Diabetes Insipidus and SIADH | Clinical Medicine

what's up Ninja nerds in this video today we're going to be talking about diabetes insipidus Di and siadh which is syndrome of inappropriate ADH secretion again this is a part of our clinical medicine section and if you guys are really enjoying these videos you're learning a lot from them they help you please support us you can do that by hitting the like button commenting down the comment section and subscribing also I really urge you guys go down the description box below there's a link to website where you guys can become a member and have access

to thousands of notes thousands of illustrations thousands of quiz questions and there's even exam prep courses that we're developing as well so go check that out but without further Ado let's talk about Di and S ADH so these two disorders are really disorders of ADH production is really what it comes down to you have to remember that ADH is produced from the posterior pituitary right there's these neurons that extend from the hypothalamus down to the poster pituitary and basically ADH is already synthesized it's just sitting in the syap I vesicles waiting to be released well

in diabetes and CPUs what happens is is ADH production is reduced significantly reduced right and there's two different reasons why it well there's one reason why it can be reduced so when we talk about this we have to remember again the posterior pituitary is the source of ADH production right so one of the reasons why patients May exhibit diabetes and citus is a problem where the hypothalamus and the pituitary could be functional that's usually the reason why so maybe there's some type of dysfunction in the poster pituitary or in the hypothalamus and we'll talk about

a little bit of that but what we call this is we refer to that as Central di so it's a diabetes in sympetalous receptors here at the collecting duct these receptors are referred to as the V2 receptors another name for ADH is also referred to as vasal pressent so ADH what it does is is it binds onto these receptors here called the vasopressin 2 receptors or The adh2 receptors and what it is designed to do is is it's designed to help to express these little like proteins on the surface luminal surface called aquaporin and these

aquaporins whenever ADH is present they'll get shoved into the actual luminal membrane and what they'll help to do is is they'll help to move water from the actual collecting duct tubules into the bloodstream right and so ADH is responsible for stimulating that process if you have a reduction in ADH production will you be able to reabsorb that water no and so this process is in inhibited because you don't have ADH being produced to bind onto the V2 receptors to stimulate water reabsorption therefore water reabsorption is reduced and then unfortunately tons of this water get lost

into the urine and so often times these patients have like profound poly areia now that's one concept is that there's something wrong with the hypothalamus of the post pituitary but there's another reason you can have Di one is called nephrogenic di in nephrogenic di the problem is ADH production could be normal but the V2 receptors are having some type of dysfunction so in this scenario nephrogenic di if your V2 receptors are dysfunctional even if ADH is present in normal amounts the V2 receptors won't respond if they don't respond it's as that ADH is not even

present at all therefore aquaporins won't be plugged in you won't reabsorb water and you'll lose a lot of water in to the urine so that's the concept and we'll go over this a Teensy bit more in a second but remember di can have a central component where you're not releasing ADH or a peripheral nephrogenic component where ADH is produced but it doesn't bind to the receptor and have the same effect as a result you don't reabsorb water and lose water in the a let's talk about these two so Central di the whole concept here is

that this poster pituitary hypothalamus it's injured in some way shape or form that's what we've come to and therefore as a result there's a reduction in ADH if there's a reduction in ADH there's no stimulation of the V2 receptors so as a result V2 receptors are going to become less stimulated so less activation here as a result you're not going to plug these aquaporn into the actual luminal membrane and therefore water reabsorption will be reduced so less water will be reabsorbed more water will be lost in the urine what's the reason for all this destruction

of the hypothalamus of the posterior pituitary a couple different reasons one is there's a disease it's called shean syndrome and in C shean syndrome what happens is the patient undergos what's called postpartum Hemorrhage so after they've had birth they maybe lose greater than a liter of blood blood within 24 hours or they lose enough blood that they become hypmic and hypotensive so as a result they lose blood volume so their blood volume will drop from the blood loss and if their blood volume drops from the blood loss so can their blood pressure so often times

what we see as the result of this blood loss is a reduction in blood volume which leaves the hypovolemia and a reduction in blood pressure as we reduce blood pressure and on top of that you know what else happens in patients who have postpartum Hemorrhage they throw off a lot of their coagulation factors and they end up causing clots that consume a bunch of their clotting proteins and it can lead to diic so sometimes they can get a low BP and they can get what's called diic either way the combination of these factors what ends

