Di

[IveGotTwins]

CA2 here.

42 yo M with GBM and no other PMHx comes to day surgery for crani taking dexamethasone and keppra. He was dx 2 weeks ago after persistent headaches. He says in holding that he has to pee. Circulator says she can take care of that with a foley in the room. Over the course of the 4 hrs he has 4000mL of UOP. No mannitol, no diuretics of any kind. 1L of NS, 1L albumin from me. Serum lytes from ABG are all completely normal. Bicarbonate starts 28 and is 32 by end of case. Mild metabolic alkalemia. Completely hemodynamically stable throughout. Attending doesn't want to send urine lytes to further investigate since we won't likely follow up on it.

My purpose for posting was to see if anyone has had any similar experiences, have any thoughts on other possibilities pertaining to the cause/diagnosis/treatment and if anyone would have further worked up this patient even if the "follow-up" would be done by ICU team.

Thanks.

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[gasp]

Sounds like a straight forward case of DI after craini with tumor resection in a young otherwise healthy pt.. What were you getting for the base deficit? Only thing I would have done different is given DDAVP after the first liter of UO. I would not necessarily send urine lytes unless I was really interested for some reason. I've had cases like that and a little ddavp goes a long way or even 1-2U of Vasopressin (if the BP permits and there's no other contraindications).

I am curios as to why Mannitol was not given? Was that the surgeon's decision?

 

[IveGotTwins]

Though I've never seen a case of DI my understanding was that serum Na would be high, urine Na and SG would be low. Since we had none of those we did not treat with DDAVP. I still felt that it was DI and we would see the Na rise eventually. The bicarbonate and BE both rose slowly topping out at 32/+5 perhaps due to a contraction alkalosis. I wanted to do urine lytes to support my theory but my staff didn't want to. We held off on the mannitol to avoid further diuresis and they said they didn't need it for exposure. The patient actually had 4800cc of UOP but I subtracted 800cc from the OR total because I read that 500-800cc is the maximum capacity of the bladder. Since he said he had to pee in holding I figured I could make the adjustment.

I'm surprised that you are so sure it's DI without any additional info. Is it common (not uncommon) in otherwise healthy patients getting a crani? I always thought SIADH would be more likely if a neuro-hormonal problem were to occur. Perhaps it's because I'm still green.

 

[HollywdAnesth]

In my limited experience, the best way to manage electrolytes in a patient with DI is to let the patient do it themselves.
If the patient was hemodynamically stable and without mental status changes, then you can give him free access to water. The thirst mechanism should still work.

There is no reason to do urine lytes because it is just going to tell you what you already know, that the urine is very dilute.

 

[Idiopathic]

Though I've never seen a case of DI my understanding was that serum Na would be high, urine Na and SG would be low. Since we had none of those we did not treat with DDAVP. I still felt that it was DI and we would see the Na rise eventually. The bicarbonate and BE both rose slowly topping out at 32/+5 perhaps due to a contraction alkalosis. I wanted to do urine lytes to support my theory but my staff didn't want to. We held off on the mannitol to avoid further diuresis and they said they didn't need it for exposure. The patient actually had 4800cc of UOP but I subtracted 800cc from the OR total because I read that 500-800cc is the maximum capacity of the bladder. Since he said he had to pee in holding I figured I could make the adjustment.

I'm surprised that you are so sure it's DI without any additional info. Is it common (not uncommon) in otherwise healthy patients getting a crani? I always thought SIADH would be more likely if a neuro-hormonal problem were to occur. Perhaps it's because I'm still green.

Some cases in the literature of steroid therapy unmasking DI, i think in patients with sarcoidosis. You are right about needing the urine lytes to make a diagnosis, as you need to have large volume of inappropriately dilute urine (i.e. serum Na rising and urine still not concentrating).

As far as how common it is, its rare in the OR, Ive seen some cases associated with dexmedetomidine, and this is in the literature as well. Typically, you dont see it for hours after pituitary resection, which would be the most likely associated lesion. When we see DI in association with TBI or intracranial bleed/mass, it suggests to me a more severe injury, so i would not expect to see central DI associated with a typical crani. In, fact, I dont believe thats what this was either. Also, remember your nephrogenic causes (lithium most common, i know there are more)

i would treat volume loss as needed, would probably not be more aggressive unless lytes were seriously out of control or patient hypotensive