Case from this weekend

[Idiopathic]

---

Members do not see this ad.

For those peeps who keep arguing for Sux>>>Roc, what benefit do you get over RSI dosed Roc? Do a few seconds quicker onset outweigh your side effect profile? You're likely gonna paralyze the guy intraop regardless. And while AssLoadOfRoc is gonna hang around for a while afterward, how many of you think it's highly probable you're gonna get this guy extubated at the case's conclusion anyhow? Thoughts?

i think this guy gets extubated at the end of the case. i would use sux. of course, i also dont think his sats are 80.

 

[W222]

I think we are ready for the answer as to how this gem played out????????

 

[VentdependenT]

lemme guess. preoxygenate with 3vital capacities 100%fio2, propofol, roc, tube, antiemetic, reversal, extubate.

If there is US you can effectively rule out PTX if there is pleural shimmering (lung pleura sliding) and B-lines(look sort of like spotlights) along with MMode showing motion artifact below pleura.

 

[glorfindel]

I didnt say that. flippen misrepresentin me dog

I believe in the context you are using it, the correct spelling is dogg.

Or, perhaps, this is just a regional difference...

(I agree, we are near the end. Tell us, OP, what happened with the case.)

 

[VentdependenT]

It would be "Dee Oh Double Gee"

 

[glorfindel]

Or else it would be "Dee Oh Gee."

 

[jetproppilot]

okay, these are all great points; however, you have to assume that for him to get to you

ready to roll back to the OR

hes had a workup of his trauma. if he is sitting there talking to you, not short of breath, not hemodynamically unstable, its unlikely hes had a

big PE

pneumo

acute right heart failure

it is more likely that he has

acute monitor failure

with that said

obviously

do a full workup, H&P, etc. get a CXR...all the stuff that will be on your boards. then, the answer you will likely come up with is

prop/sux/tube

extubate to BIPAP if you have to, overnight in PACU/23 hour obs

UMMM DUDE YOU'RE USING BOLD A S S FONTS.

For the record.

That just happened.😀

 

[lushmd]

Lots of great thoughts/input. OK, here is how I proceeded:

(1) Venue: Before discussing doing this case in the main hospital OR vs eye center with the attending ophthalmologist, I spoke with the attending anesthesiologist on call (and in house) for the main ORs re the local practice pattern about this (for those in practice, consider this comparable to running something past a senior partner). Despite my strong preference for doing this case in the main OR, he indicated that this isn't done due to specialized equipment needs of the ophtho folks. On the upside, he offered to be present during induction/intubation in case extra help was needed. Also, regardless of venue, the pt would recover in the main hospital PACU and could be admitted there if needed. I definitely would not have done this case at a free standing ASC.

(2) Hypoxemia: Certainly concerning. As far as I could tell, this was accurate (good waveform, same reading obtained with new sensor and also using a transport monitor). Interestingly, the pt wasn't dyspneic. Although PE (unlikely given that for him to have a PE large enough to cause this, he'd be in far worse shape), PTX (unlikely given negative CXR and mechanism of injury; when I said low speed I meant it: he was parked and hit by a car traveling at low speed in a parking lot), pulm contusion (no rib fx, inadequate mechanism of injury), etc... are all possible, I think that this was due to a combination of restrictive lung disease due to morbid obesity (this is likely what whomever told him about "small lungs" was referring to) exacerbated by supine positioning, OHS exacerbated by narcotics given in the ED (2 mg dilaudid), and untreated reactive airway disease (although the pt denied it, a previous ED record indicated a history of asthma). Reassuringly, his SpO2 improved to the low 90s (probably his baseline) with a bit of reverse T-berg and albuterol; 100% with supplemental oxygen.