up happening is is they throw off the profusion to the pituitary and as you throw off the profusion to the pituitary it increases the risk of what's called infarction so as a result these patients May undergo infarction of their poster pituitary hypothalamus and lead to destruction of the actual neurons that release ADH that's one reason so shean syndrome postpartum Hemorrhage as a result the other one is called pituitary apoplexy so if a patient has what's called pituitary apoplexy they have a pituitary adenoma that they bled into so they bled into that tumor bed what happens

is is that whenever you bleed into that tumor bed it ends up leading to compression of the near nearby vessels that are supplying the pituitary and the hypothalamus in that vicinity so as you have more vascular compression you may squeeze some of the arterial supply to the posterior pituitary into the hypothalamus as a result you get the same kind of concept here is that you reduce perfusion to the pituitary and as you reduce perfusion to the pituitary this may trigger death of the tissue cells and lead to and in farction and as you stimulate infarction

the cells die they lose the cap capability of producing ADH the next one is called a pituitary adenoma but it has to be really big that it's causing compression so it's called a pituitary macro adenoma how do we Define that has to be at least greater than 10 millimeters in size with this large size it compresses the anterior pituitary and it may even compress the posterior pituitary so if you cause in increase compression of the actual tissue you may cause destruction of the tissue so increased compression may lead to loss of function and so this

increased compression may lead to loss of function as a result a reduction and ADH production last one's actually probably very common believe it or not I see it a lot in the neuro IU patients who have a Neurosurgical procedure where you cut those little suckers off so if a patient under goes what's called a Trans sphenoidal reection in other words they have a procedure at or near the pituitary and they end up removing the posterior pituitary think about it dude if you remove that t if you remove the posterior pituitary you remove the literal source

of ADH production and so these are commonly the triggers of why a patient would have a reduced production of ADH all right beautiful now we go to to the next component nephrogenic Di and nephrogenic Di the pituitary and the hypothalamus these puppies are good they're working out well so these are these are normal so let's actually put that these are okay if these are okay then what they'll do is they'll be able to produce we're just going to put here a normal amount of ADH there's no abnormality with an ADH production here so ADH production

is normal right but here's where the problem is the problem exists here there's dysfunction in these V2 receptors they're just not working so ADH is being produced which means that it's circulating through the bloodstream and it's trying to come here and act on these V2 receptors but it doesn't exert any effect on the V2 receptors because of that water will not be reabsorbed and if water is not going to be reabsorbed we will lose that water there'll be less water reabsorption and more water loss in the urine the question arises what's causing this V2 receptor

dysfunction there's three common causes one is it could be due to lithium now whenever you see this in the vignette what I want you to assume is okay do they have anything written in the vignette or anything in their history that suggests why they would be on lithium such as a mood disorder such as bipolar disorder if you see that you really want to be thinking that's causing the V2 receptor dysfunction the other one is hypokalemia but it has to be really profound hypokalemia and so when I think hypokalemia I'm really looking for GI losses

or renal losses so I want you to suspect has there been any GI losses or renal losses what do I mean have they been vomiting have they had lots of diarrhea or on top of that have they have any diuretic overuse the other thing is with hypokalemia comes ECG changes so you know you really want to assess for any ECG changes do you guys remember what it kind of looks like in these patients starts off with t-wave inversions goes into U waves and then they can cause a prolonged QT interval which can increase the risk

of torsades so assess for ECG changes and assess for any losses where you could lose the potassium the last one is usually hyper calcemia this has to be really really high with Hyper calcemia you really want to think about this you want to think about that acronym the bones Stones groans thron psychiatric overtones I'm not going to write all that but I really want you guys to think about that so they had a history of like lots of kidney stones osteoporosis bone fractures pathological fractures usually pancreatitis psychiatric disorders arhythmia such as changes in their QT

