Interesting case

[CremeSickle]

27 y/o male s/p MVA comes to OR with R hip fx.

Hx: none
Rx: none
Allg: none

preop per usual - versed.

Smooth RSI with lido, fent, prop & Sux (+ defas dose of vec)
Pt to vent ancef 1 g given ISO on. V/S normal. Methadone given at start of case, some fent given for start of op.

Bear hugger, fluid warmer, HME

Op starts.

30 minutes into surgery pt now has v/s change:

HR: 130 BP: 190/89 temp: 38.9 ETCO2: 39

ISO at 1.7% and 100 fent given w/o change.

Plan? Diff Dx?

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[amyl]

forgive the freshman questions: what is HME? why methadone and fentanyl?

 

[CremeSickle]

HME (heat/moisture exchanger) is also called an artificial nose.

Fent does a nice job at blunting the initial sympathetic response (pain) during incision
Methadone is an excellent long term narcotic which i have seen the best and smoothest wake ups ever with. You need pts who arent leaving the hospital.

 

[Noyac]

Could be Thyroid storm.

 

[urge]

Or MH.


Anywho, get a Blood gas.

 

[VentdependenT]

MH: looks like a hypermetabolic picture developing.

Hypercarbia/Hypoxia

what noyac said

Volume Overload. Unlikely

Drug Reaction (check out skin for rash I suppose. Would usually be a shock picture however.)

Weirdo pheochromo or some adrenal something.

ICH especially S/P MVA. Could even be a venous bleeder which now pouring out because of the ISO 2MAC. Yeah Yeah the HR is not reflective of a cushing reflex. So what. Maybe look at the pupils. Maybe the dude is having a friggen seizure.

Check a gas. Look at the piss. Check CO2 resorber. Turn off bair hugger. Turn down room temp. In light of the rising CO2 and Temperature I'd seriously worry about MH. I'd seriously consider switching to Propofol Nitrous mixture till you rule this mother out. Give another whopper slug of fentanyl to rule out pain. Maybe pt was a narc addict? Treat the pressure if the fent doesn't work. Dantrolene in the vacinity isn't a bad idea either.

 

[fval28]

MH till proven otherwise.

I would do all that was suggested (ABG, switch to non-triggering, dantrolene in room, etc) and CALL FOR HELP.

If this is MH you'll need a lot of hands on deck, for mixing dantrolene, getting Bicarb drip, running labs, etc.

I recently went to a lecture with Charlie Watson, one of the guys from MHAUS, great lecture and lots of good info- anyway he relayed a story similar to yours when he was in the service of a young, healthy soldier who had a MH event during a case- his fast response (and the patient's protoplasm) got the guy out of the hospital in days and back to his duty station. The take home for me was that fast recognition and action is what made all the difference- and this was BEFORE there was routine use of ETCO2 monitors- diagnosed by skin temp and muscle rigidity... so probably further along the MH picture than the patient you are describing.


So, what was it????

 

[Planktonmd]

With the data provided you have to start treating as MH as mentioned above while you think about the differential diagnosis.
The other possibilities could be:
1- Methadone inhibits the re-uptake of serotonin and nor-epinephrine and causes histamine release, so if a patient is taking MAOI's or chronically using cocaine they can theoretically have a response similar to the one mentioned.
2- A thyroid storm is definitely a good thought.
3- Cocaine (or other stimulants) intoxication.
4- A seizure should also be considered and you might not see the convulsions if a muscle relaxant is still on board.
5- A fat embolism should always be considered when weird things happen after a broken bone, and it can cause all the symptoms mentioned although we don't know if the Oxygenation had changed.

 

[Gern Blansten]

I would think the CO2 would be quite a bit higher with MH. I might get things ready, but without an ABG, or other more convincing evidence, I would keep looking.
What other medicines did they receive before they got to you. Is neuroleptic malignant syndrome a consideration? Did they get haldol or some other drug in the ER?

 

[VentdependenT]

NMS has gotta be on there too.

It would be low on my differential considering the patients PMH is nada. If he was a schizo then yep.

I suppose Reglan could cause it as well. Compazine for sure. Although I've never seen it I had always thought it had a far more insidious onset as compared to MH. Hours to days. Vs Minutes to hours for MH.

 

[CremeSickle]

Geez, kick ass responses!

Pupils PERL Bilat, no sz obvious, No thyroid Hx, No illegal drugs

So..

Everyone thought it was MH and (as mentioned) started to treat with dantrolene RIGHT AWAY, switched to manual bagging (d/t gas in circuit) and TIVA Op was finished.

BTW, we called the "MH hotline" and noone answered.... go figure.

