nephrectomy case

[amyl]

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i love hearing everyones opinion of cases so -- a case i inherited today:
60 something yo woman w pmhx of cerebral aneurysm, COPD -45 pack year history quit smoking a few months ago, no meds -- for robotic p nephrectomy in R lateral recumbent, aline, 2 sixteens running well. no cardiac history - rate dependent LBBB seen during outpt stress test.

i came in shortly after insufflation, etco2 about 40, hemodynamically stable, doing well.

couple of minutes later etco2 climbing quickly despite maxing out ventilator and pt develops LBBB and flips her t waves, BP starts dropping....

thoughts?

 

[Bertelman]

gas embo, Rt recumbency ain't helping. Shut gas off, Lt side down


http://www.pubmedcentral.nih.gov/pagerender.fcgi?artid=2502512&pageindex=2

 

[Jeff05]

in that article gas embolism causes decrease in etco2. also bp drop is sudden.
here there was an increase in co2 and a gradual hypotension.

was there subq emph?

 

[TrustMe]

Did they nick the diaphragm and you are getting a tension pneumo from the insufflation?

 

[OB1🤙]

Any sub-q emphysema? Edit: already asked.

Entities that cause grossly decreased CO (i.e. large gas embo, tension pneumo) should not result in a huge increase in ETCO2. That said, embolic air in a coronary artery could cause localized ischemia and the EKG changes you mention, provided some means of a right-to-left shunt exist.

Other things to rule out: is BP dropping because you're decreasing preload with all the PPV you're now doing? Is the pt relatively hypovolemic? Respiratory variation in the a-line tracing? Just how low a BP are we talking about here, and what change from prior to insufflation? Any change after you ask them to turn off the CO2?

Call for a TEE probe and assess filling, wall motion, presence of air in the left heart and coronaries, and for the presence of a PFO.

 

[Intrathecal]

Increased CO2 production usually means a hypermetabolic state: MH, NMS, sepsis, thyroid storm, serotonin syndrome, pheo. THe only condition from this list that cause hypotension is sepsis, but patient has no infectious etiology at this point. Was the patient on SSRI pre-op? I've seen both hyper and hypo tenision from serotonin syndrome, but hypertension is more common.

It may have something to do with the head too, perhaps aneurysm ruptured on induction/intubation/positioning, but I can't explain why pt would be hypotensive unless an epidural catheter was placed and activated. I'm trying to think how elevated ICP can cause increased CO2 production... but can't make the connection. He can get EKG changes with a subdural hematoma.

 

[huktonfonix]

In general if an acute event happens after a surgical occurence, tell them to stop (cross clamp, oculocardiac reflex, insufflation). Hard to say whats going on definitively. Could be gas emboli as previously mentioned although it would have to be substantial to cause decreased BP unless there is a R-L shunt with coronary emboli as previously mentioned. It could also be relative hypovolemia or absolute hypovolemia related to either decreased return from high insufflation pressures although both should cause a decrease in ETCO2. Elevated CO2 can also cause a sympathetic discharge which may lead to myocardial supply/demand imbalance. More information regarding Heart rate, rhythm, oxygenation, temperature, etc... would be useful to rule in/out.

Regardless this is an acute event causing apparent new onset myocardial ischemia. If the event was immediately after insufflation I would inform the surgeon to release pressure on the abdomen, support blood pressure as needed with either phenylephrine/inotrope as neccesary (fluid/blood if heavy blood loss i.e. aortic puncture). Listen to breath sounds to ensure proper ETT positioning as well as r/o PTX. This is likely going to cancel the case unless the risk of the renal lesion outweighs a potential acute coronary syndrome (EKG changes with hypotension). Need to discuss that point with the surgeon. And yes although unlikely, you do have to rule out MH. Send the ABG, lytes, etc....

 

[periopdoc]

Either they are insufflating her left chest or they nicked a vessel/ vascular structure and are insufflating it. It is unlikely that a hypermetabolic state just happened to pop up coincident with insufflation and that is the only other explanation I can think of for hypercarbia in a patient with high minute ventilation.

EKG and BP changes are chicken or the egg dilemma, but both are ultimately secondary to the hypercarbia. Have them deflate the abdomen and convert to open if she stabilizes.

Late Onset of Subcutaneous Emphysema and Hypercarbia Following Laparoscopic Cholecystectomy scan down to page 1468

- pod

 

[BLADEMDA]

Any sub-q emphysema? Edit: already asked.

