilute down the actual sodium so what's supposed to happen the normal pathway what's supposed to happen is is I'm supposed to stimulate my thir centers right which is in the hypothalamus and then as a response to that I should increase my water consumption and the whole purpose of that is that I'll bring more water into the body so this is the normal physiological response but what if I have a patient who's

losing water from the git skin or the kidneys but the problem exists right here is that they will not increase their water consumption so this is where that a problem exists so in a patient who has maybe renal losses or extr renal losses this is what's leading to a decrease in our serum water so this is what's dropping their serum water right but then what are they supposed to do become thirsty drink what if I have a patient who has a decreased water intake if I combine both of these the problem with this is I'm

going to be doing the same thing I'm perpetuating this process here I'm not getting enough water back into the circulation what are some reasons why a patient won't drink enough water well often times it's because they have something going on uh such as let's say they're intubated they can't they have a tube in their Airway so they can't tell somebody that they're thirsty or they're sedated another one is they could have some type of altered mental status or elderly individuals often times sometimes geriatric patients is a very common population that we see this in and

the last one is maybe decreased or limited access so maybe you have a limited access to water for some type of socioeconomic reason or whatever it may be but this combination if you will is what is we see most often as the cause of hypernia most likely hypovolemic hypernia hypervolemic hypernia and uvalic Hyper nutr let's go through that now all right my friends let's now go through each type of hypernia based upon volume status and again this is super important just in the same way that we talked about it with hyponatremia you're assessing the patient

to look do they have decreased skin turer do they have dry mucous membranes are they hypotensive tacac cardic do they have some of these features without any edema present what way are they losing water and often times it it's pretty simple if the patient says that I've been peeing a ton that's often times pretty you know elucidative of the cause but another way that we can kind of look at this is in a patient who has hypovolemic hypernia what we really want to do is is understand something called you know where's the water being lost

and we can do that off of urine osmolality helpfully but also history so let's say that we think about some renal reasons why a patient would be losing tons of water water so here they're losing a lot of water in their urine all right if I lose a lot of water in the urine that means that the urine is very dilute if the urine is very dilute then what that tells me is that the urine osmolality would be what it would be low because I have a very dilute urine it's not a very concentrated urine

and so that's relatively helpful right away and so one of the things I can tell myself is if I check a urine osmolality and it's lower it could be indicative of di diabetes insipidus or a renal cause related to hypovolemic hyponatremia the way that I would want to do this is in a patient with the ey they appear uimate they don't appear to be volumed down in the sense that they don't have decreased skin turg they don't have any types of dry mucous membranes or hypotension tacac cardia in these patients they appear uvalic in this

patient they definitely appear to be hypovolemic so what would be some reasons I would lose a lot of water across the kidneys well it's usually a simple thing such as osmotic diuretics and the two that I would really want you guys to you know strongly remember here is going to be manitol and hyperglycemia so in the history it's pretty evident if a patient received manitol why in the heck would I give somebody manitol the reason I would give somebody manitol is did they have an ICP issue so as manol often given to help to reduce

the intracranial pressure so if someone had any kind of recent intracranial pressure issues that I'm giving the manol for another one is in patients who are diabetics who have very high glucose levels the reason why this is important is whenever you have very very high glucose levels glucose acts as an osmotic agent and imagine here now manitol glucose I represent them as these black dots here they're going to be moving moving through our tubular system and if you have a lot of these agents they're super osmotically active guess what they're going to do they are

going to yank water with them and all of this water is going to get yanked into the actual urine so these are exhibiting an osmotic type of effect so again if a patient has a very high glucose think do they have any underlying disease like diabetes so glycose Uria and the manatu are very common to cause excessive polyurea but very watery watery urine output and that would cause volume depletion in that particular scenario an extr renal cause in this situation we're thinking about okay there's a GI loss or there's a skin loss and believe it

or not this is exactly the same the hyponatremia the only difference is is in this patient they're going to lose a lot of water from their kidneys and guess what they're not going to drink the water at all and because they don't drink any water their water intake is reduced they're going to perpetuate their hypernatremia same thing if they're pooping vomiting or having excessive diaphus and burns and they're not drinking water they're not reping back the water that they're losing so in patients who have very very terrible let's say for example this patient could be

uh diarrhea it could be vomiting or it even could be excessive NG tube suction in this scenario it could be excessive diaphoresis so they're sweating like crazy or it could be severe burns in these particular scenarios what you really want to remember is something very interesting they're losing a lot of water from areas that are not the kidneys so because of that what happens all right watch this in this scenario both of these patients they're losing volume all right so they're going to lose volume we're going to go down the extrenal cause so if you

lose blood volume because you're pooping it out vomiting it out or you're having it lost from your skin what is that going to do to your kidneys it's going to tell the kidneys that the profusion is low if it tells the kidneys that the profusion is low what's that going to do it's going to activate your renin Angiotensin aldosterone system if you activate your Ren and Angiotensin aldosterone system what should that do that should go and activate ADH if I increase ADH production what will that try to do it'll try to go to the kidneys

and retain water so if I try to go to the kidneys and retain water what happens to the amount of water that's present in the urine there's less water in the urine what happens to the urine osmolality it goes up and so in these patients they have a very high urine osmo ality that's helpful so look high urine osmolality in extrenal causes low urine osmolality and renal causes and that's super important to remember this kind of process occurs here the same thing where they'll have low blood volume you'll activate the Ren otens and aldosterone system

