Thanks for the feedback. I know many of my viewers are non-native English speakers. I try to balance between speaking slower so people can understand, without speaking too slowly and making an already long video even longer. I've tried to improve the audio quality over the last 2 years, predominantly to help the non-native English speakers, and I include more text on each slide than I do when teaching in person in the US. It's not perfect for everyone, but it's the best balance I can do.
...Hopefully, someday RU-vid will create a feature in which videos can be played back at different speeds. For example, one viewer could play the video at 90% full speed to help understand what might be a different language from his/her primary one, while another viewer could play the video at 110% full speed in order to view videos more quickly, and watch more of them per unit time. That would solve this problem, though I suspect there are significant technical limitations to this.
Thanks for the suggestion! I've looked at a couple of platforms for delivering content on-line in a more robust fashion than RU-vid, but despite their huge support and publicity, I haven't felt completely convinced of their effectiveness yet. Plus, most invite their course creators (not the other way around), and the type and purpose of content I try to deliver works best if it's on-demand. Not to say I wouldn't be interested if Coursera gave me a call...
Just want to say a big Thank You Dr. Strong, for all your videos! Very helpful as supplementary material (in fact most of the time, supplanters) to my lectures in medical school.
This is awesome! I was recently diagnosed with a tumor in my pituitary. For the past 3 months, I have been to the hospital 6 times and was found I was hyponatremic. One of those visits, I was put in the ICU for 3 days with sodium levels at 112 (forgetting the nomenclature). It was awful! For I moment, I really felt I wasn't going to make it. I gues it doesn't help that I don't have a thyroid, and have Dysautonomia (POTS and Gastroparesis). I also have RA. My rheumatologist said he could not believe he was seeing me alive. My cardiologist believes I have SIADH, and has reffered me to a more experienced endocrinologist, and GI expert in motility. I am either a complicated woman or a woman with some complications 😉 Thank you for this. It helps to understand ☺
In my humble opinion the hyponatremia etiologies by mechanism is lil confusing, for the ease of remembering them I'd rather classify them by: 1.) Increase in the serum water content 2.) Decrease in the serum sodium content (in actual or relatively to the increment of other serum substances) For the list of etiologies for the increase in serum water content: 1.) Primary Polydipsia 2.) SIADH 3.) Renal Failure 4.) Endocrinopathy Whereas the etiology for the decrease in serum sodium content: 1.) Low BP (shock) or any form of trauma that leads to blood loss 2.) GI losses Eric's Medical Lectures Please enlighten me If there's any correction or let me know if this way of remembering is more practical or relatively easier besides classifying them by the volume status.
Kal. Jr There is nothing intrinsically wrong with your means of classifying these etiologies - in fact, that's how I thought about them during residency and for a while afterwards. However, while it seems really logical to divide them based on too much water vs. too little salt, in practice that differentiation is hard to make in an actual patient who you've just met and are trying to understand. The volume status differentiation, while feeling more artificial from a physiology point of view, makes diagnosis in practice easier. But in the end, whichever works for you is fine. Not just for hyponatremia, but for any physiologic derangement, there is rarely one and only one framework by which to categorize etiologies. (e.g. anemia can be categorized as hypo vs. hyperproliferative; or by high vs. low vs. normal MCV - both classification systems are totally fine).
I had similar teaching as you when in med school, and was initially confused in residency when I saw attendings prescribing salt tabs for SIADH. 2 key principles: First, you are correct that salt tabs + water = IV saline, which is why it's important to always combine salt tabs with fluid restriction. Salt tabs + unlimited water risks making SIADH worse, just like saline...
Very useful & easily digested . God bless you Regarding pseudohyponatremia due to hyperglycaemia there is a rough and rapid way to calculate decrease in sodium For each 100 mg ↑ in blood glucose the corrected serum Na = ↑ 1.3 mEq/L
Several other viewers have asked for this topic in recent months, and it's on my list of upcoming videos. I wish I could give you an approximate target date, but it's hard for me to predict. I promise I'll get to it at some point!
Distinguishing SIADH vs. CSW via urina Na: I'm not familiar with a difference in urine Na levels and a brief lit. review I just did failed to turn up mention of this either. Not to say there definitely isn't one, but it seems, at the very least, not well described. Though there are a couple of theories, the definitive pathophys of CSW is unknown. Furosemide is a well known cause of hyponatremia (though anecdotally, not as much so as thiazides), though it shouldn't cause hypernatremia.
