More clinical case talk.

[Noyac]

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Middle aged man for laparoscopic inguinal hernia repair. He is otherwise healthy and has never had general anesthesia.
Induced with prop/roc/Fent. Easy airway. Case starts and CO2 begins to rise.
BP increases precipitously from 110/60 to 180/95 then 195/100.
No rigors
Temp is 36.2

Fentanyl given and respiratory rate increased without successful resolution of elevated ETCO2. CO2 continues to rise. Case is proceeding without complication.

What next?
What is going on here?

This one should be easy but we will see.

 

[Noyac]

BTW, all you smart old guys/gals, give the youngsters a chance here to respond.

 

[PianoMedic]

First year med student so may be completely off on this, but my initial thought is probably due to the inflation for the laparoscopic procedure. End tidal CO2 increase due to the increased pressure on the lungs through the diaphragm. Might have to increase the tidal volumes in addition to the increase in respiratory rate as long as your airway pressure isn't too high.

The blood pressure has me a little more confused. Is it due to a compression of the Inferior Vena Cava causing a backup all the way to the heart and increasing your core and upper limb arterial pressures? Not sure of the best treatment (relieving a little of the pressure in the abdomen maybe?). Again this could all be wrong.

 

[axeon123]

insufflation pressure too high, could lead to systemic reactive response resulting in elevated blood pressures? and elevated insufflation pressures can lead to subcutaneous emphysema, suggested by rising etco2 that is not improved with increased minute ventilation. hypercarbia itself can cause a hypertensive response, too.

 

[ambiturner]

I agree that it's more likely to be related to the laparoscopy, especially if the increase in CO2 directly correlates with with insufflation, but you have to seriously consider MH too...what is the HR? The case should be quick and so you ideally the appendix will be out in 5 min and you can desufflate but in a long case it might be worth asking for a quick desufflation to see if things get better.

 

[Noyac]

its a hernia case not an appy.
HR was 100

 

[Noyac]

Remember this. Lap IHR is not performed intraabdominally. It is an extra peritoneal procedure.

 

[BuzzPhreed]

Prop, sux, tube.

 

[geogil]

Hypercarbia can lead to the hypertension we see here and is either due to overproduction or underexcretion (hypoventilation). This is the general aproach I would take (recognizing that Noy covered some of this already)
Beginning with pt: underexcretion:

-Is tube in the right hole? do we see consistent ETCO2 tracing? Chest rise?
-Are the expiratory and inspiratory valves working properly? Are we getting rebreathing because of a stuck valve?
-What does the CO2 absorbent look like?
-Ensure that the ventilator is delivering the Vt that you think, bag the patient and see if there is any change in ETCO2
-
Overproduction:
Unlikely MH given nl temp, although the temp can be the last thing to rise.
(other even less likely causes of hypermetabolic state like thyroid storm, salicylate toxicity- unlikely unless Noy is holding out on us.)
-CO2 embolism, although as Noy pointed out, we are extraperitoneal and the type of insufflation used differs slightly from insufflating the abdomen with liters and liters of CO2.

 

[sevoflurane]

What does a CO2 embolism do to EtCO2 again?

Can you get a CO2 embolism with a laporascopic IHR?

Hmm...

 

[geogil]

What does a CO2 embolism do to EtCO2 again?

Can you get a CO2 embolism with a laporascopic IHR?

Hmm...