(3) Airway management: Had glidescope, difficult airway cart (with fiberoptic scope set up, LMA, intubating LMA, etc...), and personnel (me, CRNA, main OR attending anesthesiologist, and anesthesia tech). Excellent pre-oxygenation (facemask with rubber strap and a bit of PEEP, ETO2 ~85%, etc...), modified RSI with lidocaine, propofol, defasciculating dose of rocuronium, and sux (sure, there's the theoretical possibility of increased IOP from sux but this is far outweighed by airway concerns; to those who advocated high dose rocuronium because this pt is unlikely to be extubated at the end of the case anyway, I'd posit that it's OK for certain pts to remain intubated/mechanically ventilated post-op but, barring pseudocholinesterase deficiency etc..., it shouldn't be due to excess paralysis). Able to ventilate with two people and an oral airway. Facile intubation with glidescope.

(4) Analgesia: No opiods or midazolam administered. At the end of the procedure, retrobulbar block done by opthalmologist. Also, IV tylenol. Pt was quite comfortable post-op.

(5) Disposition: At the conclusion of the procedure, pt positioned sitting upright and paralysis reversed fully. The trick here was to extubate this pt wide awake but still minimize bucking/increased IOP. I squirted lidocaine down the ETT while he was still deep and then gave a small bolus of propofol as the gas wore off (took a bit of time even using a low flow approach and desflurane); could have been smoother but worked OK. The nasal airway that was inserted after intubation came in handy here. We stayed in the OR for a bit following extubation to make sure that he was stable prior to the ~5 min transport from the eye center OR to the main hospital PACU. I had discussed the possibility of post-op admission with the pt and surgeon but ultimately this proved unnecessary. Within 1 hr post-op, he was off supplemental oxygen and the nasal airway was out. We watched him for another three hours during which he remained stable and then discharged him home (with follow-up the next day).

To be honest, this case went far better than I'd anticipated at the beginning; while I have no doubt that luck played a significant part, I think that my course of action was reasonable. In any case, it was a solid learning opportunity for me and, along those lines, I welcome your comments.

 

[glorfindel]

My comment is,

How is this dude getting an open-globe injury from a low-speed mva?

And it's his second open-globe?

He must be doing something wrong somewhere. Consult social work.

 

[aredoubleyou]

Lots of great thoughts/input. OK, here is how I proceeded:

(1) Venue: Before discussing doing this case in the main hospital OR vs eye center with the attending ophthalmologist, I spoke with the attending anesthesiologist on call (and in house) for the main ORs re the local practice pattern about this (for those in practice, consider this comparable to running something past a senior partner). Despite my strong preference for doing this case in the main OR, he indicated that this isn't done due to specialized equipment needs of the ophtho folks. On the upside, he offered to be present during induction/intubation in case extra help was needed. Also, regardless of venue, the pt would recover in the main hospital PACU and could be admitted there if needed. I definitely would not have done this case at a free standing ASC.

(2) Hypoxemia: Certainly concerning. As far as I could tell, this was accurate (good waveform, same reading obtained with new sensor and also using a transport monitor). Interestingly, the pt wasn't dyspneic. Although PE (unlikely given that for him to have a PE large enough to cause this, he'd be in far worse shape), PTX (unlikely given negative CXR and mechanism of injury; when I said low speed I meant it: he was parked and hit by a car traveling at low speed in a parking lot), pulm contusion (no rib fx, inadequate mechanism of injury), etc... are all possible, I think that this was due to a combination of restrictive lung disease due to morbid obesity (this is likely what whomever told him about "small lungs" was referring to) exacerbated by supine positioning, OHS exacerbated by narcotics given in the ED (2 mg dilaudid), and untreated reactive airway disease (although the pt denied it, a previous ED record indicated a history of asthma). Reassuringly, his SpO2 improved to the low 90s (probably his baseline) with a bit of reverse T-berg and albuterol; 100% with supplemental oxygen.