but it won't matter because you're continuing to lose water so that's one of the big things that are helpful here all right so UIC hybernia in this particular scenario it's two particular processes that are occurring here it's either I'm not making or releasing ADH or I'm not responding appropriately to the ADH so remember I told you that this one if there's damage to the hypothalamus post pituitary what happens are you able to produce and make ADH as a response here no so what happens to the ADH levels in this patient it's low if I have

low ADH we already know all of this we don't really need to go crazy on this we already understand that what this will do is this will go to the kidneys and you're going to lose a lot of water into the urine right straightforward the question that you need to ask yourself is what's causing this and this is a disease that we refer to as Central diabetes and CPUs so Central Di and often times this is usually due to maybe a traumatic brain injury so I think traumatic brain injuries are definitely big things to remember

um another one is I would say some type of surgical procedure that is in the vicinity of the h of the pituitary sometimes we even see these after patients have removed the pituitary adenoma and the last one is I would say What's called brain herniation so when a patient goes uh under fortunately they experience herniation um onto their brain stem this is another presentation which we see in central di all right so in this problem it's that they're not making ADH so the kidneys have appropriate receptors so they would respond to it but they don't

have enough ADH this one one this puppy is pristine he's looking good so in other words this hypothalamus poster pituitary they can pump out ADH like it's no other all right so it's working well right so I can I can make ADH if I really want to now here's where the problem exists and we already talked about this a little bit the problem exists here the problem exists here these cells the V2 receptors are not appropriately responding to the ADH so they don't reabsorb water lose a lot of water into their urine question comes up

is what's causing this we call this one nephrogenic diabetes insipidus and this one we see the most common offenders to be the use of lithium and bipolar disorder that's one really really big one so look in the history to see if they're taking any lithium maybe even check a lithium level another one is pottassium and then calcium so it's the opposite whenever calcium is extremely low this can cause nephrogenic Di and whenever calcium is really high it can also cause nephrogenic di either way both of these they present very very similarly where they're going to

lose a ton of water into their urine so the urine osmolality in both of these situations here I'll bring it over here just so that we can remind ourselves is going to be what it's a very very low uran osmolality so it'll appear somewhat similarly in what situation to the hypovolemic hypernia that we see with renal losses big difference here is that this is a UIC State that's a hypovolemic State all right let's move on to the last scenario which is hypervolemic hypernia all right my friends last one which is hyperic hypernia so in this

patient we had again hypovolemic they're volume down uvalic they appear perfectly normal all right the hyperic patient are overloaded all right and what we say is that in these particular patients they have just a lot more sodium than they do water the uvalic patient usually they have a little bit more sodium than they do water and the hypovolemic patient they have been significantly depleted of water and a little bit less depleted of sodium so let's think about again in hyper volic hypernia the patient's problem is usually that they're just their aldosterone levels are way too

high now aldosterone release is kind of a variable thing so for example I can have something called primary hyperaldosteronism so primary hyper aldosteronism so this is usually a tumor or hyperplasia um of the actual adrenal cortex and in this particular scenario it is pumping out high levels of aldosterone right so often times more than not it is usually some type of tumor such as an adenoma uh it also could be in certain scenarios like hyperplastic tissue as well but either way it's the adrenal cortex that is the problem and in this scenario it is pumping

out way too much adrone another scenario is it could be what we refer to as secondary hyperaldosteronism and in this scenario it's really there is a influx of stimulation to the JG cells that are pumping out tons of renin and what you have to know is is that renin leads to the formation of eventually Angiotensin and so if I activate my Raz system thus the name when I activate the Raz system I'm naturally going to stimulate via Angiotensin 2 I'm going to stimulate the production of aldosterone the primary stimulator for secondary hyperaldosteronism is usually low

renal perfusion we talked about this more in the Endo Endocrinology section but you can see this in things like CHF you can see this in sorosis you can see this in renal artery stenosis but either way these things are stimulating the RAS system which is increasing ostrin production so again I wouldn't you know put all your money on it but think about CHF and think about renal artery stenosis and think about sorosis as potential triggers here for secondary hyper aldosteronism or think about a tumor either way aldosterone's high all right cool what does high aldosterone

really do well if I got high aldosterone remember this is a steroid hormone some people even say that Cushing syndrome because it kind of has a little bit of a mineral corticoid activity can also act like this but I don't want to take you guys too far in that but what this is going to do is is this is going to come in it's going to activate your genes and it's going to increase not your Wrangler genes I'm talking about like you know the actual DNA genes but it's going to increase the expression of enac

channels if I increase the expression of these enac channels then what I'm going to do is is I'm going to move more water across the distal convoluted tubular cells um and then I'm sorry sodium I'm going to move more sodium and then a little bit of water often times follows so I'm going to increase the expression of enac channels which increases the reabsorption of sodium and a little bit of water often times follows into the bloodstream do you see how that directly causes hypernia but again if I add in we're going to make this a

little bit of a comparison here we'll just do one of these guys here one water molecule the combination of all of this is going to do what is going to increase the blood volume and if I increase my blood volume what will I do to my blood pressure I'll increase my blood pressure and so often times these patients will present with hypertension hyper vmia but there's one other thing aldosterone does aldosterone also increases the expression of channels that help to put pottassium into the urine and so that's another thing that you want to watch out

for is you want to watch for them to lose a lot of potassium into the urine and sometimes they even lose a lot of protons into the urine but the big thing that I think is helpful here and differentiating these is that if I dump a lot of potassium into the A and what happens to my potassium in the bloodstream it drops so hypoc Calia plus hypernatremia plus hypertension think about high aldosterone States the last thing I will say is again hyperic hypernia High aldosterone definitely is one of those that you have to remember but