interval remember it's always inverse so low Q Q QT intervals the other thing is look for a history do they have any history of like high parathyroid hormones so do they have any history of like hyper parathyroidism or do they have any history of malignancy because these are usually the only two and when I mean malignancy I mean things like multiple Myoma uh lymphomas as well as you know sometimes you can see this particularly in other patients like Squam Cel carcinomas of the head and the neck but usually I really want to think do they

have arri malignancy or hyperparathyroidism this is usually the trigger for v2 receptor dysfunction now that we have an idea of this it's the same kind of concept you're not reabsorbing water not reabsorbing water it's just this one reduction in ADH this one normal ADH but V2 receptor dysfunction okay beautiful so we got a problem when we don't release ADH you you know you end up causing a lot of water to be lost in the urine what about when you produce too much ADH so so now we get into this condition called syndrome of inappropriate ADH

secretion or Si ADH two reasons why this would happen one is the posterior pituitary has an increased release of ADH there's a lot of different reasons why but there's a pituitary problem so something is wrong with the pituitary where it's becoming hyperactive and it's increasing the production of ADH if that is the case so there is some type of increase pituitary ADH release something is going on where there is lots of increased pituitary ADH release and we'll talk about some reasons of why that would happen this is by far going to be one of the

more common ones the other one is that you have some type of tumor or you know neuroendocrine cells that have usually formed it's usually because of a tumor where there is an ectopic ADH production so we call this ectopic ADH production now what do I mean by ectopic I mean that this is not a normal site of ADH production it should be produced by the pituitary and if the pituitary is producing too much of it we'll figure out what those things are but if it's not from the pituitary and it's from a tumor some other

site that's making ADH that it's not supposed to be then I want to go looking for that and we'll talk about what those things are but either way in both of these scenarios ADH is being released in two high an amount when ADH is released in high amounts goes here really really stimulates these V2 receptors now the V2 receptors when hyperactivated will then increase the expression of aquaporn subunits if I express a lot of these little aquaporn subunits in here any water that is going to be present and the collecting duct will then move very

beautifully from the actual Lumen and into the bloodstream and so this process will be very heavily stimulated as a result I'll increase my water reabsorption and then as a result there'll be very little amounts of water that will be present in the urine this is the big difference between these two disorders Di and sadh little water in the urine lots of water in the urine lots of water in the bloodstream very little water being returned to the bloodstream the question now comes what's triggering their increased pituitary aliage release and what is this thing that's called

causing ADH production that's not from the pituitary well the increased pituitary ADH release is going to be by far the most common cause of Si ad what happens here it's not truly well understood but the concept here is that in situations where there is really low oxygen levels so some type of process that's leading to hypoxia hypoxia can be a very profound stimulus for ADH production you're like really that's weird it it can be this could be due to a stress response this could be due to a lot of different things like whenever you're hypoxic

sometimes patients can have a lot of like profound organ failure and your body tries to generate ways of increasing your blood pressure and profusion ADH is one of those and so that may be more of like a stress response effect but either way scenarios where there's really low oxygen could also be a trigger well what are things that could cause disease of the lungs well a couple different pulmonary oh son of a gun a couple different pulmonary diseases that I want you guys to to be able to remember is the following one is do they

have something like pneumonia do they have something like COPD or are they intubated because patients who are on mechanical ventilators can commonly get this so you want to think do they have COPD do they have pneumonia do they have ards or are they intubated so anybody who's receiving like some type of positive pressure ventilation in some form can also have this type of process and this could be a trigger for hey let's tell that pituitary to go ahead and start pumping out more of the ADH another one is it could be intracranial disease so a

lot of intracranial diseases this is usually something that's either at or very close to the hypothalamus in the pituitary area so if you have some type of brain pathology in that vicinity for example if a patient has something like a stroke or they have something like a bleed or they have even like sometimes traumatic brain injuries that are at or near the hypothalamic area this could definitely be a trigger so it's usually injury that is near the hypothalamus what are a couple of these that I want you guys to think about well a couple of

these again I kind of mentioned it stroke bleed traumatic brain injury would be the big one so some type of stroke maybe an i or a subarachnoid hemorrhage or lastly a traumatic brain injury these are some particular ular pathologies that I would really want you guys to think about and again profound stimulator for ADH production the last one is drugs there is a bunch of different drugs that may have the capabilities of increasing the activity of ADH production a couple of those that I think are worth remembering are three types one is it's going to

