Hyponatremia and acute psychosis?

[fishbum]

If you're willing, I'm hoping you experienced folks might be able to help me understand a few things about a case I walked into the middle of recently. (I should probably be more careful where I walk.) 

 

Hours 0, 1 and 2:

 

45 year-old male with a history of seizures secondary to TBI on long-term tegretol presents to ED via EMS with acutely onset visual + auditory hallucinations. Pt is alert and cooperative but confused. He has no psych history, and no other history besides.

 

VS: BP=138/74, HR=78 (NSR), RR=16, non-labored, spO2=99% on RA.

 

Labs as follows:

Na=127

K=3.4

Cl=86

CO2=25

AGAP=16

Glucose=98

BUN=38

Creat=2.14

Ca=9.8

 

Etoh negative, tegretol level=0.1 

 

Hours 3 and 4:

 

Pt given 1L NS bolus, no significant change.

2nd liter given, during which pt (rapidly) becomes agitated and combative, eventually requiring several people to restrain. BP up to 190s/120s, HR=140s-150s. A couple of doses of ativan and haldol are given without effect. Etomidate and succinylcholine worked well....

 

So here's what I'm wondering about:

 

1. Tegretol is associated with SIADH/hyponatremia, right? So, is Na=127 likely to be chronic or is this number low enough to be a flashing neon sign indicating a probable cause of the initial presentation? 

 

2. One of a few things I really remember from fluids & electrolytes class is to correct hyponatremia slowly. Using the calculator at http://reference.medscape.com/calculator/hyponatremia-correction-infusate-rate, it appears that the max rate for NS infusion should be 471.43 ml/h. The pt got about 2,200 ml in about 2 hours (1100 ml/h). Is that rate sufficiently overzealous to cause cerebral edema? If so, would you expect it to develop that quickly? How do you feel about increased ICP for an explanation of the sudden agitation/combativeness?

 

3. What do you think about excited delirium (maybe acutely withdrawn from tegretol since pt is sub-therapeutic)? Haldol is to be avoided in these pts if sympathetic syndrome is suspected because of QT prolongation, right? How do you feel about haldol in this pt with no particular reason to suspect cocaine/meth, but with combativeness+metabolic acidosis? Anyone advocating ketamine +/- benzos?

 

4. If all of the above are way off, any other differentials?

 

I'd appreciate any feedback/discussion you can offer.

[EMEDPA]

what did his tox screen and head ct look like?

a na of 127 doesn't do that. we send folks home from the ed at 127 all the time.

maybe this guy had a previously undx psych d/o? one of the primary causes of low na(other than diuretics) ,is psychogenic polydipsia.

and why is he in renal failure? it isn't dehydration with a bun/cr ratio around 15.

there is more going on here than just the na...

geodon and zyprexa IM are other options if you don't like haldol.

how about DTs as a cause of the agitation? you would expect an ETOH of 0 if he had bad DTs. maybe his etoh level is normally 500(?)

[fishbum]

what did his tox screen and head ct look like?

 

maybe this guy had a previously undx psych d/o? one of the primary causes of low na(other than diuretics) ,is psychogenic polydipsia.

and why is he in renal failure? it isn't dehydration with a bun/cr ratio around 15.

there is more going on here than just the na...

 

how about DTs as a cause of the agitation? you would expect an ETOH of 0 if he had bad DTs. maybe his etoh level is normally 500(?)

Tox screen and CT not available (further comment deferred).

 

Good thought on undx psych...plus new ones have to start some time, right?

 

I thought about DTs but kind of discounted it based on no tachycardia/normal BP (at least initially) and no reports of tremors on arrival. How rapidly would you expect that to develop? 

 

 one of the primary causes of low na(other than diuretics) ,is psychogenic polydipsia.

 

He did soak the sheets thoroughly and then fill the foley bag pretty rapidly when inserted...but he'd also just had 2 liters of fluid. 

 

 

a na of 127 doesn't do that. we send folks home from the ed at 127 all the time.

 

This answers one of my biggest questions, thank you. I know I've had patients with low 130s and high 120s before with MUCH milder sx...just made me wonder how individual that would be...and how low is really low.

