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Help with a physiology-clinical scenario question

epidural man

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First off - This was NOT my case.

I came on to relieve the call team and they were finishing up the case that I am about to describe - so the fine details are lacking.

As I understand it.....

a 19 y/o ruptured appendix some days before, IR drain not working...patient getting sicker and sicker...decision to OR for laparoscopic appy.

Patient has been tacchycardic, but good urine output and no hypotension. Induction is smooth with no hemodynamic compromise (so i am told...i'm not sure if the kid dipped at all or not)

Anyway, after insuflation, the patient immediately became hypoxic (in the 50s), CO2 dropped significantly (Attending said "hardly any wave form at all). Pulse was present and patient maintained BP but remained tacchydardic.

Patient remained easy to ventilate by hand, checking the tube with bronchoscope showed correct tube placement. Breath sounds were well heard bilaterally.

As a side note, I asked the surgeon about the case, he said when he put the trochar in, pus came out rather forcefully, and there was lots of puss everywhere. They ended up leaving the belly open because he said he couldn't close it (the why - not sure if it was tight, or because of the puss). They didn't do the appendectomy because anatomy was difficult.

Anesthesia immediately let surgery know of the troubles, and they stopped insuflation and opened the belly. According to the anesthesia team, it seemed that everything improved once they started opening the belly.

Okay - so what happened?

First thought for me is of course a significant decrease in CO (from the preload reduction) which decreased the CO2 waveform. But if this is the case, why would BP persist as high as it did, and why would he get so hypoxic (in the 50s)? Maybe he had the starting of abdominal compartment syndrome, and the insuflation was the last straw.

Second thought would be a CO2 embolism - which I have never seen so I don't fully appreciate what to expect with that - but wouldn't that cause your CO2 to INCREASE? Also, patient wouldn't immediately become hypoxic (except maybe with a complete shut down of CO).

What else could cause this scenario?
 
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nimbus

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What a weird case. Why didn’t they do an appy when he first presented?

I think CO2 embolus, like any right sided embolus, could initially cause RVOTO with decreased ETCO2 and hypoxemia. But if it’s that severe I would also expect hypotension. As you remarked, inadequate preload and RV filling would have a similar effect. The absence of hypotension doesn’t fit the picture. Is there EMR you can review? Was a lot of vasopressor or inotrope given?
 
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vector2

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What a weird case. Why didn’t they do an appy when he first presented?

I think CO2 embolus, like any right sided embolus, could initially cause RVOTO with decreased ETCO2 and hypoxemia. But if it’s that severe I would also expect hypotension. As you remarked, inadequate preload and RV filling would have a similar effect. The absence of hypotension doesn’t fit the picture. Is there EMR you can review? Was a lot of vasopressor or inotrope given?

Yeah, really need the EMR, vitals, meds, timeline, and the op note...

Actually, after describing this, I thought...that doesn't make much sense....let me go check.

I went and looked at the record. The patient DID become hypotensive, and they did give some EPI which he robustly responded.

Sounds like embolus (maybe Veress needle found its way somewhere bad due to hostile abdomen + pus) and contractility bump from epi pushed the bubble through. Although....massive preload drop post-insufflation from being septic +- hypovolemic is certainly not ruled out.
 
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DocMcCoy

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Unfortunately, now it’s really hard to trust anything you got in sign out considering they left out the whole “oh ya we had to push some epi”. Differential is wide open and all common causes possible. Stuff happens but that was a pretty important detail.

As for a hopefully uncommon iatrogenic cause, I’ve seen a similar situation created when someone forgot to adjust PCV with steep T burg and insufflation. Ventilated dead space for a couple minutes and wasn’t recognized till the sats were dropping.
 
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narcotics999

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Vagal response + preload reduction? Any transient HR drop before epi kicked in? Usually I will not use epi if only BP drops and this pt was tachy at baseline.

Cant understand why an app was not done in the first place.
 
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JiPo

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I would think that 2 differentials would be at the top.

