dopamine versus phenylephrine

This forum made possible through the generous support of SDN members, donors, and sponsors. Thank you.
using dopamine dose not prevent renal failure. i think at the doses that one would use to keep up the BP, you'll have alpha mediated vasoconstriction.
so dopamine induced urine output is just to make us feel good, but does nothing to protect the kidneys.

Phenylephrine would be my drug of choice to maintain BP.
 
I prefer fluid, usually blood. An 8-10 hour spine case is usually a bloody mess. They are always behind, as a rule. If the BP and/or UOP goes low, I reach for fluid (then blood) first, not a pressor.

-copro
 
coprolalia said:
I prefer fluid, usually blood. An 8-10 hour spine case is usually a bloody mess. They are always behind, as a rule. If the BP and/or UOP goes low, I reach for fluid (then blood) first, not a pressor.

-copro
Click to expand...

"I prefer fluid, usually blood." - Copro - I think that blood is a NO, NO for fluid replacement (and I mean whole blood) - except massive trauma resusicitation when you add fluids. Of course PRBC s are not volume.
I agree with fluids then vasopressors as a general rule for hypotension without to know the reason for hypotension. Volume, heart, SVR are part of the DD. If you think about tissue hypoxia (with acceptable perfusion) it is time for blood.
Noe between dopamine and phenylephrine - depends of the clinical picture.
Weak heart there - dopamine.
Good CO - neo.
2win
 
2win said:
"I prefer fluid, usually blood." - Copro - I think that blood is a NO, NO for fluid replacement (and I mean whole blood) - except massive trauma resusicitation when you add fluids. Of course PRBC s are not volume.
I agree with fluids then vasopressors as a general rule for hypotension without to know the reason for hypotension. Volume, heart, SVR are part of the DD. If you think about tissue hypoxia (with acceptable perfusion) it is time for blood.
Noe between dopamine and phenylephrine - depends of the clinical picture.
Weak heart there - dopamine.
Good CO - neo.
2win
Click to expand...

Man, we are having communication problems today... :laugh:

All of these patients bleed like stink, even if you use Amicar or whatever else. They inevitably need blood... not for volume or for UOP... but because they bleed like stink. If a patient is hypotensive and becoming increasingly tachycardic, and their Hct is low, I'm giving blood before I start neo.

That was my only point.

-copro
 
Jeff05 said:
using dopamine dose not prevent renal failure. i think at the doses that one would use to keep up the BP, you'll have alpha mediated vasoconstriction.
so dopamine induced urine output is just to make us feel good, but does nothing to protect the kidneys.

Phenylephrine would be my drug of choice to maintain BP.
Click to expand...

hasn't the whole "renal dosing" of dopamine been shown to not exist in a clinical setting and strictly a theoretical point?
 
RussianJoo said:
hasn't the whole "renal dosing" of dopamine been shown to not exist in a clinical setting and strictly a theoretical point?
Click to expand...

Yes, renal dose dopamine is BS.

But if a patient is having low urine output because of decreased cardiac output then dopamine in the beta agonist dosing range will be certainly helpful..
 
Appropriate doses of tranexemic acid and DDAVP can do wonders for blood loss in 8-10 hour spine cases. I am assuming you are doing scoliosis cases.

My group handles a ton of these cases and hearts and we use the same protocols for both types of cases.

Preop elimination of blood thinning meds (including herbal/holistic/all natural supplements containing high doses of platelet inhibiting substances), autologous/directed blood donation, epogen therapy, etc. are all methods to ensure optimum surgical conditions and minimize or obviate the need for transfusions.

Hopefully your surgeons are also on board with hemostasis as bleeding occurs and are not of the "ignore it and hope it clots" mindset.

I use neosynephrine in line on a microdrip to provide intermittent augmentation as needed and optimize fluid balance to the cc when at all possible. Overloading patients and blowing them up like puffer fishes can be problematic intraoperatively as well as postoperatively with dependent edema third spacing and increasing intracavitary pressures translating to increased epidural venous pressures and more bleeding.

