RA spine case

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ethilo

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Had an interesting case this CA-1 year and felt inspired to share. The details have been changed enough to be unidentifiable to them.

58 female russian-speaking only (If you speak Russian, insert any language that you don't speak here), BMI 42, with severe rheumatoid has had progressively worsening neck pain over the last year associated with facial numbness in the evening-time and inability to reach up into her cabinets at home because craning her neck back makes it so she can't lift her arms up out of weakness. MRI found to have severe hypertrophic synovitis C1-4 with diffuse severe C1-4 foraminal stenosis, C2-3 anterolisthesis of 4mm on extension films. She is scheduled for posterior O-C4 lami / fusion, C2/3 ganglionectomy.

PMH:
#. Rheumatoid arthritis - on methotrexate, chronic prednisone 10 mg daily
#. Chronic pain (assoc with RA) - Morphine 30 mg TID, gabapentin 300 mg TID, oxycodone 5-15 mg breakthrough. Pain is 7/10 this AM.
#. Depression - Escitalopram
#. HTN - Lisinopril 30 mg which she takes "when she feels like her BP is high." PACU BP 170/80. Last took it 2 days ago.
#. IDDM2 - insulin glargine 25 units BID. A1c 8.7
#. Asthma - Uses albuterol once weekly when outside on her farm.

Of note, she had a TTE 4 months ago at an ED for transient word-finding difficulties, demonstrated R>L shunt on saline bubble study and EF 40-45% with LV WMAs, moderate concentric LVH. Normal sinus rhythm. Obs, then discharged to follow-up (she didn't follow-up).

Exam:
- Morbidly obese, thick neck, MP4, limited neck extension due to pain, actively complaining of R facial / occipital pain. Edentulous.
- RRR, lungs have trace wheezing diffusely.
- 1+ pitting edema in legs.

22g IV placed by pacu RN

Neuromonitoring is SSEPs, EMGs, MEPs, prone positioning with head in pins

Plan? preop / induction / monitoring / access / maintenance / dispo

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Positive thing is she doesn't speak english so it will be harder for her to sue. Negative all the rest...
Botom line your proper fcked, if you can intubate which you should with proper positioning proceed and hope she lives to pod 1 then you're in the clear.
 
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Oral board answer:
Delay surgery for proper BP and blood sugar control, start diuretic, consult pain doc to switch anti depressant to amitriptylin and increase gabapentin, counsel for weight loss yada yada...
Real world: it ain't going to happen so you do the case get paid although not enough to cover for the days of your life lost and hope for the best.
 
Had an interesting case this CA-1 year and felt inspired to share. The details have been changed enough to be unidentifiable to them.

58 female russian-speaking only (If you speak Russian, insert any language that you don't speak here), BMI 42, with severe rheumatoid has had progressively worsening neck pain over the last year associated with facial numbness in the evening-time and inability to reach up into her cabinets at home because craning her neck back makes it so she can't lift her arms up out of weakness. MRI found to have severe hypertrophic synovitis C1-4 with diffuse severe C1-4 foraminal stenosis, C2-3 anterolisthesis of 4mm on extension films. She is scheduled for posterior O-C4 lami / fusion, C2/3 ganglionectomy.

PMH:
#. Rheumatoid arthritis - on methotrexate, chronic prednisone 10 mg daily
#. Chronic pain (assoc with RA) - Morphine 30 mg TID, gabapentin 300 mg TID, oxycodone 5-15 mg breakthrough. Pain is 7/10 this AM.
#. Depression - Escitalopram
#. HTN - Lisinopril 30 mg which she takes "when she feels like her BP is high." PACU BP 170/80. Last took it 2 days ago.
#. IDDM2 - insulin glargine 25 units BID. A1c 8.7
#. Asthma - Uses albuterol once weekly when outside on her farm.

Of note, she had a TTE 4 months ago at an ED for transient word-finding difficulties, demonstrated R>L shunt on saline bubble study and EF 40-45% with LV WMAs, moderate concentric LVH. Normal sinus rhythm. Obs, then discharged to follow-up (she didn't follow-up).