...There's a surprisingly small amount in the literature about the use of oral salt tablets for long-term management of SIADH (even compared to the conceptually similar treatment option of oral urea). I've seen salt tabs used a number of times with apparent effect, though I appreciate that my personal case series of a dozen patients doesn't substitute for a large RCT. However, physiologic principles do seem to support the approach as well. Hope that helps!
Thanks for ur response, plz continue to upload other general topics which will benefit both internists and surgeons, appreciate all your hard work. Looking forward to endless hours of such informative lectures. Sutirtha India
...Second, you're absolutely right that the oral salt will likely all be excreted. However, since sodium excretion requires water excretion, as long as the amount of increased oral water that might accompany the salt tabs is less than the min amount of water necessary to excrete the oral salt load (i.e. more water is lost than gained), the serum sodium should improve.
Dr. Strong is the reason why I want to be a diagnostician, thank you so much for your amazing amazing contribution. Your lectures are a life saver and make medicine easier for us to study, understand and practice.
It's really amazing the way you teaching medicine through those videos, perhaps I would love to see more videos and can you post more topics and frequently. Some endocrinology topics please
I remember having heard a lecture by Conrad Fischer where he put a lot of stress on the fact that THE CONCENTRATION OF SODIUM IN URINE and Sweat CANNOT BE MORE THAN THE CONCENTRATION OF SODIUM IN BLOOD - The hyponatremia is actually caused due to drinking water. This made sense as far as sweating and Urine is considered - BUT DOES THE PERSON ALSO FEEL THIRSTY IN CIRRHOSIS AND CONGESTIVE HEART FAILURE.
Great video. Other hyponatremia videos on RU-vid don't explain the physiology properly. You mention loop diuretics as a treatment for SIADH at the end but I can't find any mention of these before 35:16. Doesn't make intuitive sense so would have been good to have an explanation.
thanks doctor for your nice lectures which i watch every other time to refresh my knowledge. i would like to ask you 3 questions if your time allow: 1. if pt present with severe symptoms despite being hyperovlemic (pulmonary edema, ascites or renal failure for example), in this case shall i treat the cause specifically (diuretics or dialysis) without initiating the hypertonic saline? 2. when initially correcting the severe symptoms (seizure for example) and raise sodium say by 3 when symptoms resolve; shall i subtract this value so that the allowed amount for me now to raise over 24 hrs id 3? 3. if pt with cirrhotic ascites come with hyponatremia and hypovolemic, in such case, shall i resuscitate with NS plus managing the ascites with diuretics or total paracentesis?
HI DR Eric BRILLIANT AND COMPREHENSIVE EXPOSITION AND ILLUSTRATION OF SODIUM POTASSIUM AND WATER HOMOEOSTASIS.what about the distal delivery of sodium in this scenario and implications
As always, the video is very helpful and easy to understand. I have a question though, I was classically thought that the disorders of sodium reflect the disorders of water and so is the treatment. Can you please explain the role of sodium tablets in treatment since it appears to me that no matter how much sodium you give PO it will be excreted and not affect the serum level.I reviewed this on uptodate and it seems salt tablets plus oral water intake is equivalent to giving normal saline IV.
I remember this 21 year old patient with Ulcerative colitis, his serum sodium concentration was corrected way too fast and presented with what was suspected to be Foville's syndrome (anterior pontine infacrtion) but it turned out to be ODS due to rapid correction of Na+... very very very sad outcome for the patient indeed, he became hemiplegic sadly :< .
I think as a general rule, clinicians freak out too much about hyponatremia. If the patient is asymptomatic or mildly symptomatic, there is absolutely no reason to hurry in fixing it, and obviously (as you've shared) a big reason to go slowly.
correction of hyponatremia by NSS KG * 1.5 i think it will elevate serum NA BY 12 meq / day and not 6 meq isn.t it sir ? duration of correction during severe symptomativ hyponatremia is it have time limit or until resolution of symptoms ?
Thank you sir for your time and for creating these helpful videos. You speak a little bit fast which is ok. I need to brush up on my listening as a non-native English speaker. I have a question about hyperproteinemia which is linked to normal plasma osmolality. How that would be possible. Protein is one of the contributing components of creating plasma osmolality. Is that right? any solutes, glucose, or protein create osmolality. am I right?
hi Eric, thank you very much for the great videos! they are very helpfull. can u please try to explain in deatail why giving 0.9 saline to SIADH can worsen the hyponatremia (if the urine osmolarity is high enough). thanks
Hello, Dr. Strong. I had 2 questions: 1. Can you please give an example for the anticipated duration of therapy of saline equation? How does one know the anticipated rate of correction? 2. Physiologically speaking, why does the saline Na conc. need to be greater than the urine osms for serum Na to increase?