be what's called ssris so selective serotonin reuptake Inhibitors are a very big trigger another one is called carbamazapine that's a really big one as well and then tricyclic anti-depressants can also be very strong triggers for ADH production so when a patient has Si ADH you have to ask yourself the question do they have pulmonary disease intracranial disease or are they on particular drugs often times the most common trigger is going to be intracranial disease so look for a patient who has underlying neurological deficits altered mental status of some sort if you can't see that look

for any underlying hypoxia or pulmonary disease and then lastly think about drugs but it should be more of an exclusionary basis now the last thing that I want you guys to think about is could it be an ectopic site usually you want to look for a patient who has an underlying history of something called small cell lung cancer so in a patient who has what's called small cell lung cancer they can create this concept where the tumor can become it can kind of transform into this neuro endocrine type of cells and so what happens is

they generate something called a par neoplastic syndrome and with this this tumor then gains the capacity to be able to produce large amounts of ADH with that being said if we have large amounts of ADH what ends up happening what do they do to the kidneys they go to the kidneys and they end up causing increased water reabsorption so this is the concept that I really want you guys to understand here is that in patient with sedh think about intracranial disease neurod deficits altered mental status some type of pathology that's affecting their neuro exam then

think about pulmonary diseases pneumonia COPD are they intubated they have Arts lastly think about certain drugs and then if from there you haven't found anything also consider about ectopic sites like look for any evidence of lung cancer look for any CA weight loss uh hemoptisis of some sort that would suggest this is the source now that we've really gone into this let's now talk about what are the problems what's the issue what's the complications that can arise when ADH is too low and when ADH is too high all right my friends so we talked a

lot about di sadh we talked about the pathophys the causes behind them I think the big question is how will these present well often times it's all related to that water Factor right so is in di what's happening you're not really reabsorbing water you're losing a lot of water into the urine right so it's it's the same concept here and so these patients often times really they get rid of so much water that they lose a lot of the water in their bloodstream that their sodium actually starts becoming a little bit more profound and so

they end up developing hypernatremia concept behind this is again pretty straightforward we already talked about this that in di either there is a reduction in ADH so it's one of the two right so there's either a reduction in ADH or there's dysfunction of the ADH receptors either way same concept Central nephrogenic di in this scenario are you going to be reabsorbing water no so that's the concept is that either way it doesn't really matter in this scenario whether it's nephrogenic or it's Central the pathophysiology end point is the same is that you won't reabsorb water

as a result there'll be less water inside of the bloodstream and as a result if you're not reabsorbing this water a lot of this water is ending up inside of the urine now when you end up with a ton of water in the urine it's usually pretty large volumes and so this large volume of water in the urine ends up leading to pretty substantial urine output and so whenever the patient is producing like greater than three liters of you know urine in a very short amount of time generally like a 24-hour period we start to

say that they're kind of moving into What's called the polyurea type of phase so either they're peeing really frequently or they're peeing out very large volumes either way this is what we see due to the water loss in the urine all right the second thing is that whenever you lose a lot of water in the urine you don't get enough water reabsorption into the bloodstream so there's decreased water in the bloodstream as a result this decreased water leads to a increase in your serum sodium so now as a result of losing that water you're going

to have an increase in the amount of serum sodium now whenever sodium goes up we call this hypernia at what point do we diagnose hypernia well off the lab value is whatever it's greater than or equal to 145 M equivalents per liter whenever that goes up what happens is this high amount of sodium can do two things one is it can make the actual blood really like hypertonic or hyperosmolar really concentrated and so we call that an increase in osmolality so there's an increase in the osmolality blood super concentrated the problem with that is that

whenever the blood is really hypo I mean hyper asolar it really has a profound stimulus on the hypo alus and the hypothalamus has these different types of osmo receptors that are present on it the subicular organ right there's all these different types of uh things there but what happens is it stimulates the hypothalamus and particularly really drives up your thirst mechanism and what do we call that whenever the patient becomes really really thirsty it's called polydipsia and so what happens is we'll actually write this as a result whenever you stimulate The hypothalamic Thirst Center this