Exam:
- Morbidly obese, thick neck, MP4, limited neck extension due to pain, actively complaining of R facial / occipital pain. Edentulous.
- RRR, lungs have trace wheezing diffusely.
- 1+ pitting edema in legs.

22g IV placed by pacu RN

Neuromonitoring is SSEPs, EMGs, MEPs, prone positioning with head in pins

Plan? preop / induction / monitoring / access / maintenance / dispo
she needs to finish her workup/treatment for her TIA/cardiac issues. Once you have cardio's blessing then glidescope vs awake FIO, avoid hypoxia hypotension, ect.
 
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I am concerned that she has pulmonary hypertension (something has to be causing her R-sided pressures to be elevated enough to create the R->L shunt). Although this is probably 2/2 her obesity, she should have it properly diagnosed and treated (her edema suggests she may not be optimized in this regard). This is not trivial in that mortality for patients with CHF having elective surgery is high, higher still for decompensated CHF, and with R-sided failure, well, I don't have to tell this group. Assuming she turns out not to have a more threatening diagnosis (my experience has been that patients with primary pulmonary HTN are much more brittle than those with secondary), and assuming she can be diuresed a bit (to what endpoint?), the case itself doesn't have to be difficult.

One point that hasn't received a lot of attention in these clinical posts, but which is increasingly on the radar, at least at my center, is the language issue. None of the things we want to do for this lady, from delaying her surgery, to having her see a cardiologist, to consent, to talking her through an awake intubation, work well without an interpreter. I'm sure some of the PP guys out there will say, "the hospital doesn't pay for interpreters, there's no time to call one, and in any case, we don't have the double-phone set-up, and it's all a pain in the ars." I simply can't accept that we are going to do surgery on someone like this because it's easier than slogging through the difficult communication to do the right thing.

At my center, we've adopted a policy where formal interpreters (in person or phone) have become the standard of care. Not a family member, and not an unvetted care provider (we have a process for vetting/approving bilingual providers). It may seem like overkill to some, but I just can't imagine myself being in some foreign country, unable to speak the language, and being comfortable going to surgery without knowing what's going on.
 
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Why is shunt R to L? PHTN I assume but don't you want to know this?
 
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So I'd like functional capacity information. You mention she can't reach cabinets due to symptoms of her cervical spine disease and I'm assuming she's fairly sedentary but you also mention a farm etc. Can she walk? How far? Has this changed? Has her swelling changed? CAD equivalents? Etc. How's her brain look on MRI? Word finding difficulties and a R--->L shunt could be DVT/thrombi....

With all that said she needs a RHC/LHC just based on WMA's on previous echo and R->L shunt. But literally, there isn't a single system on this woman that's "optimized" for elective surgery. We do these cases all the time and quite frankly we're crazy, that's a complete train wreck.
 
Too many unanswered questions that should be addressed before she is in the holding area with a #22 IV!
She obviously has a septal defect in the heart somewhere (not clear from the OP) and she could have pulmonary HTN that is not quantified!
Her LVEF is low without clear diagnosis!
Her Diabetes is not well controlled.
So, she needs to go back to cardiology and get evaluated properly and she needs her diabetes better controlled.
I would say she could come back for surgery when these issues are addressed in a couple of months.
The plan then will be GA with good IV access and an Aline... nothing to complicated here.
 
Agree with postpone and need for further workup
Patient can't/won't follow up
Admit for expedited cardio/pulm/vascular workup
Carotid U/S would be nice
 
I am concerned that she has pulmonary hypertension (something has to be causing her R-sided pressures to be elevated enough to create the R->L shunt). Although this is probably 2/2 her obesity, she should have it properly diagnosed and treated (her edema suggests she may not be optimized in this regard). This is not trivial in that mortality for patients with CHF having elective surgery is high, higher still for decompensated CHF, and with R-sided failure, well, I don't have to tell this group. Assuming she turns out not to have a more threatening diagnosis (my experience has been that patients with primary pulmonary HTN are much more brittle than those with secondary), and assuming she can be diuresed a bit (to what endpoint?), the case itself doesn't have to be difficult.