don't forget what I told you about the differential diagnosis if I take a patient and I have here a bag of a solution that is super salty and I just take this solution and I dump it right into their bloodstream right and I have with it a lot of volume in there's volume right so it's going to have water it's going to have a lot of other things but it's going to have a heavy amount of salt if I take and push that sodium right into the bloodstream along with volume like water then what is

that going to do to my sodium it's going to pump it up but it's also going to pump up my water so you have to watch out for iatrogenic causes of hyper volic hyper Nutri that we often times see in the hospital setting which again is which one the big one is going to be a increased use iatrogenic use of sodium chloride solution and what are things that I want you guys to remember well one could be 0.9% normal saline another one could be what's called hypertonic saling there's 23% 3% and the other one is

we call this bicarb so we uh we often times call it hypertonic bicarbonate and even tpn to some degree has a lot of sodium in it so if you give a lot of these things which we see in like a neurocritical care units or Hospital units this can definitely increase the sodium and because you're giving them volume increase their volume but they shouldn't have to some degree this hypokalemia all right my friends that covers the pathophysiology that causes a lot of this on the sodium disorders let's now talk about why these are so bad all

right my friends so now we're going to talk about the complications of hyponatremia we'll do this one first then we'll talk about the complications of hypernia it is of significant importance that you guys really really remember the complications of hyponatremia though you're going to likely get a question or experience it at some point in time in the clinical world so with hyponatremia the biggest fear that we see with this is cerebral edema the concept behind this is actually relatively straightforward so imagine here I have my bloodstream and I'm going to use these black dots here

to represent sodium right now let's say we have a patient who has normal brain tissue here right they should have a relatively equal amount of electrolytes in this case let's say sodium in the brain tissue in comparison to the actual extracellular space which is going to be the vascul and so there should be a nice equilibrium if you will between the tissues in the bloodstream but in a patient who has hyponatremia let's say that the again the amount of solutes are sodium that they have in the bloodstream is going to be in this particular scenario

much less in comparison to what they have in the brain tissue now where does water like to move water likes to move of areas move to areas where there is higher amounts of sodium higher amounts of solute concentration so where's it going to want to move is it going to want to move from the actual brain tissue into the blood or from the blood into the brain tissue I think from the blood into the brain tissue right and so what happen is is water will flood into the brain tissue and as the water floods into

the brain tissue it starts to become emitus and swollen and as a response one of the most classic features that we see is that intracranial pressure starts Rising so as the brain starts swelling the pressure inside of the skull starts Rising because the Monro Kelly Doctrine says that again the skull is a fixed space so if you have anything like more brain tissue more blood more CSF it's going to make the pressure inside of that skull go up what are some potential clinical manifestations of elevated intracranial pressure well as intracranial pressure goes up one of

the things that we see is we see some degree of swelling and compression of the brain stem structures for example maybe I start damaging some of the the structures in the medulla or compressing some of the centers in the medulla that control emesis right and so what starts happening is these patients start experiencing things like nausea and vomiting the other thing is that whenever you increase the pressure inside of the skull it starts compressing some of the no receptors are pain receptors in the meninges and so I may start stimulating some of these pain receptors

which then leads to what increasing pain which is going to represent as headaches so I may start seeing very very bad headaches so headaches nausea vomiting here's where it starts getting a little bit worse if the swelling is big enough that it starts compressing in on the cranial nerves so imagine this swelling starts getting a little bit bigger and now I'm compressing on this nerve that goes to the eye what's this nerve the third nerve these patients can start to experience herniation findings and there's different types of herniation I think one of the big ones

to remember is when a patient has a fixed and dilated pupil this indicates potential third nerve py in this the scenario of Uncle herniation so you want to watch out is there any evidence of Uncle herniation so watch for their pupils to see if they're appearing fixed and dilated right so in other words they're dilated I shine a light they don't constrict which they should the other thing that I worry about is if I start seeing headaches changes in pupils nausea vom but here's the worst case scenario here we have this blue structure that extends

throughout the brain stem it controls our level of Consciousness if you start compressing this structure so we compress the third nerve we compress some of these menial areas here what if we start compressing the reticular activating system if I start compressing the reticular activating system my level of Consciousness starts to decline the patient can go from maybe a little bit lethargic to now you're having to stimulate them you're having to scream their name push on them a little bit squeeze them pinch them to get them to wake up so now maybe they're more obtunded or

stous worst case scenario they could go into a complete come state so you want to watch are they moving along that spectrum of lethargy to obtunded to worst case scenario are they in a coma because this is a common presentation so look for any of these findings and if this is suggestive of that often times we need to start treating these patients emergently so iccp issues is one way another thing that starts to happen is is that as you start causing swelling of the brain tissue you agitate the cortex so the cortex starts becoming really

really aggravated and if the sodium gets pretty low it can increase the risk of seizures so not only am I worried about intracranial pressure I'm worried about an increased risk of seizures so these are the real big things that I have to watch out for in these patients who have hyponatremia now with that being said this doesn't usually occur when the sodium is like 134 all right this isn't going to occur in someone who's had a sodium that's been low for a long time because the reason why is the brain tissue adapts the brain tissue

