Can someone clarify this for me? Re: Rapid/gradual correction of hypernatremia

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Knicks

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....or was it HYPOnatremia?...

We have to correct it (HYPERnatremia?,, or both?) slowly so that we prevent cerebral swelling and central pontine demyelnation.

So my question is WHY does correcting it RAPIDLY lead to those 2 things?

I don't understand it.

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You are correcting hyponatremia with saline.

From e-medicine:
One theory proposes that in regions of compact interdigitation of white and gray matter, cellular edema, which is caused by fluctuating osmotic forces, results in compression of fiber tracts and induces demyelination. Prolonged hyponatremia followed by rapid sodium correction results in edema. During the period of hyponatremia, the concentration of intracellular charged protein moieties is altered; reversal cannot parallel a rapid correction of electrolyte status. The term osmotic myelinolysis is more appropriate than central pontine myelinolysis for demyelination occurring in extrapontine regions after the correction of hyponatremia.

The bolded statement should be obvious.
In the central pontine matter, the same type of edema is choking off and killing the axon tracts.

Correcting hyponatremia FAST leads to these things... you need to correct them slowly so that the tissues respond to gradual changes, not acute osmotic shifts.

Also note that hypernatremia usually just means dehydration. Rapid correction of hypernatremia with water can also lead to edema through the same mechanisms, and according to e-medicine can also lead to central pontine myelinolysis.
 
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^^ Ok thanks, but I was confused about WHY rapid correction results in edema. LoL, it's so late right now that I can't think properly. 😳
 
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Water follows sodium. If tissue is hyponatremic and the correction is acute, salt enters the tissue with the water (net sodium and water entry), as opposed to a slower correction where on average there would be a majority net flux of sodium (with no net water entry- the sodium would enter until physiologically iso-osmotic, regulated by kidneys, adrenals, posterior pituitary, etc and all that will have time to work). I think this is a generally accurate way to think of it. With hypernatremia, tissue has excess salt, and rapid correction causes a massive flux of water into the tissue with the elevated salt, which causes edema.
 
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Water follows sodium. If tissue is hyponatremic and the correction is acute, salt enters the tissue with the water (net sodium and water entry), as opposed to a slower correction where on average there would be a majority net flux of sodium (with no net water entry- the sodium would enter until physiologically iso-osmotic, regulated by kidneys, adrenals, posterior pituitary, etc and all that will have time to work). I think this is a generally accurate way to think of it. With hypernatremia, tissue has excess salt, and rapid correction causes a massive flux of water into the tissue with the elevated salt, which causes edema.
Brilliant.

Thanks man.

Sheez! It's almost 4:30am! I'm outtie.

Thanks again.
 
Only things to add from a practicing perspective are that if you're aiming for slow correction, normal saline is the fluid of choice (Na concentration of 154, which is higher than a normal sodium, so it will work).

The exception to the rule, and I don't think you need to know htis at the med school level, is for a person seizing from low sodium, in which case rapid correction with hypertonic saline is necessary until seizures stop. At that point, slow correction once again rules.
 
^^ Thanks for that. Yes, any clinical pro-tips you and anyone else provides will be appreciated.
 
Salt and water is some of the toughest stuff in Medicine. I prob spent untold hours studying this stuff, but until you see it in a lot of patients its tough to put in perspective.

I have found the easiest way to understand salt and water is at the bedside. First I evaluate the patients volume status (TB salt), toughest thing to do by far but- estimation of JVP, rales, and intracardiac filling pressures, ascites, peripheral/sacral edema, skin turgor, mucus membranes, blood pressure and heart rate, history of GI/renal/other losses- along with focused historical clues, usuing all of this and your clinical judgement is the first and hardest step. Then its easy from there...