One point that hasn't received a lot of attention in these clinical posts, but which is increasingly on the radar, at least at my center, is the language issue. None of the things we want to do for this lady, from delaying her surgery, to having her see a cardiologist, to consent, to talking her through an awake intubation, work well without an interpreter. I'm sure some of the PP guys out there will say, "the hospital doesn't pay for interpreters, there's no time to call one, and in any case, we don't have the double-phone set-up, and it's all a pain in the ars." I simply can't accept that we are going to do surgery on someone like this because it's easier than slogging through the difficult communication to do the right thing.

At my center, we've adopted a policy where formal interpreters (in person or phone) have become the standard of care. Not a family member, and not an unvetted care provider (we have a process for vetting/approving bilingual providers). It may seem like overkill to some, but I just can't imagine myself being in some foreign country, unable to speak the language, and being comfortable going to surgery without knowing what's going on.
FYI, providing an official interpreter is not just good medicine, it's the law. One doesn't want to end up being accused of assault and battery.
 
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Too many unanswered questions that should be addressed before she is in the holding area with a #22 IV!
She obviously has a septal defect in the heart somewhere (not clear from the OP) and she could have pulmonary HTN that is not quantified!
Her LVEF is low without clear diagnosis!
Her Diabetes is not well controlled.
So, she needs to go back to cardiology and get evaluated properly and she needs her diabetes better controlled.
I would say she could come back for surgery when these issues are addressed in a couple of months.
The plan then will be GA with good IV access and an Aline... nothing to complicated here.
What if this is her baseline? ;)

I don't want to be the wiseguy here but, besides her airway, this is the regular crappy American ASA 4 patient.

She probably has a PFO, like 20-25% of the general population. It's probably open from a degree of PHTN and RV failure, possibly from a rheumatoid lung or OSA. 1+ edema is not something so exciting. Her LVEF is slightly decreased, let's assume from CAD.

I am more concerned that her diabetes is poorly controlled, which will f*ck up healing. The surgeon should be, too.

BP is actually decent for preop. God bless her for not taking her ACEI on the day of surgery. And her asthma would qualify as mild intermittent.

If only my ICU patients were this healthy. :)

Seriously, I doubt she can be brought to a much better place on her "Fatling" curve.
 
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Would postpone. But hypothetically if you were forced to proceed (say critical cord compression), how many of you would float a swan since you can't TEE here?
 
Not if intervention changes management. And we don't if she needs intervention as there's been no testing/quantification.
What intervention? Diuresis? I don't see much else that could be changed. You will not control the diabetes in this lady (she has language barriers with other docs, too), and she will not get/need a PCI before the intervention (she's asymptomatic). Her respiratory status will not get significantly better.

Not only that, but that surgery doesn't come with significant hemodynamic strain, as far as I can remember.

And it's an urgent surgery. It cannot be postponed for more than a couple of months or so, and I doubt anything major would change in that period.

The oral board answer is different from the real world answer, as usual. I am not saying postponing is wrong, I am only saying it won't change much.
 
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FFP, she could be asymptomatic because she is a poorly controlled diabetic. I would hold off for further cardiac workup myself.
That is correct. Plus she probably lives a very sedentary life, especially with that RA.

All I am saying is that postponing won't change much. I bet she has CAD. It doesn't matter; she can't get a stent, maybe a BMS (if anybody still puts those in), with an upcoming urgent surgery next to her spinal cord.


m_07944_gr1.jpeg


Going through the algorithm: No, No, Elevated risk, No or unknown. The main question is "Will further testing impact decision making OR perioperative care? (Step 6)". And here we get into the coronary revascularization problem.

We should get used to this crap. Uneducated independent CRNAs will not postpone this kind of patient, and we will look like the incompetent bad guys.
 
