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How To Treat Hypernatremia?


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#1 onearmwonder

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Posted 17 July 2010 - 04:41 AM

I cam across a case today in the hospital and I am curious of what is the pathophysiology behind treating hypernatremia(170mEq/L) due to dehydration from poor to no input. The NP in the room stated they treat it with .45%NS with D5w solution, but she didn't have the time to explain. The PT has had no input x 5 days, PIC line is not working, no TPN, no hx. of NIDDM/IDDM. Blood sugar was 40mg/dL and she was more altered than normal per family. Not asking how to treat the hypoglycemia, got that down, just the hypernatremia. Is the 170mEq/L intracellular or intravascular? Let's hear your thoughts!

Thanks,

Matt
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#2 TexRNmedic

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Posted 17 July 2010 - 08:45 AM

I cam across a case today in the hospital and I am curious of what is the pathophysiology behind treating hypernatremia(170mEq/L) due to dehydration from poor to no input. The NP in the room stated they treat it with .45%NS with D5w solution, but she didn't have the time to explain. The PT has had no input x 5 days, PIC line is not working, no TPN, no hx. of NIDDM/IDDM. Blood sugar was 40mg/dL and she was more altered than normal per family. Not asking how to treat the hypoglycemia, got that down, just the hypernatremia. Is the 170mEq/L intracellular or intravascular? Let's hear your thoughts!

Thanks,

Matt


Hey Matt, I'll give you my simple answer and if you need more just let me know. I know we have some textbook authors around here that can add more detail if you need. We are basically measuring the serum or intravascular level when we draw blood for labs. The major extracellular cation is sodium with an average normal level of about 140 mEq/L. The normal intracellular sodium is around 12 mEq/L. Intracellular K is about 140mEq/L. Sodium has a direct impact on the osmotic movement of water. In an over simplified explanation, in a patient with inadequate water intake or excess water loss, the total body water becomes depleted and sodium will become more concentrated. Extracellular and intracellular dehydration will occur.

The easy answer for treatment is we need to replace the depleted total body water. This can be done enterally or parenterally. Hence the free water NG/OG boluses given to mildly hypernatremic patients in ICU. IV fluids with low sodium content like D5W, 1/4NS, and 1/2NS can be used to replace the water. The replacement is done gradually as the high sodium levels in sensitive tissues like within the brain will have an osmotic effect on the water and a rapid resuscitation can cause rapid fluid shift and edema. I'm willing to bet the patient had some other lyte issues, albumin/protein deficiency and some pretty significant prerenal failure. Take a look at anion gap measurement. If they have had a complete metabolic panel, it might be interesting to look at the balance of measured cations and anions. If you can, follow the CMP over a few days as they correct the various issues. Might also take a look at serum and urine osmo and urine sodium, if they measured it.

Regards,
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Wes Seale
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#3 onearmwonder

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Posted 17 July 2010 - 05:12 PM

So if the sodium level is based off of intravascular readings, then I'm still not clear of how we are reducing the sodium levels. If we are infusing .45%D5w at a slow rate what is that doing if we have severe renal insuficiency? Because it seems to me that If we were trying to reduce sodium we try to rehydrate the patient which will allow the sodium to leave with the water. Is the D5w for glucose for energy production?

Matt
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#4 SerendepitySaki

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Posted 17 July 2010 - 05:43 PM

no. you have mail.

So if the sodium level is based off of intravascular readings, then I'm still not clear of how we are reducing the sodium levels. If we are infusing .45%D5w at a slow rate what is that doing if we have severe renal insuficiency? Because it seems to me that If we were trying to reduce sodium we try to rehydrate the patient which will allow the sodium to leave with the water. Is the D5w for glucose for energy production?

Matt


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#5 onearmwonder

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Posted 17 July 2010 - 09:35 PM

Didn't receive it yet...
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#6 TexRNmedic

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Posted 17 July 2010 - 09:54 PM

So if the sodium level is based off of intravascular readings, then I'm still not clear of how we are reducing the sodium levels. If we are infusing .45%D5w at a slow rate what is that doing if we have severe renal insufficiency? Because it seems to me that If we were trying to reduce sodium we try to rehydrate the patient which will allow the sodium to leave with the water. Is the D5w for glucose for energy production?