(3) Airway management: Had glidescope, difficult airway cart (with fiberoptic scope set up, LMA, intubating LMA, etc...), and personnel (me, CRNA, main OR attending anesthesiologist, and anesthesia tech). Excellent pre-oxygenation (facemask with rubber strap and a bit of PEEP, ETO2 ~85%, etc...), modified RSI with lidocaine, propofol, defasciculating dose of rocuronium, and sux (sure, there's the theoretical possibility of increased IOP from sux but this is far outweighed by airway concerns; to those who advocated high dose rocuronium because this pt is unlikely to be extubated at the end of the case anyway, I'd posit that it's OK for certain pts to remain intubated/mechanically ventilated post-op but, barring pseudocholinesterase deficiency etc..., it shouldn't be due to excess paralysis). Able to ventilate with two people and an oral airway. Facile intubation with glidescope.

(4) Analgesia: No opiods or midazolam administered. At the end of the procedure, retrobulbar block done by opthalmologist. Also, IV tylenol. Pt was quite comfortable post-op.

(5) Disposition: At the conclusion of the procedure, pt positioned sitting upright and paralysis reversed fully. The trick here was to extubate this pt wide awake but still minimize bucking/increased IOP. I squirted lidocaine down the ETT while he was still deep and then gave a small bolus of propofol as the gas wore off (took a bit of time even using a low flow approach and desflurane); could have been smoother but worked OK. The nasal airway that was inserted after intubation came in handy here. We stayed in the OR for a bit following extubation to make sure that he was stable prior to the ~5 min transport from the eye center OR to the main hospital PACU. I had discussed the possibility of post-op admission with the pt and surgeon but ultimately this proved unnecessary. Within 1 hr post-op, he was off supplemental oxygen and the nasal airway was out. We watched him for another three hours during which he remained stable and then discharged him home.

To be honest, this case went far better than I'd anticipated at the beginning; while I have no doubt that luck played a significant part, I think that my course of action was reasonable. In any case, it was a great learning opportunity for me and, along those lines, I welcome your comments.

The only thing I do not like about this is your mask ventilation of a guy this big. I think the two hand jaw lift with all your might can cause increased pressure on the eyes depending on where your hands are...and if you can't ventilate your not going to be as careful. As I said before my preference is an awake gylde to avoid this problem (as well as others). I also may have been more hesitant to extubate a guy with a baseline sat of 81%, but obviously I woulda been wrong on this one. I would however have pushed for an overnight tele, despite seemingly being fine post-op. as far as the sux issue, it's pure unfounded dogma that has never been proven to occur, but has been used extensively without problems. Also as a side note, in my humble opinion, having a fob as a backup for airway rescue is a waste of time, if you think you need a fob it should be your plan A. There's very little chance you'll have the time, oxygen reserve, or airway patenxy to wiggle that into the trachea. some people seem to want to teach residents that having every airway device under the sun out and available makes the initial plan A fool-proof.

 

[pgg]

Thanks for posting.


I'm curious about others' opinions on a related topic - defasciculating doses.

Been a while since I read about this, but isn't there some question of whether or not the increase in IOP is really due to fasciculations? I remember reading some animal studies where they cut the extraocular muscles and still observed the increase in IOP. Here's one:

http://jpet.aspetjournals.org/content/162/1/1

They did note the increase in IOP was prevented by pretreating with D-tubo, but that wasn't really a 'defasciculating' dose ... it was a full blown ED95 dose, so the animals had dense nondepolarizing blocks before the succ was given.


I bring this up because I am not convinced of the utility of defasciculating doses for anything, from succ-induced myalgias to succ-induced increases in IOP. I never pretreat a patient who's going to get succ with a nondepolarizer.

The only thing I'm convinced a defasciculating dose really does is slow the onset of succ. And if I'm using succ, its fast onset is what I'm interested in.


Just curious if there are some other dogma vs data opinions on this.