Entities that cause grossly decreased CO (i.e. large gas embo, tension pneumo) should not result in a huge increase in ETCO2. That said, embolic air in a coronary artery could cause localized ischemia and the EKG changes you mention, provided some means of a right-to-left shunt exist.

Other things to rule out: is BP dropping because you're decreasing preload with all the PPV you're now doing? Is the pt relatively hypovolemic? Respiratory variation in the a-line tracing? Just how low a BP are we talking about here, and what change from prior to insufflation? Any change after you ask them to turn off the CO2?

Call for a TEE probe and assess filling, wall motion, presence of air in the left heart and coronaries, and for the presence of a PFO.

Pretty good responses from Hawaiian Bruin and POD.👍


First, the Brain Anuerysm should have been treated already and is unlikely part of this problem. Second, her huge smoking history should put you on alert about her likely coronary disease. Third, long laparoscopic cases can lead to high end tidal C02, pneumothorax, decreased cardiac output/cardiac compromise and blood loss.


I agree with the common sense approach to this patient's problem. The increasing end tidal CO2 is a major issue along with EKG changes. Can the team decrease the insufflation pressure? Did you send an ABG? Did you try pressure control ventilation? Any response to pressors or fluid? Is a TEE available to obatin additional info. about the heart?

Never be afraid to be a patient advocate during laparoscopic cases. There will be times that the surgical team will need to STOP the insufflation while you optimize the patient. This may be one of those times. The surgical procedure can be converted to an open nephrectomy if needed; so, depending on the results of your additional data (ABG, TEE, response to PC ventilation, EKG changes) the surgical approach may or may not continue as a laparoscopic case.

As POD has pointed out those EKG and BP changes are worrisome and must be immediately addressed.

 

[OB1🤙]

Paging amyl- what happened in this case?

Another thing worth mentioning- this pt developed a LBBB during a stress test and was subsequently "cleared" for surgery-> what else was discovered or mentioned in this test?

Clearly the decision was made to proceed regardless of the presence of a transient LBBB with stress, which makes me wonder what preoperative discussions took place with cardiology, surgery, et al.

 

[Licoricestick]

Not convinced on CO2 embolism - I've always been taught that gas embolus causes a significant reduction in CO and that is the mechanism for the change (ie reduction) in ETCO2. So it doesn't fit with increasing CO2. Besides a reduction in cardiac output should be reflected in immediate hypotension, not gradual hypotension. Same for tension pneumo.

Not sure why people are so keen to dismiss MH - it needs to be considered and ruled out.

Would like to know:
what HR is doing
what ETCO2 numbers are
what the pressures/gas flows into the abdomen were
did CO2 continue to rise after abdomen deflated
what airway pressures were and what 'maxing out the ventilator' actually means

I would tell the surgeons to cease and to deflate the abdomen.
Robot needs to be undocked to allow access to patient and repositioning if required.
Eliminate the circuit, bag by hand on 100% O2 (how do lungs feel, what sort of pressures are required, can you get adequate volumes)
Auscultate and percuss chest (?tube position, ?pneumothorax), check for subcut emphysema, check trachea position, if haemodynamics continue to deteriorate despite release of intra abdominal pressure consider needle decompression
fluids and/or vasopressors for hypotension
Send ABG (interested in CO2 gradient and pH)
TEE if you can (would not be possible at my institution within reasonable timeframe)

Rapid improvement to baseline/near baseline - consider proceeding as open procedure if significant risk from kidney, otherwise wake patient up
Diagnosis clear - treat it, consider waking patient up
Diagnosis unclear - consider treating for MH

 

[BLADEMDA]

Not convinced on CO2 embolism - I've always been taught that gas embolus causes a significant reduction in CO and that is the mechanism for the change (ie reduction) in ETCO2. So it doesn't fit with increasing CO2. Besides a reduction in cardiac output should be reflected in immediate hypotension, not gradual hypotension. Same for tension pneumo.

Not sure why people are so keen to dismiss MH - it needs to be considered and ruled out.