1. severe atelectasis from FRC dropping below CC after insufflation, and they are ventilating mostly the deadspace at this point until alveoli are recruited back.

Was this patient obese? T-berg position doesnt help. Possibly a component of abd compartment syndrome which could push on diaphragm to increase intrathoracic pressure further, and insufflation took it over the edge. This would cause hypoxia, likely decrease in BP due to decrease in preload. I would think that it has to be insufflation related because it happened so soon after insufflation and disappeared after desufflation.

2. CO2 embolism. If it is a small embolism, ETCO2 would go up, but if it is massive, ETCO2 would drop, and you would see BP drop and etco2 drop immediately. This would have to be a huge embolism though, like the veress needle would be against an injured/open vessel for this to happen so soon after insufflation. With difficulty inserting the trocar and with difficult anatomy, this definitely is a possibility.

if hypoxia and hypotension resolved without epi, i would say it was prob #1, but epi muddles the water and it is hard to say. It couldve been either one. If it truly happened “immediately” after insufflation, #2 would be more likely.
 
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We actually had a sim lab for almost this exact scenario.

I was the unfortunate victim “doing” the case and at the time didn’t really pay attention to the timing of the insufflation and the CV/pulm collapse

Same thing, during the actual case they were able to bag okay, good volumes despite minimal ETCO2 tracing, clear lungs. Pressures were low but responsive to aggressive pressor use. The surgeon was able to finish and close but they kept the patient intubated.

Imaging showed diffuse b/l opacities and the (pulm) ICU attending initially labeled it ARDS from aspiration during the intubation. But you can see that pattern with nonthrombotic embolisms as well. And that really doesn’t fit the timeline of events. She apparently dramatically recovered POD 1 and was extubated, did well.

The one thing that stopped them from tying this up into a neat little bow however was that they threw in a TEE during the case and didn’t see any obvious bubble or PE.


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Beeftenderloin

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Unfortunately I’ve been in 2 of these cases. Thankfully the patient lived in both. We were fortunate to get a TEE probe in fast in both cases and saw LARGE bubbles in the pulmonary arteries and actually in the hepatic veins as well in 1 of them.

The case you describe is a CO2 embolus, plain as day. They insufflate, ETCO2 drops precipitously, you hear that gut wrenching brown noise from the pulse ox as the patient desats, then becomes hypotensive. As was previously stated big CO2 bubble causes RVOT obstruction with massive dead space ventilation and hemodynamic collapse.

Tell the surgeon to stop insufflation > call for help > position head down, left side down (so hopefully the bubble migrates away from lungs and brain if there is an undiagnosed PFO) > vapor off, 100% O2 > epi epi epi. Putting in a CVC and trying to aspirate bubbles is described in the literature but never really works.

If you can keep the patient alive for the 10-20 minutes it takes to absorb the CO2 without being profoundly hypoxic or hypotensive for that period of time they typically do okay. Both times we cancelled the case and took the patient to ICU tubed and on an epi gtt. Both times the epi was off after about an hour and patient extubated a few hours later.

I’ll never forget these cases. These can be clean kills (patients that walk in healthy and leave in a bag) if you aren’t paying close attention around insufflation.

Granted, both of mine were in elective cases. If the patient is starting to look better and this is an emergency case for source control I could see how many would press on.
 
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Planktonmd

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What threw you off here is that you are dealing with a healthy 19 Y/O who is capable of maintaining hemodyamics despite being severely septic and likely under-resuscitated. So, he was basically on the edge with maximum compensation by increasing cardiac output, then we gave him anesthesia and abruptly decreased preload by increasing the intra-abdominal pressure, so he had a sudden drop of cardiac output, but was still amazingly able to maintain some blood pressure, likely thanks to the Epinephrine given earlier, despite all our attempts to kill him.
Had this been your usual older patient with other comorbidities, he would have presented to the OR hypotensive with typical septic shock symptoms and he would have crashed on induction.
The CO2 embolus theory is less likely because if the volume of CO2 was large enough to cause a drop of CO to a point of almost no CO2 wave, he would not have recovered so quickly after stopping the insuflation, and also you would expect increase of ETCO2 when the gas starts getting eliminated after the initial drop of CO.
 