Our typical primary adult, teen, or pedi scoli patients lose less than 20% of their blood volume intraoperatively, have most of it returned via cellsaver, and rarely need transfusions intraop or postop. We extubate in the OR and they typically stay in the ICU for 2 days primarily for more frequent and specific neurochecks and pain management.
 
Agreed UTSW, nice to see you again.

Cop, I think you are just trying to defend your previously poor answer of give blood. Thats fine if you want to defend it but in reality we should use what the pt calls for. If they are prone and sagging BP with low UOP the Hct can still be more than adequate therefore, you don't need to give blood. We do plenty of prone spine cases, luckily they are rarely over 5 hrs and we hardly ever need to give blood but I typically have some background neo running. Never needed dopa either because if their heart is weak enough to need dopa then our spine surgeon probably isn't going t book them for a 5-8 hr prone spine case.

My answer would be neo for most cases.
 
MY biggest concern with long prone spine cases is visual loss. Perioperative factors that have been implicated in the development of ION include intraoperative hypotension, duration of surgery, intraoperative blood loss, use of replacement fluids, and anemia.
Errors in fluid management (usually fluid excess) were the most common cause of perioperative morbidity and mortality. Edema compromises tissue oxygenation and produces an increase in tissue pressure in spaces like the orbital cone, which is surrounded by a nonexpandable space, thereby slowing microvascular perfusion, increasing arterial venous shunting, and reducing sympathetic drainage, all of which facilitate further edema formation.

The recently published American Society of Anesthesiologists Postoperative Visual Loss Registry by Lee et al. The POVL Registry data provide some important findings. They further reaffirmed the importance of the duration of surgery (94% cases took ≥ 6 hours) and blood loss (82% with > 1 L) as significant factors associated with POVL.

Interestingly, when using the CRAO (central retinal artery occlusion) group for comparison, the authors of the POVL Registry study were also able to highlight some important points. As stated earlier, the evidence for cause of CRAO was direct facial–orbital compression, and not as complicated and multifactorial as for ION. The authors were able to demonstrate that the lack of use of Mayfield pins and ipsilateral periocular trauma were statistically significant findings in the CRAO group. The importance of the duration of surgery and estimated blood loss were reconfirmed and statistically significant when the ION and CRAO groups were compared.

Particularly notable was the use of replacement fluids in those patients with ION. There was a significant statistical difference in the volume of crystalloid infusion in patients with subsequent ION compared with those in the CRAO group. An average of 9.7 L of crystalloids were infused in cases of ION compared with 4.6 L in others, whereas the hematocrit value comparison was not statistically significant (26 compared with 31, respectively). Previously, these two factors had been discussed in the literature with an overemphasis on postoperative anemia and with sparse mention of the importance of overhydration. Both of these factors may be interrelated and their significance is difficult to discern. However, fluid overload has been mentioned as possibly playing a role in past case reports, and this is the first study to highlight its importance.9,31

Clearly, other factors may play a role in the development of POVL. Intrinsic factors such as coexisting disease or ocular vascular anatomy or extrinsic factors such as operative frame and type of fluid used may also have an important but yet unknown role in this disease origin.

http://thejns.org/doi/full/10.3171/FOC-07/11/15?cookieSet=1

Cop, if you are doing these cases you should read this. Fluids are not necessarily the answer.
 
