EtCO2 and hyperthermia

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Had a case, middle aged healthy guy getting an excision of some soft tissue benign tumor (forgot the name) on the chest. Guy had a thoracoromy, lymph node dissection, we placed a left double linen tube, had to go on OLV to aid expose for about 30 mins halfway through case. Placed an epidural and ran it for the case. Maitinance was volatile with some fentanyl. Anyway, even from the start of the case, I put the guy on the vent on two lungs, mild hypercarbia at the start of the case. Had hypercarbia during the case, increased MV a little, etCO2 up to 45 of so woth PaCO2 of 50. It did respond to increasing the minute ventilation, but I was ventilating this guy at 10 L/min or so. The guy was kind of large, maybe almost 6 feet. Halfway through the case his temp had climbed to 38.3, no Baer hugger on. No abnormalities otherwise on his ABG than a mild respiratory acidosis, no other signs of MH, curious if you guys have any idea why the hyperthermia?

The guy woke up fine, but was still febrile in te PACU, temp ended up coming down in a couple hours.
 
Are you sure it was benign tumor? Why lymph nodes?

Some malignant tumors can cause fever.
 
I've had similar cases before... Makes me wonder about some genetic mutation similar to "classic MH" but with variable penetrance/expressivity. Or could have been the epidural wasn't working, pain/light anesthesia, etc. Or the dude had excess dead space, in which case your alveolar ventilation would have been <10L/min. What was the ETCO2/PaCo2 gradient when you checked an ABG?
 
****, hopefully not light anesthesia, but totally could have been. Does this typically cause enough sympathetic stimulation tj cause a fever?

Tumor was benign, but there was a lot of it on the chest wall. He already had previous resection. Maybe from tumor lysis ? I geuss they irrigate with water instead of saline.

I was thinking maybe te left DLT was stuck in one lobe or something and I wasn’t ventilating a lobe. He did get a bit hypoxia in one lung with the right side down. Or maybe a mucous plug in a whole lobe?

In terms of etCO2-PaCO2 gradient, it was normal. Typically COPD patients have a low etCO2 as well, but are Hypercarbic on ABG, no??
 
So MH doesn’t always have to be a rapid temperature rise and a full blown episode. It can be subtle and present after a short procedure while the patient is in PACU. Also remember that historically many MH patients have had uneventful anesthetics in the past.
 
So MH doesn’t always have to be a rapid temperature rise and a full blown episode. It can be subtle and present after a short procedure while the patient is in PACU. Also remember that historically many MH patients have had uneventful anesthetics in the past.
Can you elaborate? I know many MH patients have had GA before without full blown MH. But how do you diagnose this? If you saw someone with an elevate etCO2 and developed a temp you just electively switch to a non triggering anesthetic?

I was under the jkpression that hypeecarbia that does not respond to an increased MV was suggestive of MH, but if it responds to increasing te MV then it’s not likely mh
 
I've had this happen with intraoperative thyrotoxicosis. Very high metabolic demand, hyperthemia. Was ventilating with ~12L and the ET was 50. Wouldn't be surprised if this guy maybe had an underlying thyroid issue.
 
I've had this happen with intraoperative thyrotoxicosis. Very high metabolic demand, hyperthemia. Was ventilating with ~12L and the ET was 50. Wouldn't be surprised if this guy maybe had an underlying thyroid issue.

Yeah I was just about to say it sounds like something metabolic that happened quickly. Thyroid vs sympathetic vs tumor as everyone is saying
 
This is classic differential diagnosis of hypermetabolism. 3 main culprits: MH, hyperthyroidism, pheo. Oral boards case.
 
While you can't exclude the big three FFP mentioned above, common things being common, this could simply be a big guy who needed a higher minute ventilation. He's healthy and don't underestimate the inflammatory and metabolic demand that major surgery can induce in the human body. I think it's underestimated, particularly in the post-operative period.
 
Patient had to history, otherwise healthy.

I did have drug reaction on the radar, but no changes in his respiratory mechanics, no skin or mucosal changes, no hypotension. I don’t know, can you have drug fever present that way intraoperatively?

Heart rate didn’t do anything the whole case, around 60 or so. So I didn’t suspect light anesthesia, and epidural seemed to be working with bonuses.
 
While there are a TON of things that can cause fever, hyperthermia of 38.3 in a 65 degree OR is quite unusual. Coupled with the increased MV and ETCO2, something did cook there.
 
i guess the question is when are you giving dantrolene? it's nice to have a ddx and everything but what made you not give dantrolene? in this case his ABG was pretty unremarkable but what if his lactate was 4? Could still happen in any of the hypermetabolic states
 
i guess the question is when are you giving dantrolene? it's nice to have a ddx and everything but what made you not give dantrolene? in this case his ABG was pretty unremarkable but what if his lactate was 4? Could still happen in any of the hypermetabolic states

I’m not entirely convinced that this was MH. From what I’ve heard and read over the years I think there are a few things that are more indicative of malignant hyperthermia that weren’t present in your case:

1. Tachycardia is supposed to be one of the first signs, so unless this patient was severely beta blocked he probably wouldn’t have a heart rate of 60.

2. Blood gas: I believe the classic finding is a mixed acidosis because you have both hypercarbia and a metabolic acidosis due to a hyper metabolic state.

3. I have heard that patients are completely rigid despite receiving heavy dose of muscle relaxation, which I’m assuming was the case for your thoracotomy.