Thanks, it's been a long day and obviously not thinking things through clearly. IHR does not involve insufflation to expand the tissues in the same way that intrabdominal operations do, but rather local tissue expansion with an inflatable expander

 

[Noyac]

Hypercarbia can lead to the hypertension we see here and is either due to overproduction or underexcretion (hypoventilation). This is the general aproach I would take (recognizing that Noy covered some of this already)
Beginning with pt: underexcretion:

-Is tube in the right hole? do we see consistent ETCO2 tracing? Chest rise?
-Are the expiratory and inspiratory valves working properly? Are we getting rebreathing because of a stuck valve?
-What does the CO2 absorbent look like?
-Ensure that the ventilator is delivering the Vt that you think, bag the patient and see if there is any change in ETCO2
-
Overproduction:
Unlikely MH given nl temp, although the temp can be the last thing to rise.
(other even less likely causes of hypermetabolic state like thyroid storm, salicylate toxicity- unlikely unless Noy is holding out on us.)
-CO2 embolism, although as Noy pointed out, we are extraperitoneal and the type of insufflation used differs slightly from insufflating the abdomen with liters and liters of CO2.

Very good geogil. A systematic approach the the problem. And a good one at that.
So to address the ventilation part of your question.
-tube is in the right hole
-tracing is as expected
-absorbent is darkish but not exhausted.
-valves in good working order
-do know what bagging would have shown, wasn't attempted.

Overproduction
-temp, as you noted, takes a little while to increase. Having had an MH case before, the temp did start to rise in my past CSE so I turned off the hair hugger not knowing what was the cause yet and this seemed to slow the rise enough to make the picture quite confusing.
-CO2 embolism. Well let's discuss this a bit more. What would someone expect to see with a CO2 embolism?

I think everyone has had an opportunity to respond so all you smart "old" guys and gals are free to comment.

 

[deleted171991]

CO2 embolism is CO2 + embolism. 😀

Would expect EtCO2 to rise initially with insufflation and absorption (the CO2 part) until... it falls (the embolism part) together with the cardiac output, BP etc. That's the time to get supportive and pray:
- stop insufflation
- switch to 100% O2 (nitrous loves difusing into CO2 bubbles, too)
- increase ventilation
- give fluids to increase venous pressure and decrease further gas entry
- give pressors/inotropic agents to maintain CO
- CPB

 

[risnwb]

Co2 embolism should theoretically cause an initial increase in End tidal co2 due to increased dissolved co2 in blood. However depending on the actual volume of emboli a rapid cardiovascular collapse would result in a low cardiac output state and therefore a low end tidal. I guess it's also possible that if enough was lodged in the pulmonary vasculature but cardiac output was relatively maintained, you could see an increase in end tidal co2 due to increased dead space ventilation...

 

[sevoflurane]

CO2 embolism is CO2 + embolism. This is where my knowledge ends. 😀

Would expect EtCO2 to rise initially with insufflation and absorption (the CO2 part) until... it falls (the embolism part) together with the cardiac output, BP etc. That's the time to get supportive and pray:
- stop insufflation
- switch to 100% O2 (nitrous loves difusing into CO2 bubbles, too)
- increase ventilation
- give fluids to increase venous pressure and decrease further gas entry
- give pressors/inotropic agents to maintain CO
- CPB

Of course one might get lucky and the patient might end up just with some elevated end-tidal that needs hyperventilation.

+

Immediate TEE to diagnose the culprit... + left lateral and CVL to suck out what you can....

Is this what's going on here...?

 

[deleted171991]

I doubt this case was CO2 embolism. I would expect that to happen within seconds after initial insufflation.

I would bet more on relative hypoventilation of the patient (relative to the CO2 production and absorption) with secondary sympathetic stimulation. MH if signs of increasing temperature (2-3 degrees in 10 minutes) or rigidity. MH is a zebra.

Increasing just the RR might not be enough. If the volumes are low, it might be just a lot of dead space ventilation. Also, once the insufflation starts, it's pretty difficult to decrease the CO2 in some patients; one can just hope to be able to keep up with the ventilation. That's why I always target my end-tidal to 30-ish before insufflation.

And of course, let's not forget the main cause of sympathetic stimulation after induction: the patient is light. Of course that does not explain the CO2 part.

 

[sevoflurane]

Thanks, it's been a long day and obviously not thinking things through clearly. IHR does not involve insufflation to expand the tissues in the same way that intrabdominal operations do, but rather local tissue expansion with an inflatable expander

No worries geogil. Great response man! I have not seen the inflatable expander, we still do these laporascopic with CO2.