We do a ton of spine cases. The only time I would use a pressor infusion is if the patient isn't tolerating the anesthetic. This is usually apparent from the start of the case. 1st line for me would be phenylephrine because I'm going after pressure, not cardiac output. Later on in the case, hypotension would be more from hypovolemia, especially if it's at the decortication stage. I like to run maintenance fluids with 2 or 3% hypertonic saline (to minimize total volume) and transfuse as needed based on hemodynamics and hemoglobin. I do not like pressor infusions in this setting because it can mask hypovolemia. Instead I would use intermittent boluses as needed to give me time to catch up. Low urine output in the prone position has led some to give massive amounts of fluid without improvement, and simply makes the patient edematous. Probably >95% of our adult major spine cases (like the T5 to S1 type fusions) get extubated.
 
in general, give whatever fixes what you think the physiologic derangement is. Lots of bleeding? give blood/fluid. Vasodilation from anesthetics and pooling of blood in prone position? Give phenylephrine. Myocardial depression or need more CO? Dopamine (or other inotrope of choice, but you get the idea). In general the pressors in the spine cases tend to compensate for the original physiological derangement and allow you to be more conservative on giving fluids to avoid excess administration.
 
Noyac said:
MY biggest concern with long prone spine cases is visual loss. Perioperative factors that have been implicated in the development of ION include intraoperative hypotension, duration of surgery, intraoperative blood loss, use of replacement fluids, and anemia.
Errors in fluid management (usually fluid excess) were the most common cause of perioperative morbidity and mortality. Edema compromises tissue oxygenation and produces an increase in tissue pressure in spaces like the orbital cone, which is surrounded by a nonexpandable space, thereby slowing microvascular perfusion, increasing arterial venous shunting, and reducing sympathetic drainage, all of which facilitate further edema formation.

The recently published American Society of Anesthesiologists Postoperative Visual Loss Registry by Lee et al. The POVL Registry data provide some important findings. They further reaffirmed the importance of the duration of surgery (94% cases took ≥ 6 hours) and blood loss (82% with > 1 L) as significant factors associated with POVL.

Interestingly, when using the CRAO (central retinal artery occlusion) group for comparison, the authors of the POVL Registry study were also able to highlight some important points. As stated earlier, the evidence for cause of CRAO was direct facial–orbital compression, and not as complicated and multifactorial as for ION. The authors were able to demonstrate that the lack of use of Mayfield pins and ipsilateral periocular trauma were statistically significant findings in the CRAO group. The importance of the duration of surgery and estimated blood loss were reconfirmed and statistically significant when the ION and CRAO groups were compared.

Particularly notable was the use of replacement fluids in those patients with ION. There was a significant statistical difference in the volume of crystalloid infusion in patients with subsequent ION compared with those in the CRAO group. An average of 9.7 L of crystalloids were infused in cases of ION compared with 4.6 L in others, whereas the hematocrit value comparison was not statistically significant (26 compared with 31, respectively). Previously, these two factors had been discussed in the literature with an overemphasis on postoperative anemia and with sparse mention of the importance of overhydration. Both of these factors may be interrelated and their significance is difficult to discern. However, fluid overload has been mentioned as possibly playing a role in past case reports, and this is the first study to highlight its importance.9,31

Clearly, other factors may play a role in the development of POVL. Intrinsic factors such as coexisting disease or ocular vascular anatomy or extrinsic factors such as operative frame and type of fluid used may also have an important but yet unknown role in this disease origin.

http://thejns.org/doi/full/10.3171/FOC-07/11/15?cookieSet=1

Cop, if you are doing these cases you should read this. Fluids are not necessarily the answer.
Click to expand...

when i was medical student, i had a very excellent renal fellow tell me once,

"bob loblaw, there are two games people play in the hospital. the first is 'what's the volume status?' the second is 'he's a douche bag.' when played perfectly, the latter game is played at the same time as the former. example: 'what did cardiology say? diurese?!? that guy is a douchebag!'

with this important caveat in mind, i will say that i think that there is plenty of evidence, none of which i care to chase down and cite at this hour, that suggests that crystalloid beyond 2-3L should be avoided whenever possible, with rare exception. surgery is a controlled trauma, and excess fluid in the setting of a a systemic inflammatory response quickly accumulates in the interstitium, resulting in numerous deleterious consequences. in my practice, my strategy is to be conservative in fluid administration when possible and, after two or three liters, i start to evaluate options for colloid. i prefer starches when possible, as even albumin carries non-zero risk for transmission of blood-borne illnesses. albumin is my next choice (expensive, though) and after that blood products. pRBCs are a well-established immunosuppressant and platelets a proven wholesome bacterial culture medium. i give blood products when lab values or surgical conditions necessitates but i try not to at all possible costs.