has the ability to secrete like idiogenic Osmos which helps to regulate the movement of water in and out of the cells so like usually after 48 Hours the brain's adapt and it helps to reduce the risk of Edema it's really these types of events that occur in what type of scenario so when we worry about symptoms we worry about it in a couple different scenarios one is is it acute meaning has these symptoms developed in less than 48 hours all right because if it has the brain hasn't had time to adapt second is it severe

and what do I mean is the sodium when we talk about severe hyponatremia what I'm talking about is is the sodium less than 120 so if I see that if I have symptoms and on top of that so let's say is there symptoms right so you have symptoms you want to know is it acute and is the sodium really low less than 120 if you have symptoms and it's acute you need to treat these patients emergently if it's symptoms and it's severe less than 120 you need to treat this patient emergently so you have to

know these things because this is where we will see these ICP issues and increased risk of seizures is when it's acute and very very severe all right the other complication that we can see with uh usually patients who have hyponatremia is let's say that you start off they have a sodium that's pretty low right so let's say for example we have this patient here um you start them off maybe they have a little bit of Edema right so they have hyponatremia and then what happens is water is moving into their brain tissue right so they're

getting a little bit of Edema right so they have a little bit of cerebral edema as a response of their hyponatremia then what you do is you say okay I got to treat these patients and what I'm going to do is is I'm going to start giving these patients medication so what I'm going to start doing is I'm going to start giving them hypertonic Sal maybe and so I'm going to start increasing the sodium levels in their blood right as I do this look what starts to happen I start rising up the sodium in their

bloodstream giving them hypertonic saline and when I do that maybe I just do it way too quickly and what happens is is I'm trying to treat the edema but I pull way way too much water out of the brain tissue and as a result the brain tissue begins to shrink and then eventually cells start dying and the area where cells tend to die is the ponds that is the problem so I'm starting to demate some of the neurons present within the ponds so what we see is in osmotic demalation syndrome is a patient who has

hyponatremia I treat them by giving them sodium when I give them sodium and I correct it too quickly the water will get sucked out of the brain I'll shrink the brain tissue the cells will die what's the problem at what point do we say oh if we go above this we're really increasing the risk of osmotic demolation syndrome well the textbooks again it can vary from textbook to textbook but often times what it's been been shown from the literature is that whenever you try to increase the serum sodium and you're trying to do this because

maybe they have cerebral edema maybe they have hypon and you're trying to treat it if you increase the serum sodium greater than greater than 6 to8 mil equivalents per liter in a 24hour period you increase the risk of causing this cellular Shifting the osmotic shifting way too quickly you shrink up shrivel those cells crenate them and cause death to the pontine neurons this is something that again we see in hypon net now there is certain patients who have hyponatremia that are more at risk for this for example if you have severe hyponatremia if you have

a patient has hyponatremia that's due to beer potomania tea and toast diet those kinds of patients or cerotic hypokalemic they're at very high risk and you have to be careful or chronic if it's been greater than 48 hours you should not aggressively treat these patients but that's something to remember now in this scenario it was the result of acute severe hyponatremia that I develop symptoms and this is because I have symptoms I'm trying to treat it but I overcorrect it what would that look like well often times this Pro process doesn't occur for at least

approximately upwards of one to two weeks one to two weeks they start to develop symptoms so what would this look like so one of the would be the corticos spinal tracts right now if I damage the corticos spinal tracts what you guys have to know about these bad boys is that they're supplying a lot of the muscles right so they're going to come down they're going to cross up the medulla but you're knocking out potentially both of them and you're hitting the entire ponds so you may lose the upper and um you may lose the

upper and lower extremity muscle function so these patients could develop quadriplegia so that's terrifying in itself the other component here is that you got a lot lot of cranial nerve nuclei here my friends so I got you know cranial nerve six seven eight nine a lot of these Supply muscles of the eyes right especially six which helps to allow for more of the particularly the lateral rectus so you know your horizontal movement so you may lose that you may only really get your vertical eye movement truly and so these patients may only have that vertical

eye movement uh but in general they may have diplopia so double vision and only be able to move their eyes vertically they may have dysarthria and dysphasia so they may have some of those bulbar symptoms as well and they may have some dysphasia so they have difficulty swallowing difficulty speaking difficulty with eye movements particularly they may only have vertical that's preserved and then depending upon if they hit the reticular formation they may even have impaired Consciousness so if you think about this this patient can't move they might have difficulty with their speech and they might

not be able to move their ey horizontally only vertically often times this can look like a locked in state and so this is one of the terrifying things about this disorder that's why whenever you're treating a patient who has hyponatremia you really don't want to exceed this in a 24-hour period obviously your goal is to try to get their sodium up to stop them from seizing or to reduce their ICP once you're doing that bring that sodium back down so that you don't increase the risk of them developing a couple weeks later osmotic demolation syndrome

when we talk about this we're going to put everything together now patient comes in they get a sodium less than 135 if they do that you get a seros mity all this is doing is looking at the bloodstream and looking at how the tenacity of the bloodstream is appearing so if I get that and it comes back normal 280 to 295 it's probably not a true hyponatremia there's something else that's happening here that's causing an artifact or an abnormal value and usually we call this isotonic hyponatremia I want you to think about two particular etiologies

here one is too many proteins or too many triglycerides so if there's too many triglycerides they could have hypert triglyceridemia maybe check a triglycerides and see if they're high or too many proteins do they have multiple Myoma or do have they gotten some type of like IVIG or protein kind of drug if that is the case this can throw off the way that the uh sodium is calculated into the actual system so if it's normal 280 to 295 that's a normal osmolality it's not real it's either High proteins high triglycerides in the other hand if