To clarify, it was an open thoracotomy and not a thoracoscopy? Because in thoracoscopies have often noticed patients getting pretty hypercarbic despite aggressive hyperventilation, which I suspect is due to CO2 insufficient absorption.

For the trainees out there also remember that if you suspect MH to draw a CK level.

Interesting case, thanks for sharing.
 
Light anesthesia? (was he drenched in sweat when you undraped him?) plus the surgeon used CO2 to create a mild tension capnothorax to press the lung down and aid exposure?

How long into the case did his temperature climb? Temperature probes take a while to equilibrate, maybe he had a pre-existing fever. Although it would be odd that his temperature became normal within hours.

It is possible he had undiagnosed hyperthyroidism. Go track him down and palpate his neck
 
Light anesthesia? (was he drenched in sweat when you undraped him?) plus the surgeon used CO2 to create a mild tension capnothorax to press the lung down and aid exposure?

How long into the case did his temperature climb? Temperature probes take a while to equilibrate, maybe he had a pre-existing fever. Although it would be odd that his temperature became normal within hours.

It is possible he had undiagnosed hyperthyroidism. Go track him down and palpate his neck

He could be drenched in sweat from his fever as well
 
A few thoughts on the high MV.

10 L/min isn't absurdly high minute ventilation for a big adult. My understanding is that a hallmark of MH is a rise in CO2 that you are unable to keep up with by increasing MV, or at least struggle greatly to keep up with. A PaCO2 of 50 with a MV of 10 would not make me suspect MH. Beyond tachycardia and (late) temperature increase, another hallmark of MH is an audible whine from the surgical side of the drapes as the surgeon complains about lack of muscle relaxation ... i.e. there are other early physical signs.

With OLV, we use smaller tidal volumes. This means that the percentage of each TV that is dead space is higher. A minute volume of 10L with 550 mL tidal volumes includes a lot less dead space (and therefore more alveolar ventilation) than a MV of 10L with 300 mL tidal volumes. The rise of CO2 with reduced alveolar ventilation is mitigated by its solubility, but it does rise. A panting dog has high MV but doesn't get hypocarbic; OLV with higher rates and lower volumes is essentially a panting patient.

Dead space also increases simply with the use of a DLT because of the extra apparatus volume distal to the Y. It's not huge, but it's not negligible, and it's compounded by higher ventilatory rates, as are common with OLV.

In short I am completely unsurprised that you had a CO2 of 50 despite a MV of 10 L/min during OLV with a DLT. I'm not sure I'd have even consciously noticed this during a case with OLV.


The temp increase is interesting, I don't have any ideas to add there beyond the differentials above.
 
Had a case ten years ago or so just like this.

Young healthy guy for scope type of urology surgery.

Twenty minutes into the case, steady HR increase from 60 to 108, end-tidal CO2 rise to 55-60, and steady temp increase to 38.8. Hyperventilating didn’t help. Stopped the volatile, deepened anesthesia with propofol, nothing stopped the rise of all perameters. A-line inserted, high CO2, but completely normal pH.

Things still crawling up. Gave first round of Dantrolene... 5-7 minutes later, everything returns to near normal.

To ICU overnight. Happened again up there, they infused more Dantrolene, cured it. Patient dismissed the next day.

Our in-house seriously expert (MHAUS quality) person, didn’t think it was MH because of no metabolic acidosis.

I am not smart enough to argue, but if it wasn’t MH, for me, it will do until the real thing comes along.
 
A few thoughts on the high MV.

10 L/min isn't absurdly high minute ventilation for a big adult. My understanding is that a hallmark of MH is a rise in CO2 that you are unable to keep up with by increasing MV, or at least struggle greatly to keep up with. A PaCO2 of 50 with a MV of 10 would not make me suspect MH. Beyond tachycardia and (late) temperature increase, another hallmark of MH is an audible whine from the surgical side of the drapes as the surgeon complains about lack of muscle relaxation ... i.e. there are other early physical signs.

With OLV, we use smaller tidal volumes. This means that the percentage of each TV that is dead space is higher. A minute volume of 10L with 550 mL tidal volumes includes a lot less dead space (and therefore more alveolar ventilation) than a MV of 10L with 300 mL tidal volumes. The rise of CO2 with reduced alveolar ventilation is mitigated by its solubility, but it does rise. A panting dog has high MV but doesn't get hypocarbic; OLV with higher rates and lower volumes is essentially a panting patient.

Dead space also increases simply with the use of a DLT because of the extra apparatus volume distal to the Y. It's not huge, but it's not negligible, and it's compounded by higher ventilatory rates, as are common with OLV.

In short I am completely unsurprised that you had a CO2 of 50 despite a MV of 10 L/min during OLV with a DLT. I'm not sure I'd have even consciously noticed this during a case with OLV.


The temp increase is interesting, I don't have any ideas to add there beyond the differentials above.

Yea though he mentioned etco2 of 45 and paco2 of 50 so dead space isn't that large with his olv
 
Some dudes just run hot. Like those guys wearing shorts when it's 20 below. And you wouldn't have this problem if you do what I do and don't check temperature.
 
Some dudes just run hot. Like those guys wearing shorts when it's 20 below. And you wouldn't have this problem if you do what I do and don't check temperature.

LAW #10: IF YOU DON'T TAKE A TEMPERATURE, YOU CAN'T FIND A FEVER
 
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