Metabolic alkalosis case

[Lidolover]

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69 year old F w/ no major PMH except for HTN, admitted with severe IVH owing to ruptured aneurysm. She failed interventional radiologic aneurysm repair and we met her in the operating room four days later for emergent craniectomy in the setting of rebleeding.

Prior to our caring for her, she received a fair amount of 3% NS and PlasmaLyte and was on Nicardipine gtt.
She was also non Pivot TFs.

In the OR, we took all measures recommended for increased ICP including hyperventilation. First ABG comes back 7.49/44/260/31.6 anion gap not recorded, Na 153 and Chloride 117 BE 6.1. Despite metabolic alkalosis, we continued to hyperventilate. Of note, renal function within normal limits. Mg and calcium within normal limits.

suggested to neurosurgery discontinuation of 3% NS but they wanted to continue.

Second ABG pH 7.52/39/170/32.1 BE 6.7, Na 153 and chloride 121. Anion gap 1.

of note, lactate always ranging between 1.1 and 1.4.

Albumin 2.9-4.2 the previous days.

from BE equation we concluded that pt had a large amount of unmeasured cations that probably accounted for her metabolic alkalosis but we are still baffled as of where these cations are coming from to have such a big impact.

she only got 1u pRBS during this time if anyone of you was thinking of citrate and that unit was given after the 1st ABG

any thoughts? I still believe I’m missing something given these numbers.

would u continue to hyperventilate or hypoventilate to neutralize the pH?

thnx

 

[GassYous]

What is a non pivot tf

Ventilation is irrelevant

You have 153 Na. What are you talking about unmeasured cations and who cares?

 

[Lidolover]

Sorry meant “on Pivot TFs” which I checked and does not have anything crazy in it.

even with Na 153, a base excess of 6.4 is not justified. And not all pts who have Na 153 are so alkalotic. In contrast, they have hyperchloremic metabolic acidosis.

 

[Radetzky]

What have her CO2s been historically? Has she received frusemide? Had she had large NG losses? Does she have hyperaldosteronism as a cause of by hypertension (pretty unlikely). The first three would be the most likely causes.

I would ventilate to try achieve a normal CO2 for this pt. I would not hyperventilate.

 

[chessknt]

Above post is spot on, would look for common explanations first (upper GI loss, diuretics, endocrine)

 

[Lidolover]

Nothing of the above. No diuretics, no GI losses. Hyperaldosteronism ... idk ... I would expect her K to be low but we have not checked levels. Her admission ABG was normal

 

[GassYous]

?

I'm sure she got mannitol and lasix. How do you have a na level but not a k? 7.49 isn't anything to write home about. But she's probably peeing from cerebral salt wasting. Also she has a contraction alkalosis. You're mentally masturbating over cations and I am not sure why.

 

[deleted162650]

You're mentally masturbating over cations and I am not sure why.

Because they’re sexier than anions.

 

[IlDestriero]

I see this all the time after mannitol head injury/brain tumor patients.

 

[Lidolover]

?

I'm sure she got mannitol and lasix. How do you have a na level but not a k? 7.49 isn't anything to write home about. But she's probably peeing from cerebral salt wasting. Also she has a contraction alkalosis. You're mentally masturbating over cations and I am not sure why.

i don’t blame you because I might have not expressed myself well or enough...but regardless...our goal in here is to level it up ... not down...so be careful pls with your wording

K was normal (I would expect it low if she had hyperaldosronism, but actually was normal) and we hadn’t checked aldosterone level (and actually is the only thing we couldn’t rule out at that time).

cerebral salt wasting has a totally opposite electrolyte profile. Her UOP is lower than I would expect with the hypertonic tx and mannitol she got.

 

[GassYous]

Yeah cause she has already been diuresed for days and she's getting 3% saline

 

[DrOwnage]

These numbers wouldn't give me cause for concern regarding her metabolic alkalosis where I would look into it too heavily and let it sway me from other things important to this patient. Sounds like an chronic ICU issue, not something that will be remedied in the OR acutely. Would be more concerned regulating her sodium and glucose levels for this case with an eye on volume status.