it's way too high it's not possible to have hyponatremia with a hyperosmolar bloodstream okay that means you have something else in the bloodstream that's increasing the tenacity and masking and hiding that sodium usually this is hypertonic hyponatremia and it's due to high glucose or high manitol okay so either they have very very high glucose check the glucose and you can actually calculate the glucose and look at that in comparison to the sodium and get a new corrected sodium level so again if you ever see that a patient has a super high glucose and a low

sodium plug it into a calculator and actually make that modification it's not real all right if they've had a recent ICP issue and they've received manitol that can also skew their sodium these are really really important things that they can get you on the exam what you want to see is hypotonic less than 280 that's a true hyp onia that means that the sodium is really low in the bloodstream and you need to figure out why I then need to diverge is it ADH dependent or ADH independent how do I determine that I check the

urine osmolality I know if it's high greater than 300 it's ADH dependent if it's less than 300 sometimes we even say less than 100 it has nothing to do with ADH it's ADH independent which means the ADH is appropriately suppressed okay I'm going to go the ADH dependent route now when I look at this again I want you to think backwards here for a second in a patient who has a decreased effect of arterial blood volume that's going to activate the Raz system right and patients who have siadh that's going to increase ADH right so

in patients who have hypovolemia or hypervolemia they're going to increase their Ras system and increase ADH production in UIC hypon nmia like sadh that's going to increase the ADH production by the pituitary or bi and ectopic site what's the ADH going to do go to the actual V2 receptor in the collecting duct reabsorb water there's going to be less water in the urine the urin osmolality is going to be high in a patient like this this is super common for ADH dependent hyponatremia for the ADH suppressed it was low solute intake high water intake in

these patients their plasma osmolality was low they suppressed ADH if ADH wasn't present what did it not do it did not reabsorb water what happened to the water in their urine it was high and therefore it was dilute and that's going to be a low urine osmolality so this is where you have TN toast beeram Mania primary polydipsia instad adrenal disease this is where you're going to have all the hyperemic and hypovolemic causes and uvalic hyponatremia that we have to sift through so now that you've done that let's kind of move down this arm let's

see that you obsess um obtain the volume status if I do that and I notice that the patient has decreased skin turg so I stretch their skin and it kind of doesn't kind of return that sells me hypovolemia if I notice a Fisher tongue signifying some dry mucous membranes that's indicative of hypovolemia if I see left if I see lower extremity edema that could be in indicative of having a lot of pitting edema this is concerning an indicative of hypervolemic state and if I see jugular Venus distension this is more indicative again of a hyper

volumic state so with that being said I can usually have a pretty good idea of how to determine if a patient has hypo or hyperemia based upon that exam if they have a dry mucous membranes if they have decreased skin turg low blood pressure high heart rate they're probably hypovolemic if they have moist mucous membranes jvd they have um pulmonary edema pitting edema AES that would suggest hypervolemia now let's say that a patient you look at their volume status and they don't have any features of hypo or hyperemia that's a uvalic hyponatremia what was the

most common one here for this one siadh for here what I want to do is before I actually make the diagnosis of Si ADH I have to rule out endocrinopathies remember I told you that so you want to check tfts to rule out hypothyroidism and cortisol to rule out adrenal insufficiency if you have done that then it's probably s then you got to go looking for brain injury pulmonary disease and drugs all right what else is another important Point here for sidh it also had a very high urine sodium all right that was was an

important point to remember as well now if I look at the volume status and they have dry mucous membranes they have a decreased skin turg hypotension they have um flat jugular veins they have features of tacac cardia and they definitely look hypoy liic what did I tell you to do it's either reenal or extrarenal how do I determine that urine sodium the reason why is if the urine sodium comes back and I say oh okay it's high that tells me that it's coming from the kidneys that's all renal and that that's really easy to think

about right because that was adrenal insufficiency which was one big one that's going to drop your aldosterone siadh is another one that can also do this and either way all of these things are suppressing aldosterone and that's going to lead to what less sodium reabsorption here and you're going to lose that sodium in the urine and that's going to lead to high sodium losses and so any kind of low aldosterone State siadh can cause this but what is the big one diuretics any kind of dtic can also do this as well so adrenal insufficiency uh

cerebral salt wasting uh Loop dtic thide Diuretics and siadh all can cause high urine sodium all right that's pretty interesting now again you're only going to see this in renal losses for low urine sodium that tells me that the kidneys aren't the reason why they're dumping sodium and the body's trying to conserve the sodium to improve their blood volume that means they're losing volume from somewhere else that's coming from the GI or the skin that's extr renal sodium losses remember if you have all these extrarenal losses your effective arterial blood volume is dropped the RAS

systems activated aldosterone's activated the kidneys are going to be reabsorbing sodium and they're not going to have a lot of sodium in their urine that is the key difference here extrenal low urine sodium renal High urine sodium now from here if I think hyperic they have jvd they have pulmonary EMA so they have crackles rails on oscilation they have um maybe even some weight gain they have some pitting edema if those things are present it suggests hypervolemic hyponatremia for Then I then need to kind of say Is it CHF is it therosis oh do I

have to really do any of that not really I can just check their urine sodium it will be low if it's extra renal that's your CHF or curosis all right I'm done with that this is pretty straightforward right that's not too bad if it's low less than 300 that's ADH suppressed if I look at the volume status there's only two UIC and hyperemic so it's a hyperic oh that one was easy that was inst stage renal disease if I really wanted to I could check the urine sodium if the urine sodium is going to be