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That is correct. Plus she probably lives a very sedentary life, especially with that RA.

All I am saying is that postponing won't change much. I bet she has CAD. It doesn't matter; she can't get a stent, maybe a BMS (if anybody still puts those in), with an upcoming urgent surgery next to her spinal cord.

How urgent/emergent is this surgery? People live with spinal stenosis for years.
Maybe she needs a stent/CABG first.

It's crappy either way you look at it, but God forbid she has a preoperative MI with morbidity/mortality on a non emergent case, you know you will get eaten alive. If her family or she sues that is. And then of course she also needs diuresis for the CHF, better glucose control, etc.

I had a patient I cancelled recently whose cardiologist had recently told him he needed a defibrillator, but it never happened for some reason. No one knows why. I said, go see the cardiologist, let him write me a nice little note of why this hasn't happened yet with your know non-perfusing arrthymia history and then we can talk.

Sounds like the wall motion abnormalities need further exploration.
 
I could be wrong, but I think that +-nuke scan and LHC is indicated for new-onset WMA regardless of symptomatology. Some data from the CathPCI registry was recently published...the majority of patients who underwent lhc before noncardiac surgery were asymptomatic, finding obstructive CAD was pretty common, and nearly half of those with obstructive disease ended up requiring revascularization. http://www.ncbi.nlm.nih.gov/pubmed/27018942

Granted, the biggest problem with her is that there's no point putting in a stent cause she'd have to stop DAPT almost immediately. However, it's possible there's a lesion that could be ballooned...ASA for 14 days then surgery.


vvv left heart cath
 
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How urgent/emergent is this surgery? People live with spinal stenosis for years.
Maybe she needs a stent/CABG first.

It's crappy either way you look at it, but God forbid she has a preoperative MI with morbidity/mortality on a non emergent case, you know you will get eaten alive. If her family or she sues that is. And then of course she also needs diuresis for the CHF, better glucose control, etc.

I had a patient I cancelled recently whose cardiologist had recently told him he needed a defibrillator, but it never happened for some reason. No one knows why. I said, go see the cardiologist, let him write me a nice little note of why this hasn't happened yet with your know non-perfusing arrthymia history and then we can talk.

Sounds like the wall motion abnormalities need further exploration.
Sorry, I missed the WMAs. That is more concerning to me than the LVEF.

You all are of course right. All I am saying is that she will come back probably in the same shape, except with the surgeon documenting that she has to have the surgery. Which is basically what we need.

And she could get paralyzed in the meanwhile, which is why I whould have a risks/benefits discussion with her and the surgeon about the value of postponing.
 
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I disagree here FFP.

She has WMAs, seen via a sensitive test for ischemia. She's diabetic and likely sedentary therefore less likely to be symptomatic, this does not mean she's normal risk for perioperative MI. This is not an urgent surgery from how I read it. So just looking at her likely CAD that's 1 modifiable risk factor. Sure, we can quibble over whether her spinal stenosis/listhesis whatever can wait X months, from what I see it can, surgeons of course will say no. Can I assume she has flow limiting CAD and maintain CPP at baseline with an a-line, limit CMRO2? Sure.

Next, her likely elevated PA pressures. Definitely may change my management, therefore I'd like to know. She may be elevated risk, which may be modifiable with treatment or periop management decisions. Do I think she's bad enough that I float a PAC? No. I'd assume she has increased PAP's and manage accordingly by minimizing fluctuations in CO2, preload etc. But unknown/unquantified Pulm HTN is certainly an increased risk.

What about her shunt? Sure, it's likely related to PAPs, which we discussed above. But they're also going to prone her, open a bunch of venous access for who knows what biological matter or air to enter. May that end up in her brain? Possibly. I call that modifiable.

I'm not concerned about the poorly controlled DM, the fact she needs stress dosed, or her ****ty airway. But the above concerns me enough that I want some answers prior to an elective case. If it's urgent etc am I comfortable proceeding with decent access and an a-line? Yup, but just cuz I can doesn't mean we should or that it's best to do from a risk standpoint.
 