Matt


I hope Sean's email helped unmuddy the water for you. Try to look at the intravascular, interstitial and intracellular spaces as compartments. These compartments have "passages" that allow certain content to move between them. Some of this movement happens without the use of energy and some requires energy. The body tries to maintain homeostasis. This means that with a little thinking about overall clinical picture, when can interpret labs to give us an idea of not just what's going on in the blood, but also in the whole body. In your case, if the patient is intravascularly volume depleted we can pretty well assume the whole body is dry. We are not really trying to remove sodium from the body, but dilute it and replace the missing TBW back to the normal, around 60% body weight.

IV fluids. I don't know of a .45%D5w. It is more than likely 0.45NS or D5Water. D5W is only worth about 200 Kcal per liter. Not really enough to provide adequate nourishment. The idea is to replace the water intravenously. The body does the rest to redistribute it.

Renal insufficiency. Remember you can have prerenal causes of renal failure. The azotemia is secondary to the dehydration and decreased renal blood flow. The patient may have progressed to tubular necrosis, but adequate rehydration and lyte correction, using the correct fluid and rate are one of the top goals.
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Wes Seale
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#7 SerendepitySaki

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Posted 17 July 2010 - 10:49 PM

via FB...

Didn't receive it yet...


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LET THE WILD RUMPUS BEGIN !!!!!!
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#8 medsrgw

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Posted 23 July 2010 - 04:15 PM

I cam across a case today in the hospital and I am curious of what is the pathophysiology behind treating hypernatremia(170mEq/L) due to dehydration from poor to no input. The NP in the room stated they treat it with .45%NS with D5w solution, but she didn't have the time to explain. The PT has had no input x 5 days, PIC line is not working, no TPN, no hx. of NIDDM/IDDM. Blood sugar was 40mg/dL and she was more altered than normal per family. Not asking how to treat the hypoglycemia, got that down, just the hypernatremia. Is the 170mEq/L intracellular or intravascular? Let's hear your thoughts!

Thanks,

Matt


This is more complicated than just looking at the sodium concentration, and is a dangerous condition. Without knowing more about the patient, and ignoring the glucose issue, the patient seems to be suffering from HYPOVOLEMIC HYPERNATREMIA. There is a very good article about hypernatremia in general at http://emedicine.med...766683-overview, and the following is a paragraph from it:

Using isotonic sodium chloride solution, stabilize hypovolemic patients who have unstable vital signs before correcting free water deficits because hypotonic fluids quickly leave the intravascular space and do not help to correct hemodynamics. Once stabilization has occurred, free water deficits can be replaced either orally or intravenously.

This is a critical part of treatment, and the IV fluids chosen must be based on the etiology of the disorder, as the patient may be hypovolemic, hypervolemic or euvolemic.

RW
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#9 SerendepitySaki

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Posted 23 July 2010 - 05:31 PM

good one. thanks.
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LET THE WILD RUMPUS BEGIN !!!!!!
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#10 onearmwonder

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Posted 23 July 2010 - 09:37 PM

Wow! Great article... Clear on that...
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#11 old school

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Posted 26 July 2010 - 01:51 PM

Is the D5w for glucose for energy production?


The dextrose is not meant to supply calories, it is given because after the dextrose is metabolized, you have effectively added free water to the system.

You can't just give free water IV because it is so hypotonic that it rapidly shifts into the cells and causes hemolysis. The dextrose simply acts as a solute to provide enough osmotic pressure to keep this from happening during administration - the water enters the bloodstream attached to the dextrose molecules, and as the dextrose molecules are metabolized the water gradually is freed to lower serum osmolality and sodium concentrations.

If the patient is hemodynamically and neurologically stable, hypernatremia can be managed largely through PO free water administration over several days time. Of course electrolyte levels and renal function need to be closely followed.

I don't know of a .45%D5w


D5 .45%NS, or "D5, half-normal" is pretty commonly used in these scenarios. It is close to isotonic but has half the sodium load of normal saline, allowing for gradual correction.

If the causative factor is simply lack of intake (dehydration), and as long as the renal system is working alright, the body will correct the problem itself (by eliminating sodium) with gradual PO free water or IV administration of half-normal or even NS.
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