high it's inst adrenal but if the patient appears to have UIC kind of volume status there's really only a couple things Tean toast primary poly dipsia and beer potomania and that's really it increase water intake primary pipia decrease solute beer podam Mania Tean toast tide this is the way that you can take everything that we looked at and put it together what about hypernia for hyper netrum when that sodium is greater than 145 you don't even need to check the cumos molality it should always be high okay because sodium is is controlling their osmolality it's

contributing to it urine osmolality is the big answer you want to know if the water is high in the urine or not so if it's low less than 600 that means that you have a low urine osmolality that means that there's a lot of water that's being lost into the urine that's a renal problem that's a renal water loss that was osmotic diuretics and that was ADH poor ADH release or poor ADH response and that's it because again osmotic diis you're causing lots of water to be lost and on top of that di so either

less ADH or no ADH effect you're not reabsorbing the water in both of these scenarios you're losing tons of water into the urine you're diluting down your urine and making it have a low urine osmolality if it's high that tells me that the kidneys are having ADH present and it's reabsorbing it right um the other thing I would be thinking about is aldosterone kind of maybe on a higher side too so in these patients I'm thinking that they have a low effective arterial blood volume in this particular situation this could be because of an extraen

L skin GI they're depleting their water the RAS system gets activated ADH gets activated goes to the kidneys reabsorbs water to repl their water loss and then what happens to the water and their urine it's low so what happens to the urine osmolality goes up this is going to be your GI losses and so that's really pretty straightforward right so here let's now say that I look at the volume status here because I can take diuretics and I can take ADH or Di and separate them based upon their volume status if I look and I

say it's UIC that's di all day so it's then I have to say okay if it's di I need to determine if it's Central or nephrogenic how the heck do I do that I give them ADH also known as ddavp which is desmo press now here let me explain I give a patient desmopressin when I give them the desmopressin their urine osmolality goes up that's Central di now here's why in these patients they're not making ADH all right from their poster pituitary you're going to give them ddavp to replace that it's going to stimulate the

receptors reabsorb water are you going to get water in their urine no not as much there's going to be less water what happens to the urine osmolality it goes up up that tells me that the problem is an ADH production problem if I give them ddavp and there's no change it means that they're making ADH appropriately it's just the receptor not responding so I they have ADH present I give them ad ddavp they both bind to the same receptor it's not going to matter are they going to reabsorb water no so what's going to happen

to the water it's going to be dumping into the urine and they're going to have no change in the urine osal it's going to remain diluted that's the concept of how you differentiate these two all right now for hypovolemic it's just diuretics right that's pretty straightforward if you really wanted to you can say diuretics for the renal water losses and that's done so if the urine sodium is high what do I got to do oh that's osmotic diuresis that's it that's probably going to be those patients who are having lots and lots of water loss

so osmotic diuretics are going to be the big one all right hyperic hybon nmia this one's actually all primarily hyperaldosteronism so I I can just chain it check a renin and aldosterone level if the patient has hypertension hypernia and hypokalemia if I do that and it comes back high aldosterone low renin which one's that um that's primary because that's the adrenal cortex problem if it comes back high and high that's a secondary problem secondary hyperaldosteronism for extr renal all I want to do is check the urine sodium and if that's low again what it's telling

me is that aldosterone is cooking baby aldosterone is going over to the kidneys and is trying to get lots of sodium and water into the bloodstream that means the kidneys are working you're losing volume from somewhere else where are you losing it from probably from the G or from the skin and that's how we EV evaluate hypernia baby now we've thoroughly evaluated hypo and hypernia how do we treat these patients patient comes in they're saying okay let's than 48 hours I've had hyponatremia symptomatic meaning they're having high ICP or seizures so what's the highest CP

look like headaches nausea vomiting reduced level of Consciousness maybe even worst case scenario they're developing herniation signs if that happens you need to treat the edema or treat the seizures and get the sodium up until they stop having those issues so concept here is if they have cerebral edema you got to get the sodium up and you're going to do that often times by giving them a very concentrated sodium solution it's called 3% hypertonic salum all you're going to do is give them lots of sodium to pull water out of the brain tissue and reduce

the ICP or stop them from having seizures often times what we'll do is we'll give them a couple bises we'll give them like 100 milliliters we'll recheck the sodium in a couple hours and if we haven't gotten at least four to six increase then we can keep going a little bit more once we get to about this you're not going to get any more benefit in reducing ICP or stopping seizures so you don't need to go anymore you're just going to cause harm if you go too high so initially we'll give them 100 milliliters of

3 % hyponic salum bump it up stop the seizures reduce the ICP check the sodium see what happens have I got up to 4 to six okay stop if I haven't I can give them another Bolis and re-evaluate it's important though that after you recheck that sodium and you've given them like two bises that they're above 68 in a 24-hour period you can't give them anymore and you might have to give them a little bit of water to bring that sodium down so that after the 24-hour period it's not above six to eight of a

bump from their initial sodium okay you don't want to cause osmotic demolation syndrome so that's how we'll treat cerebral edema or seizures if the patient has hypovolemic hyponatremia though and you've actually let's say that this patient comes in with this feature you treat them afterwards you then kind of treat their underlying cause what's the problem with hypo liic they lost sodium Rich fluid give them back the sodium Rich fluid yeah that's it normal salum would be good enough and you're basically going to do two things you're going to give them water which is going to