 

[soonerfrog]

http://mobile.journals.lww.com/anes...ewer.aspx?year=2003&issue=07000&article=00033

I stand corrected. I was thinking there had been at least a few documented case reports in the literature somewhere about a Sux-induced extravasation of ocular contents. Guess it was either anecdotal or theoretical. Or at least more likely attributed to any of the other thousands of things that more appreciably increase IOP. Still......great case----------to share, not to do. 😉

 

[pie944]

The only thing I'm convinced a defasciculating dose really does is slow the onset of succ. And if I'm using succ, its fast onset is what I'm interested in.


Just curious if there are some other dogma vs data opinions on this.

Never do it for this exact reason, if you are utilizing succinylcholine for onset, it seems counter-intuitive to give a drug prior that will compete with the mechanism of succinylcholine.

I think the article in the previous post is a great one that shows how concern over succinylcholine use and IOP all started.

This article explains the following

1) IOP increases within 1 minute and peaks at an increase of 9 mm Hg within 6 minutes after succinylcholine administration
2) The exact mechanism of this increase is unknown.
3) Some feel that tonic contractions of the extraocular muscles may explain this IOP increase.
4) In a study of 15 patients undergoing elective enucleation, succinylcholine was given after all the extraocular muscles to the diseased eye had been detached. There was no difference in IOP increase between the detached and intact eyes
5) It is now thought that succinylcholine-induced IOP increase is a vascular event, with choroidal vascular dilatation or a decrease in drainage secondary to elevated central venous pressure, temporarily inhibiting the flow ofaqueous humor through the canal of Schlemm

 

[45408]

Do the right thing. Have him transferred to a real facility. He ain't going home afterwards, in fact, it sounds like with that sat of 81% he will be getting a trach and peg afterwards in the coming weeks.

He was at home, driving, with a (supposedly) isolated orbital injury. Why would he be getting trached and PEG'd for that? I've never had to do either of those for someone in this situation.

 

[gasp]

Lots of great thoughts/input. OK, here is how I proceeded:

(1) Venue: Before discussing doing this case in the main hospital OR vs eye center with the attending ophthalmologist, I spoke with the attending anesthesiologist on call (and in house) for the main ORs re the local practice pattern about this (for those in practice, consider this comparable to running something past a senior partner). Despite my strong preference for doing this case in the main OR, he indicated that this isn't done due to specialized equipment needs of the ophtho folks. On the upside, he offered to be present during induction/intubation in case extra help was needed. Also, regardless of venue, the pt would recover in the main hospital PACU and could be admitted there if needed. I definitely would not have done this case at a free standing ASC.

(2) Hypoxemia: Certainly concerning. As far as I could tell, this was accurate (good waveform, same reading obtained with new sensor and also using a transport monitor). Interestingly, the pt wasn't dyspneic. Although PE (unlikely given that for him to have a PE large enough to cause this, he'd be in far worse shape), PTX (unlikely given negative CXR and mechanism of injury; when I said low speed I meant it: he was parked and hit by a car traveling at low speed in a parking lot), pulm contusion (no rib fx, inadequate mechanism of injury), etc... are all possible, I think that this was due to a combination of restrictive lung disease due to morbid obesity (this is likely what whomever told him about "small lungs" was referring to) exacerbated by supine positioning, OHS exacerbated by narcotics given in the ED (2 mg dilaudid), and untreated reactive airway disease (although the pt denied it, a previous ED record indicated a history of asthma). Reassuringly, his SpO2 improved to the low 90s (probably his baseline) with a bit of reverse T-berg and albuterol; 100% with supplemental oxygen.

