Na correction in Hypernatremia

[ontime]

You have a patient in Acute DKA Glu 490 and Hco3 of 7, with a high Na>163. We corrected the Acute DKA first, and then when the glu was less than 250 we started giving 5% dextrose and half NS. the resident said this was the normal way, but she never made any of the Total body weight calculations to figure out how much total fluid to give in 24 hours with a goal serum Na conn. It just seemed wierd to be giving dextrose to someone with a glu over 200. Also i would not want to over correct too fast in fear of cerebral edema or pontin demylination. What do you all think. its only my second week of IM as an MS3, so if stupid question dont flame me.

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[dredd]

The dextrose is being with insulin maintain the glucose >200 while they correct the anion gap. You have to keep giving insulin while you still have a gap because insulin will stop the ketogenesis, but you don't want glucose to fall too low because you are worried about cerebral edema. The one half normal saline is likely given with the dextrose to prevent central pontine demyelination so that the hypernatremia will not be corrected too quickly. Ideally, you should figure otu a total water deficit with hypernatremia to figure out how much to give, but in the setting of DKA, I don't think that those equations apply anymore.

 

[irlandesa]

The dextrose is being with insulin maintain the glucose >200 while they correct the anion gap. You have to keep giving insulin while you still have a gap because insulin will stop the ketogenesis, but you don't want glucose to fall too low because you are worried about cerebral edema. The one half normal saline is likely given with the dextrose to prevent central pontine demyelination so that the hypernatremia will not be corrected too quickly. Ideally, you should figure otu a total water deficit with hypernatremia to figure out how much to give, but in the setting of DKA, I don't think that those equations apply anymore.

good explanation. I think the danger of dehydration in DKA is also great enough that you wouldn't have to worry so much about being overaggressive with giving IV 1/2 NS. Also, hypernatremia, esp. at the level you mentioned, tends to require very aggressive IV hydration. One of my patients came in with an Na+ of 158, and didn't correct until we pumped her 1/2 NS infusion up to 200 cc/hr for several days. The Total water deficit calculations didn't come close to predicting that she'd need that much. Of course, she was 88, had ARF secondary to severe dehydration, and was not concentrating her urine well at all due to some underlying CRF. I wouldn't be surprised to see similar issues in a diabetic patient.

 

[Annette]

Doesn't the patient have psuedo hypernatremia? You have to correct for the glucose by decreasing the na level by 10 for every 100 of glucose over 100. She is ~300 over in glucose, so drop the Na by 30~133= hyponatremic.
Treat the DKA, and the sodium will correct automatically.

 

[marchiafava]

Annette, your grossly incorrect, so much so that I am nauseated and don't want to tell you why right now. Hopefully some else will.

 

[MustafaMond]

Doesn't the patient have psuedo hypernatremia? You have to correct for the glucose by decreasing the na level by 10 for every 100 of glucose over 100. She is ~300 over in glucose, so drop the Na by 30~133= hyponatremic.
Treat the DKA, and the sodium will correct automatically.

You are backwards.
See this site.
http://www.medcalc.com/correctna.html

 

[Apollyon]

Annette, your grossly incorrect, so much so that I am nauseated and don't want to tell you why right now. Hopefully some else will.

Grossly inappropriate and uncalled for. By the way, it's "you're", and, if viewing SDN makes you nauseated, go away.

 

[Annette]

Thanks, Mustafamond and Apollyon! I stand corrected.

 

[DR]

Annette...don't sweat it. That's a ridiculous response to your post. People have to chill out. Responses like that cause people to become stifled and not ask questions...the very recipe for ignorance and the cessation of learning. Keep asking questions. Remember this great quote I've come across: "He who asks a question is a fool for 5 minutes. He who does not ask a question is a fool forever."

 

[dredd]

Speaking of corrections, I actually made in error in my original post as well. Central pontine myelinosis is a complication of correcting hyPOnatremia too quickly, cerebral edema comes from correcting hypernatremia too quickly. Also, besides using half normal saline to more slowly correct that patients hypernatremia, it was also probably being used to continue volume resuscitating the patient. Pure D5W will not replete intravascular volume as much as 1/2 NS or NS, the saline will cause fluid retention within the intravascular space as opposed to most of the fluid going out into the interstitial and intracellular space which would occur with D5W.