improve their water and then if you give them normal saline it's high in sodium chloride you're going to improve their sodium and then on top of that you're going to improve their blood volume all of these things are the perfect scenario for uvalic hyponatremia this is all to do with SI ADH okay so they're making too much ADH how can I stop them from reabsorbing a lot of that water restrict the water intake all right decrease it to like less than a liter a day or a liter a day avoid any sodium chloride Solutions this

is super super high yield a lot of the times there used to be back in the day they would have a patient who comes in hyponatremia give them a sodium chloride fluid bows and see what happens when you recheck their sodium and if it's s ADH the sodium will drop here's the reason why in a patient who has sadh they're pumping out a ADH you give them any bit of water guess what they're going to do every bit of water they're going to bank that and reabsorb it and you're going to drop their sodium so

it's important to avoid water in any way shape or form if possible and minimize it as much as you you possibly can in these patients if that doesn't work often times what we can do is we can give them Loop Diuretics the reason why Loop diuretics are helpful is because it blocks sodium potassium and chloride reabsorption and pulls water through the tubules and Yanks all the water into the urine all right lots of water can be lost if you lose a lot of water you then theoretically can do what and you liic they had just

have a little bit more water than they do sodium so I can just decrease their water down a little bit you just have to be very careful with giving too much Loop Diuretics because you can make them hypoy if you go too aggressively all right lastly is if I tried water restriction I've tried Loop Diuretics and they're still having hyponatremia that's when I can go to the next thing which is an ADH antagonist I can block ADH if I block ADH I will not reabsorb any of the water that they're taking in and I will

dump that water into the urine they'll lose a lot of water from the body so it's either you limit water you pee out water or you pee out water that's the ways that we approach UIC hyponatremia the next thing is hypervolemic hyponatremia and these patients It's usually the chfers the endstage renal diseases and then on top of that cerotic patients often times we try to do the same thing limit as much water in sodium intake as you can because again they're going to pump out ADH and they're going to reabsorb all that water right the

other thing is that I like to give Loop Diuretics because what Loop diuretics are going to work by doing what they are going to again inhibit the sodium chloride reabsorption they're going to cause lots of water lost into the urine and that's going to help to get rid of the water from the body that's a beautiful thing because these patients tend to be hyper volate they have too much more total body water than they do sodium so giving them a loop diuretic would be the first good drug to give to these patients to really pull

off water and bring the water down and the sodium will start to rise a little bit so often times I remember hypo liic give them normal saline you iic restrict water first Loop Diuretics next ADH antagonist last hyperic restrict fluids and Loop Diuretics often times that'll get you what you need to do let's say here they have symptoms it's been acute onset of hyponatremia it's severe hyponatremia and that scenario if they do have that you give them hypertonic saline if they don't then you kind of treat the underlying cause but here's the thing if you

initiate hypertonic saline on a patient you just want to again be very careful to avoid osmotic demolation syndrome what can you not go over you can't go greater than 6 to8 you can't go greater than 6 to8 that's important within a 24-h hour period if you do give them water or desmal pressing to bring that sodium back down so that you don't overcorrect if a patient has uh particularly an underlying cause that you have to address you have to figure is it hypo you or hyper if it's hypo what's their problem they're probably volume down

give them normal saline if it's UIC what do you do restrict water if that's not working then what do you do okay I'm going to give them loop di if that's not working ADH antagonist and that's usually going to be like tolvaptan if I have a hyperemic patient I'm going to restrict water and I'm going to try to restrict their sodium a little bit too and then if I do that what's going to happen all right hopefully that'll you know avoid a lot of the ADH that's getting reabsorbed but often times what's a really good

drug to get rid of the excess volume Loop Diuretics and that should be it all right now let's talk about the treatment approach to hypernatremia so in this particular patient you have let's say a hypovolemic hypernatremic patient right in this patient when you look at their vascular system what do they have a lot of that they've lost they lost a lot of water way more water than they've lost of sodium but they've lost both of them your job is to give them back sodium and to give them back water but more particularly give them a

lot of water so in this particular patient often times if they're hypotensive or they're a little bit unstable best thing to do is fluid resuscitate them give them normal saline or lactated ringers improve their sodium improve their water prod some hemodynamic stability once you've stabilized them then you can start saying okay my sodium maybe is a little bit normal my water still on the Lower Side what can I do give them water that's where you want to replace What's called the free water deficit so again hypovolemic hypernatremia often times right off the get-go you need

to give these patients normal saline or lactated ringers to improve their volume and improve their blood pressure then once you've improved their hemodynamic stability then you correct their free water deficit and that's very simple you give them free water by having them drink it or through an NG tube or you give them IV D5W all that's going to do is improve their water because you gave them sodium you gave them water you improve their sodium you improve their water but you got to give them more water if you give them more water what's going to

happen their sodium will be normal and their water volume will be normal that's the goal all right A lot of the times the textbooks will say you know try to avoid half normal Salan the reason why is you have sodium chloride and also this can increase the risk of cerebral edema if you drop them down too quickly but it's not as an efficient drug if you have a patient with hypernatremia the best thing to do is to correct their free water deficit by giving them free water and avoiding the water in like half normal saline