triggers them to become super thirsty which is referred to as poly dipsia so one effect of hypernatremia is that the patient can become profoundly thirsty now here's another thing when a patient's putting out lots of urine right and maybe in a scenario where they have an inadequate intake of water there's something terrible can happen so let's say that a patient becomes hypernatremic and what happens is they don't intake enough water so they become hyperic or actually I would say more specifically with the polyurea Factor so I say that you lose a lot of this uh

you lose a lot of water in in the actual urine if you lose a water a lot of water in the urine what happens is less water in the bloodstream this could lead to a mild hypovolemia So the patient's blood volume could drop a little bit right now what we do is that this will trigger the patient to become thirsty they'll drink a lot of water and then replace their blood volume but often times this can occur whenever there's inadequate hydration so usually this is a result of inadequate hydration may be the trigger for these

patients becoming hypovolemic either way in this hypovolemic State these patients will exhibit signs of maybe dehydration and hypovolemia can manifest in a bunch of different ways right the blood pressure could be low they could have dry mucous membranes they could have a decreased skin turg they may have a flat jugular vein or they may have a flat IVC their urine output may be a little bit lower so that's usually the the scenarios that these patients can become dehydrated particularly if there is inadequate hydration that's the big big factor here usually this happens in like older

individuals or patients with an altered mental status or delirium who don't have adequate access to water but either way in a patient with di you really want to watch out for high sodium polydipsia where they're super thirsty dehydration usually an inadequate hydration so in other words they don't drink enough because they don't have access to it they're altered they're geriatric some sort of that way or even intubated in ICU and lastly they're producing large volumes of urine polyura s primarily will cause a disease called hyponatremia which is when the sodium level is less than 135

mil equivalents per liter what happens at hyponatremia is very straightforward in this scenario here ADH is usually producing way too high of an amount so there's very profound levels of ADH production we talked about that from increased pituitary ADH release ectopic ADH production either way you're getting hyperactive stimulation of the V2 receptors so these puppies are just pumping and what is it doing again what is it doing it's ended up increasing the expression of aquaporn subunits on the luminal surface surf you're stimulating the selection of those to increase the amount of water that's being reabsorbed

into the bloodstream right so theoretically there should be less amount of water that you're actually putting into the urine in that that theory right so in this scenario here there should be less water or decreased volume or decreased amount of water that's lost in the urine because you're banking all the water that's really kind of getting to your kidneys so usually they're UR is profoundly concentrated but here's the big thing when you increase the reabsorption of water what happens is you end up causing a dilution of the amount of sodium and as a result the

sodium levels will tend to drop so these patients may have a drop in their sodium levels that's referred to as hyponatremia whenever sodium levels dropped if they drop profoundly and acutely they can cause a lot of osmotic shifts and so this is usually what happens is is that they can trigger the these osmotic shifts one of the effects here from the osmotic shifts is the terrifying one is that here's a normal siiz brain right normal size brain and then what happens is we're going to kind of convert this normalized brain into a very large emitus

Brain so what happens is with these osmotic shifts is patients often will develop something called cerebral edema it's a pretty straightforward concept so in the actual brain tissue right what happens is there's a normal movement of water which is usually going to be moving in and out of the actual neurons of the brain if the sodium level in the bloodstream is low maybe the sodium inside of the actual brain cells will be a little bit higher and what happens is is this starts to pull water into these actual brain cells and when you pull lots

of water into these brain cells it starts causing swelling which leads to cerebral edema the problem with cerebral edema is this can present a variable type of ways in other words one of the biggest things is that the swelling it gets big enough you know there's What's called the Monro Kelly Doctrine it says inside the skull is like a fixed space so if you have more brain tissue or abnormal amounts of brain tissue more blood or more CSF the pressure inside of the actual skull will increase we call that an increase in the intracranial pressure

and that's oftentimes one of the biggest complications is that the ICP will go up as ICP goes up patients can develop a variable amount of presentations one is they may present with a very terrible headache one is they could also have nausea and vomiting the other one is they could start having Frank herniation now you're like what the heck herniation that sounds terrible and so herniation can look a bunch of different ways often times they start compressing their brain stem and they start having pupilary changes like and an aoran a non-reactive pupil and their level