[EMEDPA]

the absolute na # isn't as important as the rate of drop. lots of folks on diuretics live in the 120s. I have seen a few sub-100s and a memorable 105 who was seizing. also had a 172 last week who was confused. I had a guy with DTs last year brought in by police who was found running naked in a snowstorm(to a liquor store apparently). 10 mg of IM haldol and 14 mg of IM  ativan(in divided doses) before we could get close enough to get him in restraints to perform an exam...

[fishbum]

 I had a guy with DTs last year brought in by police who was found running naked in a snowstorm(to a liquor store apparently). 

If only he'd made it to the store....

 

Kidding, of course.

 

Thanks for the input...very interesting stuff.

[EMEDPA]

If only he'd made it to the store....

 

Kidding, of course.

 

Thanks for the input...very interesting stuff.

actually, if he had made it to the store and successfully purchaed etoh he probably would have been ok.

I have seen docs write on d/c instructions" go home and have 3 beers to avoid withdrawl sx".

I don't write that.

[winterallsummer]

As others have mentioned, the absolute Na number is not nearly as important as how fast the level fell or rose.  I have seen a patient with beer potomania who had a sodium of 104 and was 100% lucid.  That being said, 127 does not explain this case, unless we imagine a circumstance that he was perhaps hypernatremic and then it fell rapidly, but that seems unlikely. 

 

When you question if a hyponatermic lab finding is acute or chronic, you have three things to rapidly guide you: 1) prior labs - that is easy enough when avaliable, 2) symptoms (chronic symtpoms are more like malaise, acute symptoms are more like AMS and seizure), 3) suspected etiology.

 

To really differentiate, you will need to know PMH, and have some other lab values such as serum and urine osmolality and urine sodium.  The treatment for psychogenic polydispia, for example, is water restirction; in contrast, renal losses require correction with NS or hypertonic solution.

 

Now in this case, he seems to have AKI or AoC renal failure, a gap, hypochloremia, that is more like a volume depleted state.  Did you make him worse with a liter of NS?  Doubtful.  Probably his hypertension and tachycardia reflects his agitation.

 

The question is why is he severly volume depleted?  UDS and and CTH would be imperative once he is chemically sedated enough to undergo foley and scanning.  My guess is this is probably not psychosis induced by hyponatremia, but rather the hyponatremia is consistent with his AKI.  AKI, dehydration and psychosis plus a negative ETOH could suggest ETOH withdrawal.  Or he could have two separate issues - one psychiatric or neurologically, and the other of volume depletion.  All that being said, I don't think your answer here is in the sodium - I don't think he has hyponatremic induced psychosis, and I don't think you corrected it so rapidly that you somehow led him down that course.

 

My money is on the UDS, personally.  Of course I want the head CT as well.  And I would like to know his CMP results, and of course what happened next!

 

As a rule of thumb, when presented with hyponatremia and unsure what to do, but the patient is stable and not needing 3%, order a quick serum osm, urine osm, urine elctrolytes, then give 250-1000 bolus and then put them on maitenence fluids.

 

Please let us know the final outcome of this interesting case.

 

** I wanted to add a quick caverat to the above "rule of thumb."  Some cases are better treated with fluid restriction (eg 1L total qd) alone.  In some circumstances, the serum osmolality makes it so that NS is actually still hypotonic, and thus NS will not correct the issue.  However, the most common cause of hyponatremia is hypo-osmolar hyponatremia (eg volume depletion), and this is typically reflected in the H&P and other labs such as creatinine.  Typically at 110-115 or below, you should order your labs but discuss the case with nephrology before doing anything.  When a patient has neurological symptoms (caused by brain swelling), 3% saline may be given in 100 boluses.  However, when the patient lacks any neurological symptoms, volume depletion seems plausible, then from my anectotal experience, ordering S and UOsm and lytes, giving 500 ml and then 100 ml/hr or no further fluid and sitting tight has worked well for me; this probably reflects the epidemiology which is that most cases are volume depletion. 

 

Another low hanging fruit is to see if the patient (ESPECIALLY if older and female) is on HCTZ, which is another very common cause of hyponatremia.