finally, and this is what prompted me to post, i feel that for some strange reason we, as anesthesiologists, feel that we are admitting defeat as physicians if we start a patient on a phenylephrine infusion to maintain blood pressure. this i do not understand. when approaching hypotension in a patient--anesthetized or not--the approach is the same: treat the underlying cause and support the hemodynamics. septic? site control, antibiotics, and support the blood pressure/myocardial suppression. cardiogenic shock? reperfusion, diuresis, balloon pump, surgery (etc.) and inotropes. anesthetic-induced vasodilatory state resulting in hypotension? discontinue anesthesia once surgery complete and SUPPORT THE BLOOD PRESSURE. exceedingly few patients' cannot tolerate a low dose phenylephrine infusion to support their blood pressure to address the vasodilatory state induced by anesthesia. why do so many of us resist? hypoperfusion causes end-organ damage, not 'hypovolemia.' certain vascular beds will recieve less perfusion in the setting of phenyephrine infusion but the important ones will not. if you are worried about depressing cardiac output...start low-dose epinephrine. i routinely do this in my elderly lobectomy patients getting high-thoracic epidurals. usually a couple of mics/min is all it takes.
 
Loblaw and Noyac,

I respect your guy's opinions. But, please do not send the wrong message here. Positioning is probably the most important preventive measure for AION, and I make it a habit to place my patients in slight "head up" while they are prone.

My experience, antithetical to Loblaw's, is that people are far too unwilling to pull the trigger on giving blood for often the nebulous and nefarious reasons he elucidates in his post. Again, if the patient has proved to you they need blood (the ultimate colloid), give it. That's my opinion.

Noyac, I actually - literally - have the APSF article on AION right in front of me now. This was translated to a practice advisory by the ASA. Here it is online:

"Colloids should be used along with crystalloids to maintain intravascular volume in patients who have substantial blood loss."

"At this time there is no apparent transfusion threshold that would eliminate the risk of perioperative visual loss related to anemia."
Click to expand...

http://www.apsf.org/resource_center/newsletter/2006/summer/ASApub.html

This is the current state of practice for this incredibly rare complication. Nowhere does it say to run a pressor. However, if the HCT is low and the patient is acting like they need blood, why wouldn't you give it? I'm not talking about willy-nilly transfusion here, but most of the patients who are multi-level and are going to need blood at some point during the procedure. If you're going to argue with that, you're being intellectually dishonest.

I respect what you guys are saying, but I can tell you that running a pressor will probably only mask hypotension and make the numbers look good, and will not prevent chemosis, as well as be likely to get you behind during the case. We're talking about an inherently bloody procedure with a large exposure and massive insensible losses.

Now, UTSW's suggestions are something that I have done inconsistently and probably should revisit. Perhaps his institution has genius surgeons that barely scrape the patient's spine when doing these too. However, we have run Amicar at low dose doing these cases and, at least anecdotally, I didn't feel that this made a huge difference in blood loss. Again, chemosis is going to happen no matter what you do and, if you consider this a surrogate marker for optic disk swelling, probably the best solution is to put the patient slightly head-up and position your a-line at the level of the tragus.

Poor answer? No. Just a different answer than yours. Personally, I don't run a pressor until I'm convinced that the patient has had their fluid balance optimized, and this includes replacing blood cells when it's clear they need them.

I guess that makes me a douchebag.

-copro
 
coprolalia said:
Man, we are having communication problems today... :laugh:

All of these patients bleed like stink, even if you use Amicar or whatever else. They inevitably need blood... not for volume or for UOP... but because they bleed like stink. If a patient is hypotensive and becoming increasingly tachycardic, and their Hct is low, I'm giving blood before I start neo.

That was my only point.

-copro
Click to expand...