 

[twoliter]

I doubt this case was CO2 embolism. I would expect that to happen within seconds after initial insufflation.

I would bet more on relative hypoventilation of the patient (relative to the CO2 production and absorption) with secondary sympathetic stimulation. MH if signs of increasing temperature (2-3 degrees in 10 minutes) or rigidity. MH is a zebra.

Increasing just the RR might not be enough. If the volumes are low, it might be just a lot of dead space ventilation. Also, once the insufflation starts, it's pretty difficult to decrease the CO2 in some patients; one can just hope to be able to keep up with the ventilation. That's why I always target my end-tidal to 30-ish before insufflation.

And of course, let's not forget the main cause of sympathetic stimulation after induction: the patient is light. Of course that does not explain the CO2 part.

This. I think CO2 embolism was just being discussed as a side note since the case involved some CO2 insufflation, but an embolism would result in the opposite of what's going on here, i.e, significant HTN and a steadily increasing etCO2 (assuming we're talking about an embolus large enough to have any significant effect).
My thought is CO2 buildup from insufflation + not enough minute ventilation + light anesthesia.

 

[Noyac]

Ok, we are off and running here.
Minute ventilation was increased from 6000 to 15,000. ETCO2 continued to rise 70, 80, 90's.
Losing ground rather rapidly. Still hypertensive.

 

[deleted171991]

Wow! This is the point I would be definitely thinking about MH at (but again, not very likely, especially in the absence of both hyperthermia and rigidity). The thyroid storm doesn't sound bad either, but it's a zebra, too.

I would also involve the surgeon, see if stopping the CO2 insufflation changes anything. That's where my bet is.

The other alternative would be this huge dead space ventilation for some reason, so obviously tube position, listening to chest etc. are important.

 

[chmd]

How quickly would urine turn color from myoglobinuria? Quicker than an abg can be drawn and resulted at a surg center? Would have surgeon stop and get dantrolene ready.

 

[OB1🤙]

While doing the obligatory workup for MH, I turn to my anesthesia tech and say "I wonder if this frigging guy has a pheo..."

 

[Noyac]

Just to move this along, ventilation is not an issue. Tube is properly placed and both lungs being ventilated at full capacity. But definitely an issue that would need corrected if not already verified.

Dont really know how soon urine color changes. In my confirmed case of MH it was dark in the PACU 5 hrs after induction. But this case was not typical for many reasons. Anyway, the urine color won't help here because we don't have a foley.

 

[deleted171991]

So, Noyac, what happened when you asked the surgeon to turn off the insufflation?

 

[Ignatius J]

Ok, we are off and running here.
Minute ventilation was increased from 6000 to 15,000. ETCO2 continued to rise 70, 80, 90's.
Losing ground rather rapidly. Still hypertensive.

What is the patient's temperature?

CO2 refractory to increasing minute ventilation makes me think malignant hyperthermia. I would check clinically for signs: temperature, muscle rigidity, etc. If any doubt, send labs and get ready to hunker down.

 

[Noyac]

Very good.

Temp is up .2 degrees to 36.4
Labs sent:
ABG- 7.12/92/245/-3/25/99% (this is from discussion with partner who's case this actually was)

Surgery cancelled.

 

[Noyac]

While doing the obligatory workup for MH, I turn to my anesthesia tech and say "I wonder if this frigging guy has a pheo..."

why?

 

[OB1🤙]

Why the increasing CO2, if pheo?

So, Noyac, what happened when you asked the surgeon to turn off the insufflation?

I mean it's an albino zebra, but an acutely, severely increased metabolic rate from an epi- secreting pheo could theoretically do this.

These folks usually have headaches and symptoms, but they sometimes don't seek treatment for them.