(3) Airway management: Had glidescope, difficult airway cart (with fiberoptic scope set up, LMA, intubating LMA, etc...), and personnel (me, CRNA, main OR attending anesthesiologist, and anesthesia tech). Excellent pre-oxygenation (facemask with rubber strap and a bit of PEEP, ETO2 ~85%, etc...), modified RSI with lidocaine, propofol, defasciculating dose of rocuronium, and sux (sure, there's the theoretical possibility of increased IOP from sux but this is far outweighed by airway concerns; to those who advocated high dose rocuronium because this pt is unlikely to be extubated at the end of the case anyway, I'd posit that it's OK for certain pts to remain intubated/mechanically ventilated post-op but, barring pseudocholinesterase deficiency etc..., it shouldn't be due to excess paralysis). Able to ventilate with two people and an oral airway. Facile intubation with glidescope.

(4) Analgesia: No opiods or midazolam administered. At the end of the procedure, retrobulbar block done by opthalmologist. Also, IV tylenol. Pt was quite comfortable post-op.

(5) Disposition: At the conclusion of the procedure, pt positioned sitting upright and paralysis reversed fully. The trick here was to extubate this pt wide awake but still minimize bucking/increased IOP. I squirted lidocaine down the ETT while he was still deep and then gave a small bolus of propofol as the gas wore off (took a bit of time even using a low flow approach and desflurane); could have been smoother but worked OK. The nasal airway that was inserted after intubation came in handy here. We stayed in the OR for a bit following extubation to make sure that he was stable prior to the ~5 min transport from the eye center OR to the main hospital PACU. I had discussed the possibility of post-op admission with the pt and surgeon but ultimately this proved unnecessary. Within 1 hr post-op, he was off supplemental oxygen and the nasal airway was out. We watched him for another three hours during which he remained stable and then discharged him home (with follow-up the next day).

To be honest, this case went far better than I'd anticipated at the beginning; while I have no doubt that luck played a significant part, I think that my course of action was reasonable. In any case, it was a solid learning opportunity for me and, along those lines, I welcome your comments.

Glad the case went well.. Why did u go with modified RSI with mask ventilation (with 2 people) instead of just tubing him right after the sux? Did his sat drop?

 

[BLADEMDA]

I'd have used high dose rocuronium in this case. 1-1.2 mg/kg of rocuronium and da tube. Most f these cases take 2 hours anyway so reversal is almost always possible even at 1.2 mg/kg.

But, I don't work at an eye center so I've got lots of experience with trauma, obesity and difficult airways.
A more junior person may be reluctant to use high dose roc over sux here.

 

[BLADEMDA]

Use of succinylcholine as muscle relaxant although theoretically is contraindicated and controversial 5 but no published report has come so far causing further eye damage. In rapid sequence induction, Libonati and coworkers 23, 24 did not encountered aspiration of gastric contents or extrusion of eye contents. Other worker Bourke25 used succinylcholine successfully and carefully without encountering much problem. However, the significance of lack of reported cases is strengthened by an argument based on biologic plausibility. When an open globe injury has occurred, it is often associated with crying. Valsalva maneuver, forceful blinking and rubbing the eyes, all of which create a much larger rise in IOP than associated with the use of succinylcholine 3, 26, 27. Thus increase in IOP produced by succinylcholine may be tempered by sedatives28 and the induction agents in setting of rapid sequence induction for the repair of acute injuries and may prevent more devastating eye injury by profoundly paralyzing the muscles of chest and avoiding coughing. Advocating the evidence based practice and controversies regarding use of succinylcholine, ultimately majority have agreed to modify the technique of rapid-sequence induction with presently available faster acting dose dependent non depolarizing blocking agents for providing good relaxation 5, 29. In practice the risk is minimized by the prior administration of the induction agents which reduce IOP, e.g. small dose of non depolarizing muscle relaxant, diazepam, lignocaine, acetazolamide, and self taming dose of succinylcholine. The anaesthesiologist must however weigh the risk to the eye against the risk of aspiration of gastric contents 2, 3, 4, 5. - See more at: http://archive.ispub.com/journal/th...y-with-full-stomach.html#sthash.NXThe5Qt.dpuf

 

[aredoubleyou]

I'd have used high dose rocuronium in this case. 1-1.2 mg/kg of rocuronium and da tube. Most f these cases take 2 hours anyway so reversal is almost always possible even at 1.2 mg/kg.