 

[Docxter]

Speaking of corrections, I actually made in error in my original post as well. Central pontine myelinosis is a complication of correcting hyPOnatremia too quickly, cerebral edema comes from correcting hypernatremia too quickly. Also, besides using half normal saline to more slowly correct that patients hypernatremia, it was also probably being used to continue volume resuscitating the patient.

Although central pontine myelinolysis (CPM) is classically seen as a complication of rapid correction of hyponatremia and cerebral edema as a complication of treating hypernatremia, this is not always true. Central pontine and extrapontine myelinolysis can be seen in correction of both hyponatremia and hypernatremia (more so in the former).

 

[Tenesma]

dredd... D5W osm=280 1/2NS osm=150.... so based on oncotic pressure D5W is way better than 1/2 NS.... so if you give somebody 1/2 NS or D5W, either way it will leave the intravascular space within about 10-15 minutes. Don't use 1/2NS or D5W for fluid resuscitation in fact, even if the patient is hypernatremic, if they need to be volume resuscitated you better be using NS or another balanced solution (such as LR)... which stays intravascular maybe 30 minutes... once they are stabilized (no longer requiring resuscitation) then you can go ahead and use your formulas to try to correct the numbers

 

[SoCalDreamin']

dredd... D5W osm=280 1/2NS osm=150....

If I am not mistaken, 1/2NS osm = 77, as NS osm= 154.

 

[Tenesma]

you are mistaken (but no biggie)

you are referring to the mEq of NA... which is different from the Osm...

 

[Annette]

Now, I got the correction wrong but I thought the last thing you wanted to give someone who was hypernatremic was more sodium. I was taught (yelled at) that only the first liter should be NS then switch to D5W. If you need to keep the fluid intervascularly, use a colloid in addition.

 

[Tenesma]

annette

like i said... you use balanced isotonic solutions (NS/LR) first until the patient becomes hemodynamically stable/resuscitated, and then you can address the free water deficit if that is the cause of the hypernatremia.

and you can start throwing out of the window the whole colloid idea!!! just read the recent SAFE trial in the NEJM which once and for all proves that there is absolutely no difference between albumin (Colloid) and crystalloid.... other than here at MGH we charge $475 for 5% albumin (250cc) vs. $19 for 1,000cc of LR.

 

[KGUNNER1]

Tenesma,

Not exactly. The SAFE investigators excluded patients that have had previous outcome benefits from albumin used as a volume expander (e.g. Cardiac surgery, liver failure - transplant, and burn patients).

Subgroup analysis showed improved mortality in the septic shock subgroup and increased mortality in the head trauma subgroup.

Normal saline is not a "balanced" isotonic solution. It is 154 meq of Na and 154 meq of Cl. Our body does not usually have a "normal balance" of Na and Cl in either ratio or plasma concentration. LR is closer to a "balanced" electrolyte solution.

A big question that SAFE did not answer is the role of other synthetic colloids such as gelatin base solutions (used in Europe and Australia) or hetastarch. Typically hetastarch is mixed in NS which again leaves us with an "unbalanced" colloid (Hespan).

However, a newer product, which has some cool properties, is Hextend. This is hetastarch mixed in a balanced electrolyte solution similar to LR. Same price as Hespan. No I don't work for Abbot.

KG

 

[Tenesma]

KG - as usual, makes excellent points

 

[WhataBreeze]

Although central pontine myelinolysis (CPM) is classically seen as a complication of rapid correction of hyponatremia and cerebral edema as a complication of treating hypernatremia, this is not always true. Central pontine and extrapontine myelinolysis can be seen in correction of both hyponatremia and hypernatremia (more so in the former).