Anyway, I don't think it's likely to be a pheo, but it's on my differential, alongside other zebra cousins like thyroid storm. People usually know about thyroid issues preop though, but a pheo could slip by undetected in an otherwise healthy person.

MH is still the most sinister possibility here, of course, and needs to be front and center of diagnostic efforts while in the heat of the moment.

If the case involves CO2 insufflation of any kind, that is the most likely contributor. I admit I don't do laparoscopic hernias so I'm not familiar with the equipment and technique. Maybe this "inflatable expander" is leaking, I dunno.

If I'm in this case and things progress down this path, I think it's important to call for help if a colleague is around. You get another head to ponder things, another set of eyes to see what you may not have seen, and another pair of hands to do stuff with.

In addition to the ABG, I want to get a VBG to look at consumption, and I would have a surface echo on this heart to see what I could see.

This ABG is somewhat reassuring in that it seems to be a pure respiratory acidosis (if acute, which it should be). MH you'd have a metabolic component in there for sure.

 

[Noyac]

Very very good HB. RESPIRATORY ACIDOSIS

Now we are onto something significant.

Insufflation discontinued and ETCO2 began to decrease. Hypertension resolving.

What was the problem?

Why didn't it cause total CV collapse?

 

[B-Bone]

Very very good HB. RESPIRATORY ACIDOSIS

Now we are onto something significant.

Insufflation discontinued and ETCO2 began to decrease. Hypertension resolving.

What was the problem?

Why didn't it cause total CV collapse?

Misplaced insufflator causing tissue dissection and massive dissolution
of CO2 via large surface area exposure? I've seen this one before. Doesn't cause CV collapse because there's no embolus to obstruct flow (which would also cause decreased ETCO2 rather than increased CO2).

 

[narcotics999]

Had a similar scenario in residency. 40ish female, a bit fatty, otherwise healthy for Lap TAH/BSO. EtCO2 increased from 30s to 80s with VT 500ml/f 25-30. No tube or machine problems. Temp 36C, mild tachycardia and hypertension. Attending was a CT guy and cool about it. Surgery finished, CO2 down, no complications.

 

[Noyac]

Ok, I'm gonna call you two out B-Bone and narcotics999. Where were you two for the last 29 posts? Hanging in the wings ready to swoop down?

Yes, this is CO2 entrainment from the insufflation of CO2. The reason it didn't cause CV collapse is just as B-bone described. Unlike the case Sevo saw not long ago where massive CO2 embolism occurred.
Here's the difference, in Sevo's case a veris (?) needle was inserted into the liver. You ain't gonna save that one without CPB instantaneously. Right Sevo?
In this case it isn't a massive infusion of CO2 but rather entrainment of CO2 into the venous system maybe through a venous tear. I've also seen this during endovascular saphenous vein harvest for CABG.

So,what distinguished this case from MH? Many may say the lack of temp rise or the slow rise. But the key was a resp acidosis on ABG. In the heat of the moment however, I would suspect you would tell the surgeon to stop. So this would also clue you in but not eliminate the possibility of MH. Therefore, send gases if you at not certain.

Next question, where to go from here?

 

[20x20]

Med Student here. We had a similar situation at the beginning of a robotic TAH/BSO I observed. We didn't do any additional work-up, since the cause of the hypercarbia and HTN was clear when it quickly resolved with increased ventilation and halting insufflation We turned off the insufflation for few min and optimized the patient by hyperventilating to correct the resp acidosis. Then, we removed and reinserted the insufflator to correct for any positioning errors. (Surgeon thought it was due to poor seal of insufflator at insertion site causing subcutaneous emphysema.) Attempted to continue case with high minute ventilation, which went well for ~10min. Then, CO2 became unmanageable again (>70 or 80), so surgeon switched to open to complete the case without any complication. No need to cancel the case.

 

[pgg]

I've also seen this during endovascular saphenous vein harvest for CABG.

This exact thing happened to me when I was a resident. Typical CABG up until the CO2 rose. Before long minute ventilation was over 15L/min and CO2 was still climbing through 50 then 60.