Solutions the other big thing to remember is in patients who have hypernatremia and you're giving them water you have to be careful because you're giving them a hypotonic solution so if you give them hypotonic solution you're dropping the sodium in the bloodstream if there's less sodi in the bloodstream what's going to happen the water will start moving into the brain and induce cerebral edema this really only happens whenever you've dropped the sodium more than 12 mil equivalents in a 24-hour period don't go more than this because you can cause risk of cerebral ad demon to

occur all right so now let's move on to the next component here which is uvalic hyp hyponatremia and uvalic hyponatremia the problem here is that the patient doesn't have ADH release or a good ADH response the problem here is that that they were just losing lots of water from their body you're going to give them back fluid in the form of isotonic Solutions and then replace their free water deficit all hyper netas they to some degree they have a free water deficit that you have to replace and we'll talk about how to calculate that in

a second for uum Kyo Tre you have to fix their problem has nothing to do with the volume you got to either improve their ADH or give them something to help with the ADH response so here's what we do for and patients who have Central diabetes insipidus what we like to do is say okay what's their problem well the sodium is normal they just they've lost a little bit more water from their vascular system okay what if I gave them desmopressin for Central di because that improved it on the diagnostic test if I give them

ddavp it should hit the receptors they should reabsorb water and there should be less water loss from the body and that should improve their amount of water and actual sodium in the actual bloodstream right that's pretty straightforward simple one here's what it's complicated for nephrogenic Di has nothing to do with ADH it's the ADH receptor here's what we found that actually works and it's kind of a weird mechanism in a patient who's peeing a lot you're going to give them a diuretic that sounds absolutely insane that's what we prefer so thides they what they do

is they block the sodium chloride sorter here and if they reduce sodium reabsorption what happens here is that you're going to lose sodium and water in the urine when you lose that sodium and water in the urine what happens is your blood volume gets a little bit reduced so it reduces like a mild hypo Almia when you have mild hypovolemia what does that do to renin pumps up the renin production when you have lots of renin what does that lead to Angiotensin 2 aldosterone but guess what guess what Angiotensin 2 loves to do it loves

to act here in the proximal convoluted tubule and reabsorb sodium and even a little bit of water if you do this in the proximal tubule you have less water in sodium that's going to be lost into the urine you're reducing the actual polyera that's the concept here behind thides it's inducing mild hypovolemia and causing the kidneys to say hey I need to retain some of that sodium in water and stop dumping it that's the mechanism and so it's kind of cool now that's covering uvalic that's pretty straightforward for the last scenario here is hypervolemic so

in hypervolemic hypernatremia the problem here is that the patient has a lot of sodium and they have just a little bit more water than they should all right so this is your hyper Aldo States usually or a lot of sodium chloride Rich Solutions so what I would say is give the patient a loop diuretic the reason why is if you get Mal Loop diuretic it'll block sodium chloride reabsorption it'll reduce water loss here in the descending limb water will be retained in the tubules and you'll lose it out in the urine if I get rid

of water what's going to happen that's going to help to get rid of sodium and water solid reduce my sodium and my water a little bit right here's what I like to do next add on a thide diuretic because these patients one of the benefits of giving them Loop is you're getting rid of volume because these patients are hyperemic and you're also getting rid of sodium but if you add on a thide uretic that blocks sodium reabsorption here and if you block sodium reabsorption you lead to a little bit of sodium loss and water loss

the benefit here is is that you get a little bit more sodium loss with thides then you do with the loops so if I give them a loop diuretic that'll CA sodium and water loss more so a thide diuretic will cause more sodium loss than water loss either way in both of these scenarios what am I doing I'm going to then kind of help to normalize my sodium and then normalize my water that's the beauty behind this then after I've normalize their their hyperemia and got them to emia I replace their water losses with just

pure water I know this sounds like a lot let's make sense of it in a step-by-step process patient has hypernia sodium gr to 145 first thing that you have to do is determine what their free water deficit is so if I determine that I do that by taking their total body weight so you take 70 kg for example multiply it by 0.5 if they're a female and 6 if they're a male once you do that you're going to get their total body weight then you're going to multiply here in parentheses what their serum sodium is

divided 140 minus 1 once you get this this is the amount of water that you have to give to them over the next 24 hours to replace their water losses once you do that you're going to give them free water usually via the oral kind of drinking it or via an ngog tube we do this in kind of patients who have mild to moderate hypernia if they have severe hypernia or they can't tolerate oral water that's when we go to D5W infusions all right so every single patient who has hypernia regardless if it's hypo hyper

or uvalic they get their free water deficit replaced you then need to figure out okay if I give them water I got to monitor their sodium to make sure that I don't drop their sodium too quickly greater than what I don't want to drop it more than 10 to 12 in a 24-hour period why because it can cause cerebral edema all right that's that's got to be careful of it hypernatremia give them free water every type of hypernia gets this then think about what's actually the cause if it's hypovolemic what do you do for these

patients if it's hypovolemic hypernia you have to ask yourself the question are they hemodynamically unstable if they are then you give them normal saline or lactated ringers if they are not you can give them a hypotonic solution like half normal or quarter normal saline if it's uvalic hypernia this has nothing to do with volume or any kind of IV fluid you give them desmopressin if it's Central di all right and if it's nephrogenic di then you you give them thyoides if it's hyperic hypernia Loop dtic and if you need to get more sodium off of

them add on the thides this is the way that you'll treat the cause which again if you have a hypmic patient you'll give them fluid and give them water if it's UIC you're giving them desmo pressent or thides plus some water if it's hyperic you're giving them water and a loop diuretic plus or minus a thide that's the way that we trade hypernia my friends this was was a monster of a lecture I really hope it made sense I hope that you guys enjoyed it and learned a lot love you thank you and as always

until next time [Music]