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chocomorsel

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I am gonna go with the scenario that it is BOTH a CO2 embolus as well as increased abd pressures causing the drop in O2 and BP.
Patient was borderline but not quite hypotension due to sepsis and decompensated due to young age. Then you decrease the Preload by increasing abdominal pressures and he decompensates and BP drops. At the same time, CO2 has found its way on a vessel and caused some level of RVOT obstruction. You see the drop in ETCO2 as no gas exchange is taking place. There is minimal forward flow happening for these two reasons.
Once the insufflation pressures disappear you now have forward flow blood plus EPI that pushes the bubble forward into the lungs.
It wasn’t a massive CO2 bubble, but combined with low preload it became transiently massive. But now with increased contractility and forward flow things improve and and patient recovers.
I tied it up nicely in my head.

Oh and a CO2 bubble large enough to cause desaturation and hypotension is going to block the pipes and lead to low or no ETCO2.
 
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abolt18

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How about a distended RV?
We actually had a sim lab for almost this exact scenario.

I was the unfortunate victim “doing” the case and at the time didn’t really pay attention to the timing of the insufflation and the CV/pulm collapse

Same thing, during the actual case they were able to bag okay, good volumes despite minimal ETCO2 tracing, clear lungs. Pressures were low but responsive to aggressive pressor use. The surgeon was able to finish and close but they kept the patient intubated.

Imaging showed diffuse b/l opacities and the (pulm) ICU attending initially labeled it ARDS from aspiration during the intubation. But you can see that pattern with nonthrombotic embolisms as well. And that really doesn’t fit the timeline of events. She apparently dramatically recovered POD 1 and was extubated, did well.

The one thing that stopped them from tying this up into a neat little bow however was that they threw in a TEE during the case and didn’t see any obvious bubble or PE.


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Urzuz

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What physician with any modicum of self-respect or integrity would pass off a case after having to push epinephrine and run a pseudo-code in the patient, much less a case that is usually <60 min skin to skin (maybe slightly longer since the appendix is ruptured)?

Anesthesiologists stamp their feet and lament about how no one respects us as physicians, and then they pull **** like this. No wonder so many people view us being interchangeable with nurses.
 
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chocomorsel

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What physician with any modicum of self-respect or integrity would pass off a case after having to push epinephrine and run a pseudo-code in the patient, much less a case that is usually <60 min skin to skin (maybe slightly longer since the appendix is ruptured)?

Anesthesiologists stamp their feet and lament about how no one respects us as physicians, and then they pull **** like this. No wonder so many people view us being interchangeable with nurses.
Totally agree. It does not make us look good. I had a case of severe hypotension and me pushing Epi right as soon as someone came and asked if I needed a break.
Should have said yes and ran.
We gotta do better than this.
I bet this was academics where cases get handed over three times sometimes.
 
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Hoya11

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First off - This was NOT my case.

I came on to relieve the call team and they were finishing up the case that I am about to describe - so the fine details are lacking.

As I understand it.....

a 19 y/o ruptured appendix some days before, IR drain not working...patient getting sicker and sicker...decision to OR for laparoscopic appy.

Patient has been tacchycardic, but good urine output and no hypotension. Induction is smooth with no hemodynamic compromise (so i am told...i'm not sure if the kid dipped at all or not)

Anyway, after insuflation, the patient immediately became hypoxic (in the 50s), CO2 dropped significantly (Attending said "hardly any wave form at all). Pulse was present and patient maintained BP but remained tacchydardic.

Patient remained easy to ventilate by hand, checking the tube with bronchoscope showed correct tube placement. Breath sounds were well heard bilaterally.

As a side note, I asked the surgeon about the case, he said when he put the trochar in, pus came out rather forcefully, and there was lots of puss everywhere. They ended up leaving the belly open because he said he couldn't close it (the why - not sure if it was tight, or because of the puss). They didn't do the appendectomy because anatomy was difficult.