MH was of course on the differential but with the vein half harvested and the LIMA down already canceling and going down the MH algorithm was a big decision. Proceeding onto bypass in the midst of a MH crisis would be inadvisable too ...

 

[sevoflurane]

Great case Noy.

I think I remember telling you about the VATS I did a couple years back. Same type of scenario, but a little different plumbing. Decortication case that ended up with a broncho-pleural fistula developing intraop. ETCO2 was 80-90's and I couldn't get it down... then the culprit finally clicked something in my head.

The Veress needle in the liver always drops your ETCO2 to around 6-8mmhg.

 

[Noyac]

The Veress needle in the liver always drops your ETCO2 to around 6-8mmhg.

And it also drops the BP to that number as well.

 

[Noyac]

20x20, good call there. No need to cancel the case. Just proceed with open repair.

 

[Mman]

Here's the difference, in Sevo's case a veris (?) needle was inserted into the liver. You ain't gonna save that one without CPB instantaneously. Right Sevo?

Theoretically. But I'm not so sure. CO2 is awful soluble. I'd bet slamming in IV fluid and CPR might be able to get enough of it to dissolve so as to allow resumption of normal cardiac function.

 

[Noyac]

Theoretically. But I'm not so sure. CO2 is awful soluble. I'd bet slamming in IV fluid and CPR might be able to get enough of it to dissolve so as to allow resumption of normal cardiac function.

Nope. Too much air given. Doesn't matte if it's CO2, or whatever.

 

[20x20]

Had a similar scenario in residency. 40ish female, a bit fatty, otherwise healthy for Lap TAH/BSO. EtCO2 increased from 30s to 80s with VT 500ml/f 25-30. No tube or machine problems. Temp 36C, mild tachycardia and hypertension. Attending was a CT guy and cool about it. Surgery finished, CO2 down, no complications.

How long can you do the case with EtCO2 at 80? Do you have to additional things to manage the resp acidosis during the case?

 

[Noyac]

CO2 won't hurt the pt. Think about your ICU rotation. Remember permissive hypercapnea?

 

[pgg]

How long can you do the case with EtCO2 at 80? Do you have to additional things to manage the resp acidosis during the case?

In general (if you don't have a specific reason to avoid hypercapnia) a pure respiratory acidosis is very very well tolerated, even with etCO2 of 80. Nothing special really needs to be done. Just get them back to normal by wakeup and they'll be fine. I see it oftenish in spontaneously ventilating patients with LMAs whose providers are for some reason loathe to just turn on the vent. Maybe it's poor style but they do fine.

 

[20x20]

CO2 won't hurt the pt. Think about your ICU rotation. Remember permissive hypercapnea?

In general (if you don't have a specific reason to avoid hypercapnia) a pure respiratory acidosis is very very well tolerated, even with etCO2 of 80. Nothing special really needs to be done. Just get them back to normal by wakeup and they'll be fine. I see it oftenish in spontaneously ventilating patients with LMAs whose providers are for some reason loathe to just turn on the vent. Maybe it's poor style but they do fine.

Oh yea, permissive hypercapnea! I guess I was focusing too much on the side effects of hypercapnea, but I forgot the physical manifestations won't really show up in general anesthesia (except for HTN, right?).

Thanks for the replies Noyac and pgg.

 

[Mman]

Nope. Too much air given. Doesn't matte if it's CO2, or whatever.

See, I'm not sure if I believe that. With a RIJ catheter I can shove as much fluid as I want into the RA and RV and I'm betting with some CPR I can probably get it too move forward a bit or at least long enough until a great deal of the CO2 is absorbed.

I mean you can say it doesn't matter, but I doubt there is any evidence to support that. The problem for most situations like that is people die because nobody realizes what happened quickly enough.