of mental status starts to decline they become lethargic or stous or tuned or comos and so I think one of the biggest things here is that with acute hyponatremia you can cause massive osmotic shifts which lead to cerebral Emma increased ICP and the scariest thing is herniation which can lead to brain death so that's a very terrifying thing and you don't want that to happen another thing that can also happen is whenever you have hyponatremia this can cause osmotic shifting but it also may do something to the brain tissue especially near the cortex it may

start aggravating some of the cortical tissue and when you aggravate this cortical tissue it can increase the irritability of the cortex so it can cause increased cortical irritability and now if I irritate the cortex now this sucker can fire inappropriately and if it fires inappropriately it may lead to seizures and often times these are terrifying generalized tonic clonic seizures and so this is something that I want to watch out for as well because hyponatremia has been shown to lower the the seizure threshold and increase cortical irritability and lead to seizures so two common presentations that

you can see in the worst case scenario of s ad associated with hyponatremia is seizures and cerebral edema however this type of effect here really only occurs when the sodium drops acutely so if there's an acute drop in sodium so we would say if there's an acute drop in sodium or if the sodium dropped to the point of where it's less than 120 but usually it's whenever there's a cute drops so again we'll say whenever the sodium drops significantly it can cause osmotic shifting but it's usually either has to be acute or less than 120

same thing here has to be acute or less than than 120 then it can stimulate these profound osmotic shifts or it can stimulate cortical inability and lower the seizure threshold so the things that I want you guys to remember between these two is in di there's hypernatremia due to water loss in the UR polyura they will get thirsty if they drink enough cool they won't become dehydrated but if they have inadequate access to water or they have delirium that alters their in hydration or they're intubating they can't get water they could develop dehydration hypovolemia and

low blood pressure and then lastly they will have very large amounts of urine in their uh they'll have large urine outputs with sadh they can have hypon treia due to reabsorbing tons of water diluting their sodium if the sodium drops acutely or very low it can lower the seizure threshold cause seizures or osmotic shifting that leads to cerebral edema increase inoc cranial pressure and possibly herniation all right my friends now that we've talked about this let's go into the Diagnostics all right let's now move into the diagnostic approach of diabetes incipit so a patient who

has diabetes Inus often times they'll come in with polyera poly dipsia maybe even in severe cases dehydration due to not maintaining an adequate water intake and even hyper net treia is a very common presentation so if they come in polyurea polydipsia maybe they appear a little bit dehydrated I got to look for the hypernia then I'll get a BMP if the BMP shows the sodium is greater than 145 they have hypernia but then I got to ask myself the question what was one of the big things that Zach said about the ADH well if I

don't have ADH then I don't reabsorb water and I dump a lot of water in my urine and I don't have a lot of water in my bloodstream so that would change my osmolalities so in the urine I'd have a lot of water so the urine osmolality should go down and on my serum I don't have a lot of water so my serum osmolality should go up oh it does okay cool then this is definitely very suggestive of you know di but there's another disease that actually can kind of be a little interesting it's called

um primary poly dipsia or psychogenic polydipsia the concept behind this is that patients present with severe polyurea and often times in primary poly dipsia the inciting event is that they're drinking like greater than 12 lers of water per day so the concept here is if I take away the water that they're drinking they should stop having excessive polyuria and therefore their urine osmolality should actually increase if that happens they have primary polydipsia because their trigger was excessive water intake and that shut the ADH off okay well that takes care of that then so if the

urin osmolality kind of doesn't really change it tells me that it's a DI problem it tells me that the ADH is not going to be released no matter what or The receptors aren't responding to the ADH so now I think it's definitely di problem is I don't know which one it is I don't know if it's Central or if it's nephrogenic so it's Central I have to remember the problem is that they don't have ADH with nephrogenic the problem is that they won't respond to ADH even if it is present so I'm going to give

them a drug ADH ddavp also known as desmo pressent it's the same thing as ADH if I give them this and it's Central di they should bump their urine osmolality why because if I give them ddavp they're missing it it should stimulate the receptors they should reabsorb water they should have more water in their bloodstream and as a result their sodium will go kind of come down a little bit and improve on top of that they'll have less water in their urine the urine osmolality will go up and their polyura should also subside that would