ABG showed a metabolic & resp. acidosis (cant remember the exact numbers now though, sorry)

Pt was sent to ICU where dantrolene was finished. Over that 24 hour period pt seemed to do better and based on a discussion with the MH guru's MH was ruled out.

When they decided to wean the pt off the vent after just stopping the dantrolene the pt seemed unable to effectively ventilate and CO2 was rising.

Why was the CO2 rising?

What is the differential Dx at the top now?

 

[Planktonmd]

If you just stopped the Dantrolene and the patient is not ventilating effectively then it might be just muscle weakness caused by Dantrolene.
You need to give the patient some time.
The original diagnosis though seems to be most likely a fat embolus and if the patient did not die initially he will recover.

 

[CremeSickle]

You pegged it plank.

None of us were there for the failed extubation but it was a great case. Pt survived though i have no idea if there were any significant problems after that.

 

[VentdependenT]

If you just stopped the Dantrolene and the patient is not ventilating effectively then it might be just muscle weakness caused by Dantrolene.
You need to give the patient some time.
The original diagnosis though seems to be most likely a fat embolus and if the patient did not die initially he will recover.

Thats BOARDS stuff right there.

 

[Noyac]

Nice case. A few things have me wondering why fat embolism. HTN and high ETCO2 initially. Fat embolism will give you a cor pulmonale picture. I would have expected low BP and low ETCO2. Did this pt have petecheia on his chest, arms or conjunctiva? Did someone measure or stain for fat globules in the urine? I'm curious as to how they determined it to be FES.

For those of you studying for boards, this is a great case. A couple of things to focus on here are trauma and long bone fx. Think common causes first the rare ones like MH. We all like to consider MH early w/c is good since it is so devastating but it is still very rare. I thought Thyroid storm b/c of the HTN, tachycardia and relatively low ETCO2. MH will not have a low ETCO2 in most cases. ETCO2 will be one of the first things to go up in MH, temp is last. You don't need a H/O thyroid disease to get a thyroid storm. Trauma can cause it. I've seen it and this is exactly how it presented. I have also seen a FES case and my pt died 3 days later in the ICU after coding 6 times. Twice in the OR and 4 in ICU. It was a 29 yo female with a femor fx. Sucked bad. And she had hypotension. She was completely stable the entire case and I woke her up at the end. She was talking to me and we were about to move her to the stretcher when BAM severe hypotension and respiratory distress. ECG showed large p waves in lead 2. Echo showed cor pulmonale picture.

 

[VentdependenT]

Nice case. A few things have me wondering why fat embolism. HTN and high ETCO2 initially. Fat embolism will give you a cor pulmonale picture. I would have expected low BP and low ETCO2. Did this pt have petecheia on his chest, arms or conjunctiva? Did someone measure or stain for fat globules in the urine? I'm curious as to how they determined it to be FES.

For those of you studying for boards, this is a great case. A couple of things to focus on here are trauma and long bone fx. Think common causes first the rare ones like MH. We all like to consider MH early w/c is good since it is so devastating but it is still very rare. I thought Thyroid storm b/c of the HTN, tachycardia and relatively low ETCO2. MH will not have a low ETCO2 in most cases. ETCO2 will be one of the first things to go up in MH, temp is last. You don't need a H/O thyroid disease to get a thyroid storm. Trauma can cause it. I've seen it and this is exactly how it presented. I have also seen a FES case and my pt died 3 days later in the ICU after coding 6 times. Twice in the OR and 4 in ICU. It was a 29 yo female with a femor fx. Sucked bad. And she had hypotension. She was completely stable the entire case and I woke her up at the end. She was talking to me and we were about to move her to the stretcher when BAM severe hypotension and respiratory distress. ECG showed large p waves in lead 2. Echo showed cor pulmonale picture.

What did you do for the Thyroid storm and how'd you finally diagnosis it homeboy?

 

[CremeSickle]

Hey

I cant actually tell you how they made the Dx. I know a CT was done but after that... no idea. I did not make the diagnosis I was on the MH bandwagon and learned a very good lesson!

 

[Noyac]

What did you do for the Thyroid storm and how'd you finally diagnosis it homeboy?

It was fairly easy to diagnose after the fact. But the index of suspension was high intraop. It was some time ago but I remember treating her mostly with beta blockers (labetolol and an esmolol drip). I think PTU was given intraop but it may have been given in the ICU, can't remember exactly. We cooled the pt down and entertained the idea of MH but never started dantrolene. I may have switched to a MH safe anesthetic just to be sure. Other than that not much. Hydration and cooling and control of hemodynamics. Sodium iodide is also recommended but I don't remember starting it.