TB water can be figured out if you can clinically estimate the TB salt.
Hyponatremia = more water than salt (but could have too much/too little of both compared to "normal levels")
Hypernatremia = ALWAYS a water deficit regardless of salt level

Where this matters in relation to your question is relevant clinically. Basically, Hyponatremia = hypotonicity in your plasma, over time brain gets jealous and sucks water from your plasma to dilute its higher osmolar concentration. Acutely, no big deal to rapidly correct this disorder (volume depleted patient with recent GI illness - you can correct their serum sodium from 120 to 140 without penalty). Chronically this can be bad as brain has had time to adapt to serum levels and if you suddenly create a more hypertonic plasma, all that water the brain is swimming in with all its jealousy suddenly gets pulled out and "demyelination" "CPM" happens. I saw this in an alcoholic with end stage liver- walked into ED with serum Na of 112, altered, admitted to ICU and sodium corrected to 135 over the course of a day -we got him on the floor about a week later and he was lethargic, blamed on "hepatic encephalopathy" MRI sev days later showed abnormal enhancement in the central pons. ooooops, sorry bout that.

Hypernatremia is a bit different. Acutely, also no big deal, the plasma becomes transiently hyperosmolar, brain gets jealous and starts to spit out water, but wait, he is much smarter than that and starts to reabsorb some organic solutes ("idiogenic osmoles") after a couple of hours; thus he is able to keep big bully plasma from stealing his kiddy pool of water. So septic heroin shooter in the ICU with endocarditis who is breathing 50 x per minute and sweating bullets of water does ok if you rapidly correct his sodium from 160 to 140. But grandma Sally is screwed, since she has been in a nursing home demented and the staff is mean and haven't been giving her access to water. Her serum sodium is 160, but has been that way for weeks, and her happy brain is swimming in her happy kiddy pool of water because it is buffed up with extra solutes. But then comes along Joe intern in July, who thinks he is smart because he looks at some numbers on a computer- "ahhh, I need to fix that now" to impress his Attending. Grandma Sally's serum Na is 140 in the morning. The attending wasn't paying attention in the morning because he just broke up with his wife and is distracted by the ICU nurse in pigtails with the beautiful backside. Grandma sally stops breathing a couple of days later and seizes. A CT head revealed midline shift and herniation because pissed off plasma suddenly became hyposmolar and happy brain said- "hey buddy, there is an osmolar party in here with tons of nekkid hookers" water now becomes the jealous one and jumps inside to get freaky in the brain party, which subsequently becomes a block party orgy so large that it can't be contained and spills out into the street. And that is why you should use a condom in situations like that.
 
Only things to add from a practicing perspective are that if you're aiming for slow correction, normal saline is the fluid of choice (Na concentration of 154, which is higher than a normal sodium, so it will work).

The exception to the rule, and I don't think you need to know htis at the med school level, is for a person seizing from low sodium, in which case rapid correction with hypertonic saline is necessary until seizures stop. At that point, slow correction once again rules.

This is mostly correct with one minor correction. If the process causing hyponatremia is a PURE SIADH picture, then giving normal saline will usually make the blood sodium LOWER, not higher. Here is why.

In SIADH, there is an abnormally regulated excretion of ADH hormone. Remember that this affects H20 retention ONLY, salt regulation is normal. In a person without SIADH, if you give normal saline, the ADH level that the kidney "sees" will result in water retention that is grossly similar to the osmolarity of the blood.

However, in SIADH, your ADH level is abnormally high, and depending on how high it is, giving NS will result in preferential H20 retention of the sodium load you give, and this will result in your serum sodium falling lower, even though normal saline has a higher salt concentration than serum. To fix this, not only do you have to use a saline solution that is higher than the serum concentration of sodium, you have to use a sodium solution that is HIGHER than the URINE osmolarity. Thats why 3% saline works for SIADH and normal saline does not. The urine osmolarity, NOT the serum osmolarity, tells you how much ADH is being produced and therefore tells you how much sodium load you need to give to a patient in order to successfully increase their serum sodium. In essence, you can think of the urine osmolarity as giving you the "set point" that marks how much of an effect ADH is having on water retention.

The quick and dirty way to think about this is as follows: 1) If your patient is hyponatremic, check both a serum and urine osmolarity 2) If the serum osmolarity < 280 and the urine osmolarity is inappropriately high, then SIADH is a prime suspect 3) In order to raise the sodium level of the serum, give a sodium load that is more hypertonic than the urine osmolarity load. That will overcome the ADH set point and cause a rise in serum sodium levels. Up to date has a good article on the subject that gives specifics on how to calculate exactly how much sodium to give.
 
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