I had a case in residency where a patient with cystic fibrosis came down on BiPAP and their bicarbonate was 57... I **** you not. Their pCO2 was 150 (on the BiPAP) and the patient was talking to me. I've read articles where a pCO2 closely above that is equal to a MAC of anesthesia. Amazing what the body can do. What happened during the case was worse though, the perfusionist, not necessarily thinking, CORRECTED their bicarbonate while they were on bypass and normalized them to 26. I don't think I've seen the cardiac surgeon so angry before. She basically shifted the body's years worth of work in the course of 2 hours. Patient actually did fine though, surprisingly.

 

[vector2]

She's either got DI, has been receiving mannitol/lasix, or both.

 

[FiO2@21]

69 year old F w/ no major PMH except for HTN, admitted with severe IVH owing to ruptured aneurysm. She failed interventional radiologic aneurysm repair and we met her in the operating room four days later for emergent craniectomy in the setting of rebleeding.

Prior to our caring for her, she received a fair amount of 3% NS and PlasmaLyte and was on Nicardipine gtt.
She was also non Pivot TFs.

In the OR, we took all measures recommended for increased ICP including hyperventilation. First ABG comes back 7.49/44/260/31.6 anion gap not recorded, Na 153 and Chloride 117 BE 6.1. Despite metabolic alkalosis, we continued to hyperventilate. Of note, renal function within normal limits. Mg and calcium within normal limits.

suggested to neurosurgery discontinuation of 3% NS but they wanted to continue.

Second ABG pH 7.52/39/170/32.1 BE 6.7, Na 153 and chloride 121. Anion gap 1.

of note, lactate always ranging between 1.1 and 1.4.

Albumin 2.9-4.2 the previous days.

from BE equation we concluded that pt had a large amount of unmeasured cations that probably accounted for her metabolic alkalosis but we are still baffled as of where these cations are coming from to have such a big impact.

she only got 1u pRBS during this time if anyone of you was thinking of citrate and that unit was given after the 1st ABG

any thoughts? I still believe I’m missing something given these numbers.

would u continue to hyperventilate or hypoventilate to neutralize the pH?

thnx

Curious why you’d want to stop normal saline because of a metabolic alkalosis?

 

[coffeebythelake]

Curious why you’d want to stop normal saline because of a metabolic alkalosis?

Yeppppp

 

[anbuitachi]

what is a pivot tf?

edit: nvm just realized tf is tube feed. 🙂

 

[deleted697535]

She's either got DI, has been receiving mannitol/lasix, or both.

Yes, its basically this id say. Especially in a head injured patient without GI losses

CWS with Na=153? wow. id like to hear more about that

saline causes acidosis, so stopping hypertonic wont fix this. Driving her sodium higher probably wont help either so you could stop it but you should have regular serum and urine osmolality to guide therapy also

 

[leviathan]

I wouldn't be hyperventilating this patient unless they were actively herniating. Presumably they're in the OR and their skull is open sooo, don't hyperventilate them unless you want to fry off more neurons.

 

[Planktonmd]

Curious why you’d want to stop normal saline because of a metabolic alkalosis?

He said saline 3%, that's hypertonic saline not "normal saline". Hypertonic saline for several days explains the increase in plasma sodium and chloride and also causes a significant diuretic effect with other diuretics which explains the metabolic alkalosis. They need to stop the hypertonic saline. Very simple.

 

[GassYous]

Yes, its basically this id say. Especially in a head injured patient without GI losses

CWS with Na=153? wow. id like to hear more about that

saline causes acidosis, so stopping hypertonic wont fix this. Driving her sodium higher probably wont help either so you could stop it but you should have regular serum and urine osmolality to guide therapy also

I meant cws and di which can happen in the same patient. But when you're constantly infusing 3% saline that has 513 mmol/L of sodium...

 

[Lidolover]

Sorry for late response...basically I was so curious about these numbers that I went and checked all neurocrit pts admitted to the neuro crit unit that day. Guess what? 100% of pts with increased ICP who had hypertonic treatment had pretty much similar numbers. I think its contraction alkalosis but what triggered my interest is why hyperchloremic metabolic acidosis is not compensating this alkalosis at all. Idk the answer to that. DI and CSW are out of equation.