But, I don't work at an eye center so I've got lots of experience with trauma, obesity and difficult airways.
A more junior person may be reluctant to use high dose roc over sux here.

Roc with sats 81% preop? This guy is gunna desat quick and you'll have to wait a bit for the roc to guarantee he aint going to buck on intubation.

 

[slunk]

Slim,

A Saturation of 81% sets off alarm bells. I'd place an arterial line right off the bat or at least send an ABG. Yes, I would make sure the pulse oximetry is functioning properly.
I would also get a CXR. At my institution I could get an ABG and CXR in under 10 minutes with a Radiologist assisting me (if needed) for the read. I could also get a CT scan in under 30 minutes (total time needed) if I spoke with the Radiologist. We need to rule out pneumothorax, rib fractures, pulmonary contusion, etc. so at least do a quick exam and get the CXR.

As for the bedside Echo I can call a tech or do the exam myself in under 5 minutes in the holding area. If I call the echo tech then it would take 20 minutes. This quick Transthoracic echo would provide additional info to me which may help in the care of this patient. (Pericardial Effusion from MVA, decreased LV or RV function, Significant MR, etc).

I could work this guy up pretty well in under an hour with labs, tests, etc. and if that Saturation is 81% then he needs some basic tests. Please note I didn't order a single consult except a quick conversation with a radiologist via phone.

I've been at this gig a long time including Trauma anesthesia and this guy shouldn't just be slamed off to sleep without any further work-up due to an eye injury.

Ultimately, he needs a General Anesthetic so you could argue then is no point in delay but I've seen more than one death in the O.R. due to poor preop workup in a trauma. So, It ain't gonna happen on my shift if I can help it.

One last thing I've seen EVERY thing imaginable missed by the ER over my career including Pneumos, Pericardial Tamponade, Cervical Fractures, etc so NEVER assume they didn't miss something.

What are you looking for on the ABG that the room air Sat of 81% doesn't tell you? CO2 level? Severity of acidosis? You can already approximate the PaO2.

Looking for a cause of such a low Sat in a sick guy and/ or a trauma patient is reasonable.

Not sure I would delay the case for an ABG though.

 

[pgg]

What are you looking for on the ABG that the room air Sat of 81% doesn't tell you? CO2 level? Severity of acidosis? You can already approximate the PaO2.

Looking for a cause of such a low Sat in a sick guy and/ or a trauma patient is reasonable.

Not sure I would delay the case for an ABG though.

It would give you an idea of whether his current level of CO2 retention is chronic vs acute. In a COPD'er who's just come off an exacerbation and steroid taper, who just had some vague trauma story (slo-mo MVA in a parking lot but open globe injury is weird), who is hypoxic ... there's enough color to this story, and enough doesn't obviously add up that I'd like to see an ABG and CXR.

For all I know his primary emergency is respiratory failure, not the open globe.

 

[BLADEMDA]

Roc with sats 81% preop? This guy is gunna desat quick and you'll have to wait a bit for the roc to guarantee he aint going to buck on intubation.

On 100 percent oxygen with bag assist this patient's saturation is pretty decent. IMHO which includes more than 2 decades of trauma this patient won't buck at all after 1.2 mg/kg of rocuronium. I'd place an arterial line and induce with propofol and rocuronium. The arterial line wouldn't take long to place either (in my hands).

I've seen it all slim. I mean all. This guy's airway is not that atypical and his history at the VA should give you reasonable assurance the glidescope is more than enough backup here

 

[EtherBunny]

Interesting case...thanks for posting it! Great discussion, too.

Just a quick question for the attending anesthesiologists on this forum. The one thing that I'm curious about is the limited mouth opening issue. I understand the perioperative concerns with the low sat of uncertain etiology, morbid obesity, trauma, OSA, operative setting, and open globe. But what about the limited mouth opening issue?