Would like to know:
what HR is doing
what ETCO2 numbers are
what the pressures/gas flows into the abdomen were
did CO2 continue to rise after abdomen deflated
what airway pressures were and what 'maxing out the ventilator' actually means

I would tell the surgeons to cease and to deflate the abdomen.
Robot needs to be undocked to allow access to patient and repositioning if required.
Eliminate the circuit, bag by hand on 100% O2 (how do lungs feel, what sort of pressures are required, can you get adequate volumes)
Auscultate and percuss chest (?tube position, ?pneumothorax), check for subcut emphysema, check trachea position, if haemodynamics continue to deteriorate despite release of intra abdominal pressure consider needle decompression
fluids and/or vasopressors for hypotension
Send ABG (interested in CO2 gradient and pH)
TEE if you can (would not be possible at my institution within reasonable timeframe)

Rapid improvement to baseline/near baseline - consider proceeding as open procedure if significant risk from kidney, otherwise wake patient up
Diagnosis clear - treat it, consider waking patient up
Diagnosis unclear - consider treating for MH

MH is a possible but unlikely diagnosis. An ABG should rule this out. You do know what the ABG should show for MH, right? Temperature is a late sign but may begin to increase a few minutes after C02 starts rising.


When you hear hoof beats think horses and not Zebras.

 

[BLADEMDA]

Note: The more criteria an individual fulfills, the more likely that a malignant hyperthermia (MH) episode has occurred. Thus, with only temperature elevation during anesthesia, an individual is not likely to be susceptible to malignant hyperthermia. An individual who fulfills criteria for all clinical findings is almost certain to have had an MH episode.
Table 1. Criteria Used in the Clinical Grading Scale for Malignant Hyperthermia


Clinical Finding 1 ManifestationRespiratory acidosisEnd-tidal CO2 >55 mmHg, PaCO2 >60 mmHgCardiac involvementUnexplained sinus tachycardia, ventricular tachycardia, or ventricular fibrillationMetabolic acidosisBase deficit >8 mEq/L, pH <7.25Muscle rigidityGeneralized rigidity, severe masseter muscle rigidityMuscle breakdownSerum creatine kinase concentration >20,000/L units, cola-colored urine, excess myoglobin in urine or serum, plasma [K+] >6 mEq/LTemperature increaseRapidly increasing temperature, T >38.8° COtherRapid reversal of MH signs with dantrolene, elevated resting serum creatine kinase concentration Family historyConsistent with autosomal dominant inheritanceFrom Larach et al 1994, Rosenberg et al 2002
Signs occurring during or shortly after general anesthesia in the untreated individual
1. Clinical findings (except family history) are in order of relative importance.

 

[huktonfonix]

Not convinced on CO2 embolism - I've always been taught that gas embolus causes a significant reduction in CO and that is the mechanism for the change (ie reduction) in ETCO2. So it doesn't fit with increasing CO2. Besides a reduction in cardiac output should be reflected in immediate hypotension, not gradual hypotension. Same for tension pneumo.

Not sure why people are so keen to dismiss MH - it needs to be considered and ruled out.

Doesnt necessarily have to be an embolus. It does decrease CO IF the embolus is large enough to cause PHTN or airlock same as any other gas emboli. However, if the insufflation pressures are high enough the CO2 is absorbed into the bloodstream as well. A lot of the OP post is kind of chicken and egg stuff. It would be helpful to have more info and know the timeline of events. Was it decreased venous return causing hypotension leading to myocardial ischemia and further hypotension with coincidental rising of CO2? Was it emboli causing hypotension and ischemia? PTX leading to the symptoms? Dunno, could be any of them. After assessing physical signs and monitors the treatment as you mentioned is likely gonna be fluids, pressors, and desufflation regardless (unless PTX). MH is unlikely but does need to be ruled out. Although I suppose if youre unlucky enough to be having myocardial ischemia and MH concurrently your number might be up anyway.

 

[amyl]

sorry... got busy (CA-1 and all)....
temp 35.9, had previous anesthestic and no sux (i know this technically doesn't rule it out but makes less likely) so MH wasn't at the top of my list but i checked for masseter spasm any ways... none.
heart rate was stable -- mostly in the 60s, briefly into the 70s.
maps fell into upper 50s, i pushed neo a few times and then went for the drip, which we eventually weaned...
told surgeons to deflate asap and CO2 was SLOW!!! to come back down, felt like forever actually.
i wanted to send a gas right away but my attending wanted to wait a few minutes.... probably didn't want to know how bad the numbers were. gas as we were starting to get the co2 down: pH 7.18. didn't give any bicarb, just let the ventilator do the work. she just would not tolerate insufflation and lateral recumbent. some esmolol brought out NSR intermittently but it didn't stick around. convinced the surgeons to open. hypovolemia likely contributed as we were trying to keep her a little dry to normovolemic d/t aneurysm. for the very first time i was super happy just to be the resident and have staff to call ;-) the rest of the case went okay... staff wanted albumin for fluid resuscitation but then staff change and new staff wanted hextend instead. probably didn't really matter...

apparently some demand ischemia bringing out the LBBB and more COPD than her pack year history suggested.
another pt for discussion: surgeons really, really didn't want to open and wanted to use helium to insufflate... but i think they passed as it would have taken to long to set up at last minute.... anyone out there w any experience w helium insufflation?