Thank you Dr, I have question "why occur hypervolemia in advanced kidney failure although the Urine Na elevated(Una >40 meq /l)? -In advanced renal failure, kidney excreted sodium and retention water with out sodium?
Thanks once again for this great content! I have a question though regarding Step 3 in the Diagnosis Process. How can I reliably determine a patient's volume status? Hypervolemic might be easy due to odema, but what about differentiating between hypo- end euvolemic? Thank you
Great lecture and thank you for your extensive answer to my previous question on the ABG. I have a question regarding dehydration and the sodium profile. Many sources state that dehydration without fluid intake causes hypernatremia, and if water intake is initiated, hyponatremia ensues. As far as i recall from physiology, the ADH response to hypovolemia (seen with severe dehydration) would override the inhibition caused by a fall in osmolality, which should cause hyponatremia even in the absence of water intake. How would you explain this conundrum? Thanks in advance!
A great question! Paradoxically, both hypo or hypernatremia can develop from dehydration. In hypovolemic hyponatrememia, patients develop hyponatremia predominantly from replacing solute loss (i.e. diarrhea, sweat) with solute-free water. There is also a contribution from tubular water reabsorption via effect of ADH as you suggest. For some reason, this ADH contribution isn't mentioned as frequently, and I am unaware of any comparison as to the magnitude of its contribution when developing hyponatremia. However, there is a limit to how concentrated the urine can get. Thus, even if ADH is able to prevent hypernatermia from developing initially, if severely decreased water intake persists, a minimum obligate loss of free water via maximally concentrated urine will eventually lead to hypernatremia. This issue is most commonly encountered in infants and the elderly as they have impairment in renal concentrating ability, likely due to relatively decreased renal responsiveness to ADH.
Hi iv had a couple of discussions with friends who say that hypervolemia means an increase in intravascular fluid compartment ONLY - hence the ending -emia (to do with blood). If this is true then why do we call cases of CHF, nephrotic syndrome and cirrhosis - Hypervolemic? My answer is that Hypervolemia can be defined as an increase in total body water compartment, and not necessarily intravascular (though this is the most common use of the term). What is the correct answer please? Does anyone out there know?
This is a great question that unfortunately has no universally accepted answer. In discussion of hyponatremia specifically, almost all literature and textbooks classify its etiologies by "volume status" and list heart failure, cirrhosis, and nephrotic syndrome under "hypervolemia". Your friends are correct in stating that, in general, words ending in -emia suggest a state of the blood (e.g. hypoxemia, acidemia, etc...). But for some reason, the convention doesn't hold true 100% of the time. I wish there was a concise, universal way to distinguish states of intravascular and extravascular hypervolemia (e.g. decompensated heart failure) from states of intravascular hypovolemia and extravascular hypervolemia (e.g. most cases of nephrotic syndrome). But there isn't. In common practice, "hypervolemia" is usually used to refer to total body water (as you've suggested), but that usage is suboptimal. Regarding the actual diagnoses you mentioned. Heart failure (at least heart failure exacerbations or decompensated heart failure) is typically intravascularly hypervolemic. Cirrohsis and nephrotic syndrome may be either intravascularly hypovolemic, euvolemic, or hypervolemic. It predominantly depends upon the balance of hypoalbuminemia to activation of the RAA system in the former, and the balance of hypoalbuminemia to primary impairment of water excretion due to renal failure in the latter.
Hi thank you for a great answer. Just a couple more questions please. I have read elsewhere and been told that in CHF there is actually intraarteriolar volume depletion - and you've written there is intraarteriolar hypervolemia. Also you wrote that in nephrotic syndrome there is hypoalbuminemia and impairment of water excretion due to renal failiure. I was under the assumption that in both cirrhosis AND nephrotic syndrome it "predominanrly depends on the balance of hypoalbuminemia to activation of RAAS" So just a bit confused with those 2, but thanks I get what you're saying. I imagine that with cirrhosis and nephrotic syndrome there isnt one fixed volume state and rather its some kind of continuum, or a dynamic state where the fluid is moving from intravascular to extravascular compartments and back and forth though there is a total increase in body water - lol but thats just my guess :)
MukeshPandya1985 Be sure not to confuse intraarterial (arteries only) volume for intravascular (arteries + veins + heart) volume. In decompensated CHF, there is probably less than normal volume in the arteries (i.e. intraarterial hypovolemia) since arterial vasoconstriction is a natural response to low BP from low cardiac output, and this would reduce volume in the arteries. However, there is much more volume within the veins and heart itself, leading to intravascular hypervolemia. (Note that the concept of intraarterial volume is not commonly discussed in clinical medicine). I think your last paragraphs hits the nail on the head. Nephrotic syndrome and cirrhosis are very dynamic states, and even when the total body water is excessive, patients' intravascular volume can swing back and forth. The most dramatic common example of this is in cirrhosis, in which a very large volume paracentesis, when done without supplemental albumin, can shift a patient from intravascular hypervolemia to mild intravascular hypovolemia in a matter of hours (or even shorter).