Yes it's a fact this thread is over two years old. I would assume Dr. Docxter is well on the way to a wonderful career in the "Healing Arts." I happen to be one of the few CPM Surviors. (5 years) As I view many posting here at SDN, many of my own questions in regard to what has happened from the present back to 1959 when Dr. R.D. Adams was the first to bring light on this CPM issue of fatal or chronic importance. As many physicians in several areas all state, CPM goes both undiagnosed and under reported. From my readings here at SDN, I've found actually a parallel to over four years of reseach including several thousand world wide articles viewed as a Layman Advocate.

It's very common knowledge that CPM is a "Concequence of Incorrect Treatment," many times call an "Iatrogenic Cause." Please let me make one fact clear to you future doctors, I presently work on a volunteer basis along with Institutes from the NIH as we just had NINDS recognize Central Pontine Myelinolysis with an updated Information Page. The "Bottom Line" is for the few of us CPM Survivors, a new organization called the, "CPM Awareness Foundation" is about to see life.

I would love to personally be honored if in fact you may have any info in regard to "ANYTHING" about CPM as this is the first official effort to give Dr. Adam's findings the life it should have. Also on the other side, I guess you can say the main connection to our group of CPM victims. If I can help you with "First Hand Info," please don't hesitate. G-d Bless....


Franky and Breeze

Note: Franky is my neuro canine 3 year old Boston Bull Terrier associate, therapy director and loving companion.

 

[Igor]

A couple of comments.

Clinical Facts:

All DKA is acute - there is no "chronic DKA"

High serum Na means the patient has total body water depletion. In this case, it's from the osmotic diuresis (sugar pulls out water).

Cerebral Pontine demylenation (CPM for some strange reason) is the result of correct HYPOnatremia too quickly. Your patient is hypernatremic so this is not relevant to your case.

Serum Na DROPS 1.6 points for every 100 points of glucose over 100 (add 16 to the serum glucose for a sugar of 1100). Serum Cl drops the same amount so the anion gap doesn't change. If your sugar is 500 and Na is 163, your corrected Na is 168.

You are right about the osmotic shift. The size of brain is based on where the water in the body is located (the cell is mostly water). If your serum glucose is 500, the water is trying to get into the blood stream. If your serum Na is high, the water is trying to get into the blood stream. The brain will swell as this is corrected (all the organs will but the brain is only one housed in cage called the skull).

Most really smart folks recommend getting the serum glucose down to somewhere between 200 and 300; I was taught to use 250. This is an attempt at fixing the underlying problems but trying to prevent brain swelling. It may be that this is just hooey but it's what everyone does.

I am guessing your resident is using some sort of DKA protocol. Form your description (obviously I wasn't there) she didn't explain the logic of treatment plan to you.
Not knowing the case, I'll try my best:

If a patient came in with just a serum Na of 163 (not in DKA) you would calculate the free water deficit and replace half in the first 24 hours. Usually these are patients who do not have access to water (s/p CVA, nursing home residents who can't do their own ADLs, infected, whatever). Occasionally you will see diabetes insipitus (you have to think of it) but it's usually not the cause.

In DKA the patient has an osmotic diuresis. The first stage is to turn off ketosis and then get the sugar under control (insulin does this). It also helps if you know what caused the DKA but that's another story.

Anyone who has working kidneys gets very volume depleted while in DKA - all osmotic diuresis. You're not supposed to bolus 1/2 normal saline (too low osms, it can cause hemolysis). The patient is dry. Most authorities recommend treating the volume depletion first and then the hyponatremia (give 6 to 8 liters of normal saline) then change to hypotonic fluids.

Asumming you have a 60 kilo male patient, the water deficit is about 7 liters so he needs about 3500 of free water in the 1st 24 hours of the admission. There are a lot of ways to fix this; I had one attending who would have given both NS and D5W in 2 different IVs (to each his own). Others would give NS for a certain amount (say 4 liters) and then change to hypotonic fluids.

Personally, I would have started 1/2 NS at 300cc/hr (assuming BP was stable and he got some NS bolused in the ER). Again, there are a lot of ways to do this.

Just make sure the lytes are monitored - he's going to need lots of K and P and probably some Mg as well.

Great case!