 

[VentdependenT]

It was fairly easy to diagnose after the fact. But the index of suspension was high intraop. It was some time ago but I remember treating her mostly with beta blockers (labetolol and an esmolol drip). I think PTU was given intraop but it may have been given in the ICU, can't remember exactly. We cooled the pt down and entertained the idea of MH but never started dantrolene. I may have switched to a MH safe anesthetic just to be sure. Other than that not much. Hydration and cooling and control of hemodynamics. Sodium iodide is also recommended but I don't remember starting it.

SOme books say propanolol because it also inhibits peripheral conversion of t3-->t4. DO all beta-blockers do this or is it just propanolol specific? Because I don't know where the hell to find propanolol now-a-days.

 

[Planktonmd]

SOme books say propanolol because it also inhibits peripheral conversion of t3-->t4. DO all beta-blockers do this or is it just propanolol specific? Because I don't know where the hell to find propanolol now-a-days.

I think any Beta-blocker that blocks both B1 and B2 receptors should work fine.
Labetalol should do it.
In a patient with unknown thyroid history it is usually very difficult to distinguish a thyroid storm from MH, they are both hypermetabolic states and present in a very similar fashion initially, So, if a patient is showing signs of unexplained hypermetabolic state under GA and even if the CO2 is not extremely high I would start Dantrolene based on suspicion only.

 

[gasnewby]

a friend was asked on an interview "where is the dantrolene kept in your hospital?"

Is this a trick question- does it have to be refrigerated or something? is it usually in the pyxis?

 

[CremeSickle]

Its in our MH cart.

 

[tussionex]

Its in our MH cart.

we stock drug carts for our OR's...no pyxis there yet. and we keep the dantrolene on every cart.
ps - i dont know if this is a problem for anyone who needs some dantrolene in a hurry [once had to make one for ER patient in psych hosp with NMS]; it will dissolve faster if it's warm. if a water bath is not possible, which i'd imagine it isn't, even holding it the crook of your arm will help!

 

[sdn1977]

Dantrolene is expensive. It expires before it gets used (fortunately!) So, its considered a loss which is expected & anticipated.

So - you need to know where dantolene is kept. Always in the pharmacy. This is a time issue when you need to get the nursing supervisor at night. If you've got a 24hr pharmacy - that's where it will ALWAYS be.

It will also always be in the OR - somewhere. Probably in the OR pyxis - go check.

It will also be in the ER pyxis. That is normally where most every drug which might be needed anywhere is kept.

If you don't find it where you think it should be - bring it up with the dop realizing it is expensive & will expire (which means - the more places it is kept there is always a possibility we don't catch it before it expires - not good!).

We want it where you need it to be -- accessible & easy to find & use.

 

[sdn1977]

SOme books say propanolol because it also inhibits peripheral conversion of t3-->t4. DO all beta-blockers do this or is it just propanolol specific? Because I don't know where the hell to find propanolol now-a-days.

They all do this, but not to the same degree. I THINK it is due to the lipid solubility & thus the affinity for the cytochrome P-450 system. The stronger the binding of one compound to the cytochrom p-450, the greater its potential might be for inhibiting a competing molecule for the same system.

Propranolol is most lipid soluble, metoprolol intermediate & atenolol is least. Since one of the speculations for the differing effects beta blockers have on antipyrine metabolism, this might be one of only many possiblities. Researchers looked at antipyrine since it is metabolised by the liver similar to thyroxine & is an easier molecule to follow.

This may be very old information since I believe it was reported in the British Medical Journal many, many years ago - I have a torn & tattered copy.

You can still find propranolol if you can find your pharmacist. Look for that person & you'll find it. If you want it at hand, ask to have it be put in pyxis - it costs pennies & if you use it, its easy to put there.

 

[tussionex]

They all do this, but not to the same degree. I THINK it is due to the lipid solubility & thus the affinity for the cytochrome P-450 system. The stronger the binding of one compound to the cytochrom p-450, the greater its potential might be for inhibiting a competing molecule for the same system.

Propranolol is most lipid soluble, metoprolol intermediate & atenolol is least. Since one of the speculations for the differing effects beta blockers have on antipyrine metabolism, this might be one of only many possiblities. Researchers looked at antipyrine since it is metabolised by the liver similar to thyroxine & is an easier molecule to follow.

This may be very old information since I believe it was reported in the British Medical Journal many, many years ago - I have a torn & tattered copy.

You can still find propranolol if you can find your pharmacist. Look for that person & you'll find it. If you want it at hand, ask to have it be put in pyxis - it costs pennies & if you use it, its easy to put there.

propranolol goes in our pyxises and on our OR carts. so, you can still find it if you come to NY!