Would any of you be concerned about the possibility of NOT being able to instrument the airway via DL or glidescope because of the limited mouth opening? That was one of my concerns in reading the case, but it seems you all weren't concerned about that issue.

Just curious what your thoughts are.

 

[IlDestriero]

Interesting case...thanks for posting it! Great discussion, too.

Just a quick question for the attending anesthesiologists on this forum. The one thing that I'm curious about is the limited mouth opening issue. I understand the perioperative concerns with the low sat of uncertain etiology, morbid obesity, trauma, OSA, operative setting, and open globe. But what about the limited mouth opening issue?

Would any of you be concerned about the possibility of NOT being able to instrument the airway via DL or glidescope because of the limited mouth opening? That was one of my concerns in reading the case, but it seems you all weren't concerned about that issue.

Just curious what your thoughts are.

If the airway is big enough for a glide, it's big enough. Anyone use a Bullard anymore? I loved that scope. Only needed about 1cm mouth opening. Slick in a trauma. My old go to. It did take some practice to get used to though. Now everything is glide>> fiber. I question the fiber skills of the new trainees.

 

[sucstotherescue]

First off. I appologize about responding to this post so late. I just found this forum, and I must say you guys have some hell of good cases/discussions (sprinkled in with the necessary SDN BS). A hell lot better than what happens on our dental forum. Anyway, awesome case and discussion

Completely agree with everyone the low PaO2 is the largest concern For the sake of discussion I am going to say that the probe was on a bloody fingernail from the MVA and read 93% on RA on a different digit. I also going to assume trauma workup was sound and no pneumo/tamponade etc. Not sure about you guys but people at my hopsital get worked up for pneumo/tamp for what seems to be ear infections (joking on that, well kind of). I also going to give a ton of credit to my senior resident for discussing this case with me. I have long ways to go to reach his level.

Anyway, I only saw one response suggesting a Prop/Sevo induction to make sure they could ventilate the guy first. I know from experience that two divided doses of 50mg Prop (or some similar amount given wieght) about 90 seconds apart can be enough (if you give it time to work) to see if you can assist someone ventilating spontaneously.

1) If you can ventilate without difficulty, be generous with the opioid/rocuronium and turn on some sevo.

2) If ventilation is difficult, but adequate to sustain oxygenation then I would crack open the sevo and take a peak via DVL (or glide scope).

3) If I like what I see then I would back out, push some opioid/roc and intubate.

4) If the initial peak looks challenging still but I can see some semblance of arytenoid anatomy, then I may try to spray the cords with the LTA, IV lido 1mg/kg, mask a little longer for the lido to work, then spray a second time and intubate over the LTA as a conduit.

5) If the intial peak still looks impossible, then I'm deciding if my ability to oxygenate is adequate enough to proceed with asleep FOI or if he needs to be awake for the whole process.

At that point we would have done our due diligence with the issue of raising IOP. The risk of can't intubate/cant ventilate takes precedence over the globe. Not to say that the FOI cant be done without raising IOP, but it has become a secondary issue. I suppose you could do the transtracheal before waking him up. In my opinion the beauty of steps 2-4 is that you are attenuating IOP according to your ability to oxygenate. Full paralysis and opioids or topical/IV lidocaine if I feel I may need to wake this patient back up.

One important thing to note is that SUX raises IOP by cycloplegia which is independent of extraocular muscles (what I have learned). Therefore a defasciculating dose of sux or a priming dose of rocuronium will not avoid increasing IOP. Links to articles showing this below.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1815403/pdf/procrsmed00301-0031.pdf
http://jpet.aspetjournals.org/content/162/1/1.full.pdf+html

Finally, agree with obvious not a surgery center case and agree need for full support of hospital. Feel free to correct me if I am missing something important. This is what is great about anesthesia lots of ways to skin a cat. You can always learn something (approach).