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As I said, I had missed the WMAs.

Her pulmonary artery pressure might be hidden in the echo report. Or you could just do your own TTE (my preference), or put in an awake Swan, and find out. :)

Very good point about the shunt. She is at high risk for air embolus and stroke. I don't know how modifiable that is, except for closing her defect. Absent that, one could argue she needs a Swan in place.

@ethilo, how did the story end? Because I have a feeling the surgeon did not want to postpone this surgery. The question is also why wasn't this patient sent for a preanesthesia consult?
 
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I try to avoid unnecessary central access whenever possible, but I'd feel a whole lot better doing this unoptimized, prone, arms-tucked case with the ability to see CO/PAP in realtime and deliver appropriate therapeutics to central circulation ASAP. Was the right heart size/function normal on the TTE? Any mention of PAPs or valve abnormalities? Some might think a flotrac would suffice, but you run into problems with being prone, in addition to the likelihood that you will likely be ventilating her with <8cc/kg IBW tidal volumes.

I'd also be sure this case was being done on a Jackson table since it minimizes preload/CO derangements.
 
As I said, I had missed the WMAs.

Her pulmonary artery pressure might be hidden in the echo report. Or you could just do your own TTE (my preference), or put in an awake Swan, and find out. :)

Very good point about the shunt. She is at high risk for air embolus and stroke. I don't know how modifiable that is, except for closing her defect. Absent that, one could argue she needs a Swan in place.

@ethilo, how did the story end? Because I have a feeling the surgeon did not want to postpone this surgery. The question is also why wasn't this patient sent for a preanesthesia consult?
Hx of TIA and decreased EF without workup needs to be postponed and worked up if at all elective. Agree that likely nothing will be modified from cardiac standpoint( although if they find something in her carotids she is definitely a candidate for CEA prior to spine surgery), but if you take a patient with this kind of a history to the OR for an elective case without cardio and neuro's approval, and she has an intra-operative MI or CVA you are fuc@ed. Surgeon needs to document urgency/emergency to get this to the OR.
 
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Wow! Awesome discussion guys! Really appreciate it. This was a super fun case. To answer a few questions...
- She had no exercise tolerance, limited by RA pain in her legs. Could not stress herself with any examples at home.
- The TTE she got was of very poor quality (body habitus). They only reported "R>L shunt with saline bubble study" but could not identify an opening.
- I wanted to emphasize the language barrier in this case, too. My attending and I had a long talk about how to do this awake with the language barrier. Don't know if this could have been done in PP because we definitely didn't hit a 30 minute turnover on this (this was a case-to-follow, not first case start).

Here's the story:

Pre-op: APAP, gabapentin, midaz 2mg, fent 50 mg, 0.2 mg glyco, lidocaine nebulizer and OPA with 2% lido jelly on it that she was told to intermittently try to work back into the back of her throat while waiting in preop.

in OR:
Brought interpreter with us into the OR (A physical one was present, thank goodness. Bunny suited up and followed us in).
Awake A-line
Very good topicalization 4% lido pledgets held in tonsillar recesses 1 min per side by the clock, then 1 min on both sides of vallecula using a kidney pedical clamp
Awake FOB, no cough, pre/post tube placement grip strengths and questioning her for sensory changes, etc.

slowly titrated etomidate (I think we used ~8mg total), 3 more mg midaz, 200 mcg fent for induction. No major hemodynamic changes occurred.

Found an 18g in her foot and 18g US guided IV in her other arm. Lucky us.

Alfentanil for pins
Decadron 10 mg

motors were checked and present pre-flip.

Maintenance:
etISO 0.4
Ketamine 0.5 mg/kg then 4 mcg/kg/m gtt
Sufentanil 1 mcg/kg/hr
Prop 100 mcg/kg/hr
Phenylephrine

ABGs and CBGs
Goals: MAP goal 85, glucose <180, K>4
Avoid hypercarbia, hypoxia, etc.

6 hrs later...