Anesthesia immediately let surgery know of the troubles, and they stopped insuflation and opened the belly. According to the anesthesia team, it seemed that everything improved once they started opening the belly.

Okay - so what happened?

First thought for me is of course a significant decrease in CO (from the preload reduction) which decreased the CO2 waveform. But if this is the case, why would BP persist as high as it did, and why would he get so hypoxic (in the 50s)? Maybe he had the starting of abdominal compartment syndrome, and the insuflation was the last straw.

Second thought would be a CO2 embolism - which I have never seen so I don't fully appreciate what to expect with that - but wouldn't that cause your CO2 to INCREASE? Also, patient wouldn't immediately become hypoxic (except maybe with a complete shut down of CO). Somewhere in the midst of this the surgeon took out the trocar, lots going on that COULD cause it but a brief episode of severe hypotension not picked up by the BP cuff lag may explain it all IMO

What else could cause this scenario?

Maybe it went like this:

Induction of septic patient --> Hypotension --> Severe Hypotension while cuff is not cycling --> Lung perfusion decreased (loss of CO2 wave form) --> "hypoxic to 50s" (maybe pule ox probe not picking up due to severe hypotension and barely able to pick up finger pulse) --> epi given as BP cuff cycling and surgeon desufflates --> BP gives a decent reading, C02 wave form returns, Sat improves as pulse improves.

Meaning that, for a moment, the BP was probably in the 40s-50s systolic but you didnt see it because the cuff either couldnt read anything, or wasnt reading at that time, , you saw decreased sat due to almost no pulse and decreased CO2 return, epi was promptly given and then next BP had recovered a little, say its in the 90s, then as perfusion increases sat returns and CO2 thus returns..
 
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Newtwo

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Obviously this is all just opinion and shooting the breeze as no one will ever really know (except FFP).

As a wise old timer taught me years ago in the ICU when we thought our case was some Wierd thing "it's always sepsis"

Co2 embo meets all the signs but pus shot out of the abdo in a young kid? Profound sepsis, hypovolemia, maybe even a septic cardiomyopathy plus 15mmhg Co2 in the abdo. Definitely sepsis.

Really really bad your colleague didn't handover pushing epi. Like that's terrible handover.

Why did he/she just finish the case? I've never seen an appy go over a couple hours like even a **** show like this
 
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MoMoGesiologist

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What physician with any modicum of self-respect or integrity would pass off a case after having to push epinephrine and run a pseudo-code in the patient, much less a case that is usually <60 min skin to skin (maybe slightly longer since the appendix is ruptured)?

Anesthesiologists stamp their feet and lament about how no one respects us as physicians, and then they pull **** like this. No wonder so many people view us being interchangeable with nurses.
I once got handed over a complicated case of a patient who arrested intraop and the case was wrapping up and was asked to do a TEE and cardiovert then transport pt to ICU. Case was literally 30min from ending. I died a little inside. But to be fair, the signing out dude had somewhere important to go, so it was a rare and special situation
 
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abolt18

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To me this case screams CO2 embolus. The original post saying he was normotensive was the only confounder, but knowing now that he WAS acutely hypotensive, I would think the primary mechanism is CO2 embolus. I think @chocomorsel made good points, it's multifactorial. He was less resilient than he normally would have been due to sepsis.

I've had this happen once before, immediately upon insufflation. MAP was 25. I told them to stop while it cycled again (just in case it was a false reading). MAP 32. Tachycardic. ETCO2 down in 20s from high 30s. I'm pushing drugs and we de-sufflate abdomen, she had mild immediate improvement but she recovered more completely over the next 10 minutes. I just pushed my stick of ephedrine and a couple cc of phenylephrine because it was immediately available then called my attending while I drew up Epi. She was improving by the time I had the Epi drawn up so I never gave it. After all was well we insufflated again but slower and watched her carefully, no problems.