definitely help me to diagnose Central di the other scenario would be nephrogenic di it shouldn't really do it anything it's the same scenario because the patient producing ADH appropriately that's not the issue so if you give them ddavp it won't matter if they have ADH or not the receptor is not going to respond to it they're not going to reabsorb water so therefore they're still going to have low water in their blood they're still going to dump a lot of water into their urine and their urine osmolality is going to remain low so it won't

change this is super indicative of nephrogenic Di and I've determined okay if it's Central get a look at their pituitary see what's going on if it's nephrogenic check their potassium check their calcium and look in their history for any lithium use all right what about sadh patient comes in they don't really have any problems with polyurea they don't really have any problems with polydipsia it would really just be hyponatremia right so I'd get a patient come in maybe they were seizing um maybe they had some concerns and I think that they had some cerebral edema

or features of high ICP so I get a BMP and I check to see what their sodium is oh their sodium is low right it's less than 135 all right well that could be why maybe it's s ADH related so urine serosity should give me a little bit of an idea here so if I check it I got to remember ADH is way too high if ADH is way too high it's going to reabsorb a lot of water into the bloodstream so the serum osmolality in that particular scenario should go down all right on top

of that it's actually going to have less water going into the urine so because of that the urine osmolality should go up and that would tell me that ADH is turned on all right okay that's correct it's possibly sadh all right the next thing I have to remember though is that there is other disorders that can cause hyponatremia that look like this so what I got to do is I got to look at the volume status because patients who have hypovolemia can also stimulate ADH production patients who are hypervolemic but have a very poor circulating

blood volume can also precipitate a ADH process so how am I supposed to know if it's hypovolemic or hyperic or if it's uvalic well if a patient has U emic hyponatremia meaning that they don't have a lot of Edema they don't look like they're dry mucous membranes or decreased skin turg they're not hypertensive they're not hypotensive they're they don't really look like they're that type of patient they appear to be a normal volume status that really tells me that there's only three potential causes with uvalic hyponatremia you cannot determine that it's siadh until you have

excluded other causes it is an exclusionary diagnosis there's two other diseases that that you have to rule out first I have to rule out hypothyroidism and early adrenal insufficiency so I'm going to check my tfts to make sure that they don't have any hypothyroidism and check my cortisol to make sure that they don't have any low cortisol levels if those are normal then and only then can I say that the patient has sadh all right how do we treat a patient who has diabetes and citus well you can look at it two ways you can

look at you got to treat the hypernia but we'll talk about that in the renal lectures for this patient you have to treat the cause and the cause here is that they are either having no ADH production and in that scenario you have to give them the ADH and what was the drug that we gave to do that for the test ddavp desmo pressent so often times it may be required to give these patients if they're super polyuric um and on top of that they have hypernatremia desmo Pressa may be the drug to help to

reduce the polyera and help to be able to retain some of that water and then bring down their sodium for nephrogenic Di it's actually a little odd what you want to do is you actually kind of want to to produce like a little mild hypovolemia and the mechanism behind this is it actually may help especially with nephrogenic di so drugs that we oftentimes will give to these patients is one of two uh usually it's a thide diuretic another one is amide but amide is usually the trade for that or the the buzz term for that

is lithium related um nephrogenic di but often times it's just kind of thide diuretics and a little bit of sodium restriction may help with these patients how do we treat SI ad8 well s ADH is again it's a problem with ADH production usually from inappropriate from a pituitary ADH release or it's from an ectopic Focus so it is important to treat the underlying cause of ADH siadh so if it's pain treat their pain if it's due to the particular drugs minimize the exposure to those drugs if it's due to COPD pneumonia treat that those underlying

diseases if it's an intracranial disease it's not something easy that you can actually fix so in those scenarios where you're trying to reverse the underlying cause you have to deal with the repercussions of sadh which is hyponatremia and I want to treat the hyponatremia so that they don't develop seizures so they don't develop cerebral edema and the downstream consequences related to high ICP so what do I do well the first thing is you have to ask yourself the question is this something that the patient has had for more than 48 hours and do they have