Hir Sir, in the example of calculation of infusion rate for a 100kg individual - you have taken increase to 113 over 6 hours as an example. Let's suppose this stem of the question is omitted. So for calculation of infusion rate for 100kg individual : can't I use the previous recommendation of NOT TO CORRECT OVER 6 mEq/24 hours and by that come to a conclusion that the desired rate of sodium increase is 0.25 meq/L/hr (6mEq over 24 hours). Can't we place this in the formula?
A question: in advanced renal failure, where there's an inability to dilute urine due to increase in osmotic diuresis, how can this lead to hyponatremia ?
Thank you so much for all your videos Dr.strong! I have a question about a situation in which the patient is symptomatic but his hyponatremia is chronic. Do we still need to correct the sudium slowly? On one hand he is symptomatic, on the other hand- rapid correction can cause osmotic demyelination syndrome ..
I suppose that you will correct Na fast around 4-6 mmol in the first two hours in a symptomatic patient. But as the patient has chronic hyponatremia you consider stopping correction when the remission of the symptoms.
THANK you very much it is great job but i need to ask that i had read that we can differentiate SIADH and cerebral salt wasting by measuring urinary sodium ,yes i know both will be high but more higher in cerebral salt wasting, the other issue what is the pathophysiology of cerebral salt wasting, and lastly frusemide diuretic mention as a cause of hyper and hypo natrimea due you agree about that.
sir can you explain how giving isotonic saline like 0.9 NS will worsen hyponatremia in euvolemic conditions like SIADH as its sodium content is almost similar to plasma?
Sutirtha, thanks for watching and for the feedback! Unfortunately, as a hospitalist, I'm not as qualified to teach surgical topics, and with my long backlog of internal medicine topics, I'll probably be sticking to medicine for the near future. Paul Bolin and Nabil Ebraheim both have channels with some great orthopedic surgery videos. However, excluding those focusing on patient education videos, or on videos of actual procedures, I haven't personally come across any high quality channels that cover other surgical disciplines.
In long term chronic SIADH, fluid restriction and salt tablet intake is needed. How many 500mg tabs can be taken, without adverse effect? Is more than 10 tabs a day alright?
8:45 Could you explain how in theory fluid deprivation would correct a reset osmostat hyponatremia? Wouldn't that cause more ADH release via hypotension and thus make hyponatremia more severe?
I think what Dr Strong meant was that water deprivation will improve the clinical status of the patient, and worsen that of the patient with cerebral salt wasting.
Had a challenging pediatric case of patient who received both cisplatin (may cause RSW) and vincristine (may cause SIADH). Sodium went from 130 to 113 in the course of 24 hours. Additionally, the kid had poor PO while receiving chemo so volume status to differentiate was especially challenging. I wonder if the severity of hyponatremia or urine sodium levels can help distinguish? Or can the difference between daily sodium intake and daily urine sodium output (if this could be collected) assist? Curious if anyone has any thoughts?
Hi doc .. Very good video on a very difficult and interesting topic. I have a question ... You mentioned that hyponatremia due to elevated ADH can be caused by volume depletion. Won't aldosterone and angiotensin II resolve the hyponatremia by increasing renal sodium (and also water) reabsorption ? Or is it because the release of ADH which only reabsorbs water that produces the net effect of increase in solute-free water reabsorption, rather that sodium-rich water reabsorption, that causes the hyponatremia ? Many thanks :-)
I have BP 149/98, and sodium 134, I feel very sleepy, it is very hard to drive 2,3 miles. ? If I take salt, that may increase BP high. What should I do ? Suggest me pls
No. Maybe there are very subtle differences in practice re: management, but the general principles are the same. And the etiologies and work-up are unchanged.
+Mohamad Al Shaabani Actually yes! Check out my latest video posted just now with the details: ru-vid.com/video/%D0%B2%D0%B8%D0%B4%D0%B5%D0%BE-iJiUBFsvdtg.html
+Kobe Bryant BUN stands for blood urea nitrogen. For some reason unknown to me, the US (and some other countries too probably), still report urea in terms of just the urea nitrogen. But you can effectively think of it as urea (i.e. increased in situations of poor kidney function or high protein catabolism, and decreased in situations of extreme malnourishment).