Only thing I could attribute this to is CO2 embolus. Nothing else made sense.
 
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Beeftenderloin

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Oh my God...empty heart...give volume....epi to bridge if you can't stand the suspense...a bullet proof 19 year old....next...

Yea, I guess... empty in the sense that it’s full of CO2 and not blood. But the treatment for that is inotropes, not volume. If you ever come across a true gas embolus with hemodynamic collapse just open the fluids and let me know how that works out for you...
 
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woopedazz

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Why isn't it just a pus-filled, atelectatic set of lungs and a stressed heart? Producing a massive V/Q mismatch and CVS/Resp physiology that is already maximally compensated and probably also negative-pressure dependent... all hiding behind a 19M?

I assume the SpO2 was ~90-95% after minutes of pre-ox
--> induce; cardiac depression + positive pressure vent
--> ****s the bed a bit
--> epi
--> patient looks like they are rallying, but in actuality we are hypoventing the good bits of lung and it's gonna go to **** soon regardless. The gas exchange in the vented lungs are **** so the PaCO2 is skyrocketing. At the same time the PACO2 is also progressively increasing... Problem is we ain't measuring the PACO2, we're measuring the ETCO2, which at this point is still holding, because most of the expired air is all just CO2-free dead-space getting blown straight back out
--> insufflate
--> the 30-35% shunt that was hiding behind ETCO2 and FiO2 of 1.0 decides to increase
--> what happened.

Isn't that the most likely sequence of events for a pus-filled abdo that's been marinating for a few days?
 
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deleted59964

sepsis, relative hypovolaemia, add to that pneumoperitoneum which decreases venous return and causes hypotension.
hypotension responds to epi, further responds to releasing pneumoperitoneum.

my question is why stuff around with an IR drain in the first place.
 
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vector2

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sepsis, relative hypovolaemia, add to that pneumoperitoneum which decreases venous return and causes hypotension.
hypotension responds to epi, further responds to releasing pneumoperitoneum.

my question is why stuff around with an IR drain in the first place.

A2FC586E-5F51-474D-844C-9E73AE9B751C.jpeg



The flip side is when those 10-20% of pts fail with the drain, it can turn pretty nasty like the OP’s case
 
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epidural man

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Great stuff. I love you guys (he says gently as a tear drops from the corner of his eye)

A couple of things need to be clarified.
First, The team did NOT turn over the case. Despite the patient doing well when I arrived and me telling the other attending I was ok and she was good leave, if she wanted, she stuck around and finished and I helped transport the patient to the ICU.

Second, when telling me the story, they didn’t purposely leave out any details.This is a very talented and most trustworthy anesthesiologist. She had just experienced a 19 y/o be hypoxia for 8 min, called a code and got the crash cart ready, and was a half second away from chest compressions - she was a bit razzled - and understandably so. I’m sure with some distance and a chance to catch her breath she would have remembered all the details. She was trying to piece together herself what had just happened...asking me questions, wondering if she could have done something different...all that stuff a conscientious and humble anesthesiologist SHOULD do.

Anyway, thanks for the discussion. I always appreciate them.
 
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chocomorsel

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Great stuff. I love you guys (he says gently as a tear drops from the corner of his eye)

A couple of things need to be clarified.
First, The team did NOT turn over the case. Despite the patient doing well when I arrived and me telling the other attending I was ok and she was good leave, if she wanted, she stuck around and finished and I helped transport the patient to the ICU.

Second, when telling me the story, they didn’t purposely leave out any details.This is a very talented and most trustworthy anesthesiologist. She had just experienced a 19 y/o be hypoxia for 8 min, called a code and got the crash cart ready, and was a half second away from chest compressions - she was a bit razzled - and understandably so. I’m sure with some distance and a chance to catch her breath she would have remembered all the details. She was trying to piece together herself what had just happened...asking me questions, wondering if she could have done something different...all that stuff a conscientious and humble anesthesiologist SHOULD do.