no symptoms no headache no nausea no vomiting no vision changes no encylopedic to be aggressive with this patient I'm not going to push their sodium up quickly I'm G to go a little bit slow and I'm G to be careful and cautious so what we do is in these particular scenarios you do in a kind of a an algorithmic like fashion first thing is don't give them a lot of water the reason why is any water that they get into their body and they K they get filtered across their kidneys they will retain the ADH

will just be on the actual collecting duct saying hey give me all of that water so I want to give them a free water restriction so that basically any of the water that they're taking in if it is getting into them I'm not going to be reabsorbing a lot of that water and a lot of it will actually again not cause this hyponatremia all right if they're not responding to water restriction and that's kind of tough sometimes you have to limit them to like a liter um sometimes 1.5 lers of water per day um so

in those particular scenarios where it's not working you have to get rid of a lot of water from the kidneys and so often times we'll do this via um Loop dire ICS and so Loop diuretics are very interesting because what they do is they act at the sodium potassium two claric transporter so you won't reabsorb sodium here in the ascending limb and therefore you won't draw water out going down in the descending limb so water will stay in the actual tubules and be dumped into the urine so if I lose a lot of water here

into my urine I'm therefore going to allow for my sodium to start kind of naturally rising up often times we can give this in combination with salt tablets because that'll directly cause a rise in their sodium if a patient has been on free water restriction I put them on some Loop Diuretics maybe even a little bit of salt tablets and they're still not getting their sodium up then only then will we consider something called VAP Tans these are pretty tough though you got to be very careful because they can precipitate severe hypernatremia what you're doing

is basically you're trying to put them into a state of Di and you're basically going to block the ADH and so if you block the ADH you're essentially not going to reabsorb water and you're going to dump a lot a lot of water into the urine and these patients can push their sodium up pretty quickly and they can actually develop some complications in this such as osmotic demolation syndrome so you got to be very very careful with giving VAP Tans now the other scenario of treating sadh is if they're acute so if they come in

with a sodium that's relatively low and it's occurred in the first like 24 48 hours at least less than 48 hours that one I might want to be a little bit more aggressive with but the more particular trigger for me is if they are sympt Matic in other words they come in with a headache nausea vomiting confusion seizing high icps and they look like they're going to herniate in those scenarios I will not wait and do this type of stuff and go slow I'm going to push their sodium up as quickly as I possibly can

another one is if the sodium is really low so if they're symptomatic and if their sodium is less than 120 these are two really really bad situations these patients can be pretty sick and you don't want to wait and sit on your hands while their sodium is low and they're seizing and they're having ICP crisis so in this particular situation you will give them 3% hypertonic saline often times the guidelines say give them like 100 milliliters of 3% hypertonic saline when you give them this you're going to keep checking their bmps to check their sodium

like every two to four usually every two to four hours now the point of this is that you got to check it to make sure that their sodium over a 24-hour period does not exceed 6 to8 Milli equivalence in a 24-h hour period the reason why is okay I'm going to give them this to push their sodium up quickly I want to push them up like six points but then I don't want to push them up any higher so if I get them from like 120 to 126 cool I don't want to go above that

in a 24-hour period so I keep checking their sodium and if they're going up above that give them some water right or you know you could give them other medications like ddavp because you just don't want them to pass that 68 Mill equivalent range and the whole reason for that is that if you do pass that over a 24-hour period there's liter to suggest that you can demate some of the actual neurons in the ponds and precipitate something called osmotic deyin syndrome these patients can actually present almost like in a locked in state couple weeks

after they demate so maybe two weeks later they'll develop things like dysarthria dysphasia diplopia they'll develop quadriplegia and they can even go into like a locked in state and that's a terrifying complication that you want to avoid all right we would be able to see this on an MRI of a patient maybe two weeks later you can see all of this demin on their MRI here on the t2 on their on their MRI here you can see all of this kind of Edema here demalation this would be a concerning finding especially if you overcorrected them

too quickly all right my friends that covers Di and Si ADH I hope it made sense I hope that you guys enjoyed it and as always until next [Music] time [Music]