 

[deleted171991]

The difference between CO2 and air is probably the diffusion quotient. CO2 would be probably absorbed more rapidly (although I don't know if the difference is clinically significant), and we probably see shock much more rarely than these embolisms happen. Other gases, such as air, are absorbed slower, and that's one of the reasons we use CO2 in laparoscopy. N2O would be even faster than CO2, but it's flammable (like air).

I have never seen shock 2/2 gas embolism situation, but I would also bet on the CPR to move the gas forward, into the alveolar vessels, as the main chance of survival for the patient (unless I have a central line already in place).

 

[sevoflurane]

Solubility of CO2 has nothing to do with the initial clinical presentation. When these things happen, they happen fast. The ability to successfully get someone out of the woods is dependent on quick recognition and implementation of appropriate therapy... and most importantly the AMOUNT of CO2 that makes it to the heart. If you happen to get into one of the hepatic veins, your are injecting 100% of your insufflation CO2 into the right heart, causing immediate R and L heart failure.

I've seen exactly 2 of these cases. Both ended up on bypass, but both were MASSIVE embolisms.

I concur that if the embolism is small to moderate, quick CPR in the trendelenburg position, CVL placement with aspiration and fluid loading + appropriate pressors might get you through in the young patient. Soluability, may play a minor role here. Keep in mind, however, whatever you "push" through will end up on the left side of the heart, down the coronaries and out to the rest of the body.

Both of my cases had CO2 on the right AND left side of the heart.

I wouldn't delay calling my CT surgeon either way. The last time we did a sternotomy and cardiotomy for this event, the amount of CO2 that rushed out of the anoxic heart was impressive to see and hear. The heart pinked up and recovered quickly thereafter. The patient didn't have a chance if we continued CPR for god knows how long.

Unfortunately, one of my CO2 embolisms had a PFO. This caused coronary and systemic "soluble" CO2 emboli. Despite CO2 being more soluble, the patient took hits everywhere (gut, kidneys, head, etc). This was not due to global hypoperfusion, rather from specific CO2 emboli. So don't think just because it's soluble, the patient is going to do fine.

Again, it depends on the amount of embolus. Solubility plays a role when you are dealing with smaller CO2 embolisms. During a massive embolism, you better have your CT surgeon on speed dial. Minutes count in the later.

 

[Mman]

So don't think just because it's soluble, the patient is going to do fine.

I would never suggest that because it's CO2 they will do fine. I'm just saying that I'm not certain that in the absence of immediate CPB it's a death sentence. I'm betting there is a chance you could have a patient survive with immediate pushing of large fluid volumes and CPR.

 

[Noyac]

With all due respect, I totally disagree. Of every case that I have seen or heard of, none of them did well. 100% kill rate. Worse than Ebola even. I saw an orthopedic surgeon knock off a young healthy pt during shoulder scope with this technique. CVL placed lickty split. Pulled air out in large quantities. Guy still died. Thank god it wasn't my case.

They may survive a short while but not long. The outcome is drastic.

 

[sevoflurane]

I would never suggest that because it's CO2 they will do fine.

Wasn't referring to you Mman. Just a general statement.

 

[Mman]

With all due respect, I totally disagree. Of every case that I have seen or heard of, none of them did well. 100% kill rate. Worse than Ebola even. I saw an orthopedic surgeon knock off a young healthy pt during shoulder scope with this technique. CVL placed lickty split. Pulled air out in large quantities. Guy still died. Thank god it wasn't my case.

They may survive a short while but not long. The outcome is drastic.

But how many cases is that? 3? 6? For something that had a 10% survival rate, you'd need to have taken care of something like 20 or 30 to even begin to get a feel for that sort of possibility. It's so rare that I don't think any of us have any anecdotal evidence of what the actual survival would be. And if you took care of somebody that survived it, you probably wouldn't think they had gotten much air in, but you probably would have no way of proving that they didn't, merely that they survived so you didn't think it was much.


My point is that the event is so rare and there are no studies on it that all we have is educated guesses.