Nasal airway placed intraop while in pins towards end of case with 2% lido jelly so it could numb her up by the time she was awake.

Emergence:
Suctioned early to avoid tachycardia
Esmolol titrated to keep HR <80
extubated with nasal airway, sitting upright

PACU > floor
Neurosurgery team to arrange follow-up with cardiology outpatient at discharge.
 
Lol at cardiology appointment after the biggest stress she's had in years....

So obviously we mentally masturbate over lots of stuff and we can get it done without going crazy, but one success (or dodged bullet) does not make one bulletproof.

Just as a discussion point as it looks like her pulm pressures weren't bad but what would you say a phenylephrine and ketamine gtt do to PAPs in someone with true Pulm htn?
 
Again, I've left out and changed some details to make this not an identifiable person. I agree I would definitely postpone and appreciate a better cardiac workup if I could but there were other medical, surgical, and social factors that stressed urgency.
 
How much phenylephrine did she require? And what was your fluid management plan?
 
How much phenylephrine did she require? And what was your fluid management plan?

Phenylephrine was only baby doses. Like 0.1-0.3 mcg.kg.m. we started it during the later stages of the procedure to counter a slowly slowly drifting drop in BP from the MAP of 85. At the time I felt was probably the context sensitive halftime accumulation of prop and sufenta (just a guess). UOP was surprisingly great intraop, like almost 1 mL/kg most of the case, we mainly replaced output for our fluid mgmt plan. We were worried about edema in the neck / face especially with it being an inflammatory condition and obviously avoiding volume overload.
 
this case never would've went without proper preop workup especially given her very concerning cardiac symptoms/findings of pHTN and decompensated HF.
 
Wow! Awesome discussion guys! Really appreciate it. This was a super fun case. To answer a few questions...
- She had no exercise tolerance, limited by RA pain in her legs. Could not stress herself with any examples at home.
- The TTE she got was of very poor quality (body habitus). They only reported "R>L shunt with saline bubble study" but could not identify an opening.
- I wanted to emphasize the language barrier in this case, too. My attending and I had a long talk about how to do this awake with the language barrier. Don't know if this could have been done in PP because we definitely didn't hit a 30 minute turnover on this (this was a case-to-follow, not first case start).

Here's the story:

Pre-op: APAP, gabapentin, midaz 2mg, fent 50 mg, 0.2 mg glyco, lidocaine nebulizer and OPA with 2% lido jelly on it that she was told to intermittently try to work back into the back of her throat while waiting in preop.

in OR:
Brought interpreter with us into the OR (A physical one was present, thank goodness. Bunny suited up and followed us in).
Awake A-line
Very good topicalization 4% lido pledgets held in tonsillar recesses 1 min per side by the clock, then 1 min on both sides of vallecula using a kidney pedical clamp
Awake FOB, no cough, pre/post tube placement grip strengths and questioning her for sensory changes, etc.

slowly titrated etomidate (I think we used ~8mg total), 3 more mg midaz, 200 mcg fent for induction. No major hemodynamic changes occurred.

Found an 18g in her foot and 18g US guided IV in her other arm. Lucky us.

Alfentanil for pins
Decadron 10 mg

motors were checked and present pre-flip.

Maintenance:
etISO 0.4
Ketamine 0.5 mg/kg then 4 mcg/kg/m gtt
Sufentanil 1 mcg/kg/hr
Prop 100 mcg/kg/hr
Phenylephrine

ABGs and CBGs
Goals: MAP goal 85, glucose <180, K>4
Avoid hypercarbia, hypoxia, etc.

6 hrs later...

Nasal airway placed intraop while in pins towards end of case with 2% lido jelly so it could numb her up by the time she was awake.

Emergence:
Suctioned early to avoid tachycardia
Esmolol titrated to keep HR <80
extubated with nasal airway, sitting upright

PACU > floor
Neurosurgery team to arrange follow-up with cardiology outpatient at discharge.
The Roulette landed on the right number this time...
 