[jdenning]

I follow a lot of epilepsy patients and it's really common for them to have some pretty significant psych co-morbidities especially if there is a history of TBI. If I was prescribing this guy's seizure meds, I wouldn't like that Na+ of 127 and I'd get him off tegretol in favor of something else other than a sodium channel blocker. In this guy's case though, with a level of 0.1 it seems pretty unlikely that he's actually taking his tegretol. Would be interesting to see if you can dig up any prior levels

 

If possible I'd get an EEG while he's there....some of his agitation could actually be seizure activity

[Timon]

Is there any possibility of anticholenergic OD / toxcicity? Or maybe even Rieter's syndrome, malignant hyperthermia, or serotonin syndrome in the DDx?

[fishbum]

@winterallsummer: just so you know, I saved your response in a document on my hard drive so I can refer back to it and keep digesting it...thank you for the explanations. Like you and EMEDPA, I'd love to see a UDS and CT. I should be able to f/u via ICU documentation at least...hopefully I can do that tomorrow and get those results. Totally stupid question: when you say 3%, you're referring to hypertonic saline, right? Reserved for extreme hyponatremia? Forgive my ignorance, I just haven't seen that one used yet.

 

@jdenning: interestingly, there was some extremity movement post-intubation that raised the seizure question, especially considering the hx. But nothing else to bolster that dx (ie, no nystagmus), and the pre-event benzos were pretty liberal. It sounds like dropping the tegretol level to 0.1 would take a while? As in more than just missing a dose or two?

 

@Timon: based on the limited information I got, I wouldn't rule much of anything out. I'm only familiar with MH in patients getting succinylcholine, but these symptoms were before that.  

[jdenning]

With a tegretol level of 0.1 he's not taking it. Range is 3-12 and it takes more than a few missed doses to get to 0.1.

 

Let us know the outcome please. also curious about the CT

[fishbum]

Ok, so it looks like DTs is our answer. UDS was negative...someone managed to contact some family that reported a fairly recent hx of heavy alcohol use that the pt had abruptly stopped. It also appears that the tegretol was a recent change from keppra because of side effects.

 

Pt is still intubated and being treated with MVI-12, lytes are back to good (the K dropped further from the labs reported, but has been corrected).  

 

Again, thank you all for your thoughts....I'm learning a lot here. 

[winterallsummer]

Thanks for the case.  DTs - not surprising.  Wouldn't be surprised if his UDS also had something funny in it.  This is a resounding lesson in medicine time and time again: while there are many interesting diagnoses out there we all would love to make, 9 times out of 10, it is the most statistically likely and common-sense diagnosis that is the accurate one.  So in the absurd white male who is acting psychotic with significant volume depletion and ETOH of 0, ETOH withdrawal +/- polysubstance abuse "adds up" much better than seizures (which rarely present as psychosis), hyponatremia (which rarely presents as psychosis), and so forth.

 

3% - yes I am referring to 3% hypertonic saline.  When it comes to hyponatremia, the "bad thing" that can happen is that there is so much sodium inside the brain relative to what is outside, that leads to cerebral edema (or "brain swelling").  Do not think of severe or not severe hyponatremia - what matters most is how fast it dropped.  If it's 120 and the patient is asymptomatic, it is chronic and needs a gradual, non-emergent correction.  If it's 120 and the patient is seizing or has significant focal neurological deficit and is not stable, then carefully bolus 3% at 100 ml alliquots for 1-3 doses.  I think really the only time you will use this drug will be if you have a patient with sodium 120 or less, you walk in and they are seizing or having some major neurological problem, and you need to give them something to stabilize them.  Otherwise this drug is only given by nephrology in most hospitals.

[dmdpac]

I'm a little late to this party but it was a good case and good information to read through.  Thanks to all who contributed.

 

As an aside, and to follow up with what winterallsummer posted, as far as hyponatremia goes EM:RAP had an interesting board review short on it's podcast this month.  They were saying for a Na less than 120 with seizures, AMS or focal neuro deficit then 100mL 3% hypertonic saline in the first 10 minutes then 100mL 3% hypertonic saline over the next 50 minutes. 

 

There was also a short follow up about male urethral stretching which apparently is a thing in some circles.  I guess everybody has their own kink.