 

[huktonfonix]

sorry... got busy (CA-1 and all)....
temp 35.9, had previous anesthestic and no sux (i know this technically doesn't rule it out but makes less likely) so MH wasn't at the top of my list but i checked for masseter spasm any ways... none.
heart rate was stable -- mostly in the 60s, briefly into the 70s.
maps fell into upper 50s, i pushed neo a few times and then went for the drip, which we eventually weaned...
told surgeons to deflate asap and CO2 was SLOW!!! to come back down, felt like forever actually.
i wanted to send a gas right away but my attending wanted to wait a few minutes.... probably didn't want to know how bad the numbers were. gas as we were starting to get the co2 down: pH 7.18. didn't give any bicarb, just let the ventilator do the work. she just would not tolerate insufflation and lateral recumbent. some esmolol brought out NSR intermittently but it didn't stick around. convinced the surgeons to open. hypovolemia likely contributed as we were trying to keep her a little dry to normovolemic d/t aneurysm. for the very first time i was super happy just to be the resident and have staff to call ;-) the rest of the case went okay... staff wanted albumin for fluid resuscitation but then staff change and new staff wanted hextend instead. probably didn't really matter...

apparently some demand ischemia bringing out the LBBB and more COPD than her pack year history suggested.
another pt for discussion: surgeons really, really didn't want to open and wanted to use helium to insufflate... but i think they passed as it would have taken to long to set up at last minute.... anyone out there w any experience w helium insufflation?

Why esmolol if the HR only went up into the 70's? I would suspect that this was a supply ischemia from decreased preload rather than a demand ischemia, but there may be more info to this case than what was presented.

 

[amyl]

sorry typed too fast, meant supply/demand imbalance ischemia. decreased preload, lack of sufficient venous return. base excess wnl on gas so i didn't think that we were behind on fluid or anything but she didn't tolerate regardless.
attending said esmolol b/c outpt stress test showed rate dependent LBBB -- i quietly disagreed about the esmolol being necessary but it would briefly lower the oxygen demand on the heart so i figured it can't hurt.

 

[OB1🤙]

I'm still curious about this stress test. What test was actually done- a treadmill, treadmill thallium, adenosine thallium, other?

Seems to me that a rate-dependent LBBB is an EKG finding suspicious for ischemia. Was there also a perfusion study showing normal perfusion and no reversible ischemia along with this test?

What were cardiology's comments on the test and this finding?

If it was thought to be nothing, and the anesthesiologist agreed it was nothing and decided to proceed, why are we getting worked up about it when it presents itself intraop?

Seems to me that if we decide we're going to take the LBBB seriously intraop, it should have been more thoroughly worked up preop. Now I'm not necessarily proposing to take this patient for CABG before having their renal CA whacked out (if that's what the surgery here was), but I would like an assessment of the myocardium at risk if there is truly rate-dependent ischemia going on.

I know you took this case over but there's some info still missing from the picture. I'm also still curious about whether there was sub-q emphysema and what the a-line tracing looked like.

 

[guitarguy09]

I know you took this case over but there's some info still missing from the picture. I'm also still curious about whether there was sub-q emphysema and what the a-line tracing looked like.

HB- I agree about the stress test by the way. I'm an intern still in the "learning process" so I wanted to ask what the subcutaneous emphysema indicates?... Specifically, how does it change your differential, etc.? (I'm assuming you want to know that a-line tracing both for indications of volume status... but I guess I need more info about the sub-q emphysema... would it indicate more of a pneumothorax vs. insufflation picture?)

Thanks for the help and I'm sorry for my novice-type questions... but these are the great threads... and I try and learn all I can from them. Take care.