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Just as a discussion point as it looks like her pulm pressures weren't bad but what would you say a phenylephrine and ketamine gtt do to PAPs in someone with true Pulm htn?

So, I actually give ketamine to almost all of my hearts, and I really don't see much of any change in PASP (by institutional tradition, we place our lines pre-induction), even for those with significant PAH. I'm sure there is a paper out there showing a statistically significant increase, but at 0.5mg/kg, I haven't seen any clinically significant increase in PA pressures in my practice.

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So, I actually give ketamine to almost all of my hearts, and I really don't see much of any change in PASP (by institutional tradition, we place our lines pre-induction), even for those with significant PAH. I'm sure there is a paper out there showing a statistically significant increase, but at 0.5mg/kg, I haven't seen any clinically significant increase in PA pressures in my practice.

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Interesting. We use Ketamine quite a lot at my program, mostly in the 0.5-0.75mg/kg range, but we rarely, if ever use it in the heart rooms. Sounds like I'm going to have to try ketamine out a bit more next year in fellowship. Thanks for this.

And as for the phenylephrine, we all use it, probably the most widely used drug in anesthesia outside of prop/versed/fentanyl, and the dose used here was tiny. But I think it's worth knowing that it may be counterproductive in weak or failing R hearts secondary to increased PAP. Phenylephrine has been shown to increase mPAP, RVEDP, and reduce PaO2 and CO to a statistically (though maybe not clinically) significant degree (in regards to CO at least). My point is giving phenylephrine to increase CPP in a CAD patient may in fact be counterproductive, particularly if increased RV afterload is the etiology of the RV dysfunction.
 
So, I actually give ketamine to almost all of my hearts, and I really don't see much of any change in PASP (by institutional tradition, we place our lines pre-induction), even for those with significant PAH. I'm sure there is a paper out there showing a statistically significant increase, but at 0.5mg/kg, I haven't seen any clinically significant increase in PA pressures in my practice.

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If the patient is on Beta Blockers, which is usually the case, you will not see much of a sympathetic response to Ketamine and that includes PA pressure.
 
I highly doubt that these lower doses of ketamine that we are using these days has any significant effect on pulmonary pressures. It may even lower them. It does lower airway pressures which could translate.
 
Wow! Awesome discussion guys! Really appreciate it. This was a super fun case. To answer a few questions...
...PACU > floor
Neurosurgery team to arrange follow-up with cardiology outpatient at discharge.

I realize that since you're finishing CA-1, you are stoked on these details (doing a MEP/SSEP anesthetic, suctioning early, etc).

But you and your attending, in my opinion, BLEW IT on this one.

The fact you think a neurosurgery team "arranging followup" for cardiology is adequate -- the same cardiology followup that the patient failed to go to preop, of her own volition, to treat her 3-4 major cardio/pulm/vascular issues -- shows that you missed the point. So you're saying that she essentially has NO followup.
 
@ethilo, how did the story end? Because I have a feeling the surgeon did not want to postpone this surgery. The question is also why wasn't this patient sent for a preanesthesia consult?

I have that feeling also. That feeling is surprisingly common even with patients who are presenting for surgery for problems that have been "getting worse over a year." :rolleyes:
 
Phenylephrine was only baby doses. Like 0.1-0.3 mcg.kg.m. we started it during the later stages of the procedure to counter a slowly slowly drifting drop in BP from the MAP of 85. At the time I felt was probably the context sensitive halftime accumulation of prop and sufenta (just a guess). UOP was surprisingly great intraop, like almost 1 mL/kg most of the case, we mainly replaced output for our fluid mgmt plan. We were worried about edema in the neck / face especially with it being an inflammatory condition and obviously avoiding volume overload.

Excuse my ignorance, but I have never heard of this.

Context sensitive half time only refers to the time required for a half life to occur following termination of infusion. I don't know of any point in time when an accumulation would lead to an increase in the effects of your infusion, assuming a steady maintenance state. Granted that's a minor point in the grand scheme of this case, but I have never heard of such a thing.
 
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