Anyway, thanks for the discussion. I always appreciate them.
So what does she think happened since she was actually there and you weren't originally privy to all the details. She can piece it together better.
 
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Newtwo

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I've certainly seen at least 3 'young, healthy people' late teens to mid 20s nearly die from ruptured appendix with abscess in the last 8 years. Not like this intraop but needed icu, ventilation, dic, multiple repeat washout etc...

It can be terrible Esp with the delayed presentation of macho men who would be in the marines
 
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epidural man

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So what does she think happened since she was actually there and you weren't originally privy to all the details. She can piece it together better.
Preload issue in a kid on the edge but not manifesting like an adult - like some have mentioned.

But I like the multi-factorial idea...the hypoxia is baffling....more like a CO2 embolism.
 
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fakin' the funk

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I have so many thoughts and questions
1) the pulse ox drop is almost certainly artifactual and related to your massive cardiovascular event, which was
2) almost certainly relative hypovolemia + sepsis + insufflation + vagal etc etc
3) what is this nonsense about a IR drain in a perfed appy? Wth?
4) if the surgeon opened (reasonable), they didn't even fix the perf? Wth?
5) the surgeon left open for gross contamination obvie
6) @epidural man i thought you were an attending but this case is described the way a CA-1 would describe it
7) did you all send labs? Imaging? Echo? Lines? Or just dump in ICU and run?
 
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drmwvr

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Yea, I guess... empty in the sense that it’s full of CO2 and not blood. But the treatment for that is inotropes, not volume. If you ever come across a true gas embolus with hemodynamic collapse just open the fluids and let me know how that works out for you...
So, just to be clear...you'd not include meaningful volume resus in the care of this patient as described. Because I have to tell you, given the presentation, gas embolus would not be the first place I went with this at all. Even if I did get there, the suggestion that inopressor in isolation of proper volume replacement in this case is naive. But chasing zebras here is benign enough as you'd hopefully end up in the same place regardless of the cause.
 
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epidural man

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I have so many thoughts and questions
1) the pulse ox drop is almost certainly artifactual and related to your massive cardiovascular event, which was
2) almost certainly relative hypovolemia + sepsis + insufflation + vagal etc etc
3) what is this nonsense about a IR drain in a perfed appy? Wth?
4) if the surgeon opened (reasonable), they didn't even fix the perf? Wth?
5) the surgeon left open for gross contamination obvie
6) @epidural man i thought you were an attending but this case is described the way a CA-1 would describe it
7) did you all send labs? Imaging? Echo? Lines? Or just dump in ICU and run?
I am an attending - just not a good one.
 
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chocomorsel

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Maybe it went like this:

Induction of septic patient --> Hypotension --> Severe Hypotension while cuff is not cycling --> Lung perfusion decreased (loss of CO2 wave form) --> "hypoxic to 50s" (maybe pule ox probe not picking up due to severe hypotension and barely able to pick up finger pulse) --> epi given as BP cuff cycling and surgeon desufflates --> BP gives a decent reading, C02 wave form returns, Sat improves as pulse improves.

Meaning that, for a moment, the BP was probably in the 40s-50s systolic but you didnt see it because the cuff either couldnt read anything, or wasnt reading at that time, , you saw decreased sat due to almost no pulse and decreased CO2 return, epi was promptly given and then next BP had recovered a little, say its in the 90s, then as perfusion increases sat returns and CO2 thus returns..
Depends on how quickly your surgeon moves from induction to insufflation. You are describing a period of probably three minutes. I have been in some private practices that move fast, as in the tube goes in and I get ETCO2 and the surgeon is ready to cut. But those are not the majority of practices I bet.
 
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So, just to be clear...you'd not include meaningful volume resus in the care of this patient as described. Because I have to tell you, given the presentation, gas embolus would not be the first place I went with this at all. Even if I did get there, the suggestion that inopressor in isolation of proper volume replacement in this case is naive. But chasing zebras here is benign enough as you'd hopefully end up in the same place regardless of the cause.

Sure of course I would ALSO open the fluids.
 
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