 

[OB1🤙]

Presence of SCE in and of itself doesn't change much (unless it was absolutely massive and causing airway compromise), other than to pretty much confirm the dx and rule out zebras like MH. You'd want to know that the pt would be capable of generating the relatively high minute ventilation necessary to blow off the excess CO2 on their own prior to extubation, and the potential presence of myocardial ischemia in this case means you have to at least think about the work of breathing and O2 supply/demand and such.

All this is academic pontificating about a case that was probably nothing more than relative hypovolemia in laparoscopy, but it's at least a mental conversation to have with yourself while troubleshooting the hemodynamic changes.

IMO anyway.

HB- I agree about the stress test by the way. I'm an intern still in the "learning process" so I wanted to ask what the subcutaneous emphysema indicates?... Specifically, how does it change your differential, etc.? (I'm assuming you want to know that a-line tracing both for indications of volume status... but I guess I need more info about the sub-q emphysema... would it indicate more of a pneumothorax vs. insufflation picture?)

 

[amyl]

cleared by cardiology. adenosine stress test. nuc med scan part of test normal. no gross abnormality in aline tracing, no resp variation, if thats what you were getting at. no subq emphysema.

and i agree, relative hypovolemia and some pts just don't tolerate insufflation in lateral recumbent

 

[Licoricestick]

Blade - most of the information you listed was not provided in the history given by amyl (at least at the time I posted about MH).

There was no mention of HR but there was a mention that she previously had rate related ischaemic changes and she then had ischaemic changes following the increased ETCO2 - certainly that doesn't mean she's tachy, but I was considering that possibility.

There was no information on temperature, pH, the presence or absence of muscle rigidity (which is by no means a universal sign) or masseter spasm (which is now know to correlate much less with MH susceptibility than was once thought).

Given the severity of MH and the tremendous importance of early recognition and treatment, I will continue to defend my consideration of MH in the differential. Writing increased ETCO2 (especially when it is described as "despite maxing out the ventilator") in a laparoscopic case off to absorbed CO2 without considering other causes is patently stupid. But, given what amyl has subsequently told us I doubt very much that MH would have been more than a flicker in the back of my brain if I was in the theatre at the time (with the HR information available and the patient in front of me).

And the absence of a personal or family history of MH is pretty useless in excluding MH in a given anaesthetic.

Note: The more criteria an individual fulfills, the more likely that a malignant hyperthermia (MH) episode has occurred. Thus, with only temperature elevation during anesthesia, an individual is not likely to be susceptible to malignant hyperthermia. An individual who fulfills criteria for all clinical findings is almost certain to have had an MH episode.
Table 1. Criteria Used in the Clinical Grading Scale for Malignant Hyperthermia


Clinical Finding 1 ManifestationRespiratory acidosisEnd-tidal CO2 >55 mmHg, PaCO2 >60 mmHgCardiac involvementUnexplained sinus tachycardia, ventricular tachycardia, or ventricular fibrillationMetabolic acidosisBase deficit >8 mEq/L, pH <7.25Muscle rigidityGeneralized rigidity, severe masseter muscle rigidityMuscle breakdownSerum creatine kinase concentration >20,000/L units, cola-colored urine, excess myoglobin in urine or serum, plasma [K+] >6 mEq/LTemperature increaseRapidly increasing temperature, T >38.8° COtherRapid reversal of MH signs with dantrolene, elevated resting serum creatine kinase concentration Family historyConsistent with autosomal dominant inheritanceFrom Larach et al 1994, Rosenberg et al 2002
Signs occurring during or shortly after general anesthesia in the untreated individual
1. Clinical findings (except family history) are in order of relative importance.

 

[Noyac]

Just a quick $.02.
I was doing a CABG one day and the PA was harvesting the saphenous vein under CO2 insufflation technique. The ETCO2 kept rising relatively slowly but enough to be worrisome. No other cardiovascular changes. No obvious air embolism. I was concerned about MH and asked the PA to turn off the CO2. AS I was preparing to call for the MH cart the CO2 began to decrease rapidly with ventilation. It appears that there was a small rent in the femoral vein ( I think thats the one it was) at the time of the insufflation just enough to entrain CO2 but not enough for embolism pre se.
This sort of thing could have been occuring here. Unlikely, but possible.

 

[Bertelman]

apparently some demand ischemia bringing out the LBBB and more COPD than her pack year history suggested.

I'm not following how severe COPD could lead to an acute CO2 rise mid-case in a ventilated patient.