It's weekend!!😍 Of course I got your point.
How is the new gig?
2win
 
huktonfonix said:
in general, give whatever fixes what you think the physiologic derangement is. Lots of bleeding? give blood/fluid. Vasodilation from anesthetics and pooling of blood in prone position? Give phenylephrine. Myocardial depression or need more CO? Dopamine (or other inotrope of choice, but you get the idea). In general the pressors in the spine cases tend to compensate for the original physiological derangement and allow you to be more conservative on giving fluids to avoid excess administration.
Click to expand...

Let me offer another opinion. Have you given neo in the heart room with a swan or TEE in place? I have many many times and it never fails, the CO improves. This is because the myocardial perfusion is improved. I see it almost every time. So neo can improve cardiac performance as well. But there are times when its not enough.
 
coprolalia said:
Loblaw and Noyac,

I respect your guy's opinions. But, please do not send the wrong message here. Positioning is probably the most important preventive measure for AION, and I make it a habit to place my patients in slight "head up" while they are prone.

My experience, antithetical to Loblaw's, is that people are far too unwilling to pull the trigger on giving blood for often the nebulous and nefarious reasons he elucidates in his post. Again, if the patient has proved to you they need blood (the ultimate colloid), give it. That's my opinion.

Noyac, I actually - literally - have the APSF article on AION right in front of me now. This was translated to a practice advisory by the ASA. Here it is online:



http://www.apsf.org/resource_center/newsletter/2006/summer/ASApub.html

This is the current state of practice for this incredibly rare complication. Nowhere does it say to run a pressor. However, if the HCT is low and the patient is acting like they need blood, why wouldn't you give it? I'm not talking about willy-nilly transfusion here, but most of the patients who are multi-level and are going to need blood at some point during the procedure. If you're going to argue with that, you're being intellectually dishonest.

I respect what you guys are saying, but I can tell you that running a pressor will probably only mask hypotension and make the numbers look good, and will not prevent chemosis, as well as be likely to get you behind during the case. We're talking about an inherently bloody procedure with a large exposure and massive insensible losses.

Now, UTSW's suggestions are something that I have done inconsistently and probably should revisit. Perhaps his institution has genius surgeons that barely scrape the patient's spine when doing these too. However, we have run Amicar at low dose doing these cases and, at least anecdotally, I didn't feel that this made a huge difference in blood loss. Again, chemosis is going to happen no matter what you do and, if you consider this a surrogate marker for optic disk swelling, probably the best solution is to put the patient slightly head-up and position your a-line at the level of the tragus.

Poor answer? No. Just a different answer than yours. Personally, I don't run a pressor until I'm convinced that the patient has had their fluid balance optimized, and this includes replacing blood cells when it's clear they need them.

I guess that makes me a douchebag.

-copro
Click to expand...

copro, sorry if you got the impression i was speaking to you directly. i was not, i was acknowledging that volume status is a contentious issue and remarking what my own practice was. i would never be purposefully disrespectful to a colleague, i was just trying air my views on the subject. apologies that you felt offended or targeted.

in a case with large blood loss, i would transfuse blood, but i would do it not for volume, but for anemia. though a transfusion does raise the hemoglobin, we make a lot of assumptions when we give frozen, filtered, sometimes older blood--that it delivers oxygen to the tissues the same way as actual blood, for example. i'm not convinced that the benefits of blood transfusion are due solely to increased hemoglobin, and not due to the increased volume.

i agree with your comments about addressing hypovolemia, i'm just trying to acknowledge that to optimize the fluid balance, you have to consider the fact that our anesthetic vasodilates the patient. i don't run a neo drip on every patient once i hit 2-3 liters, but on a long case such as a neck whack or back case (with lots of blood loss or not) i would prefer to correct the vascular tone issues rather than get into crystalloid volumes that i sometimes see on my colleague records: 6-10L. i mean, that is 12-20 POUNDS of fluid. these fluid loss calculations that we are taught are completely bogus and based on archaic, generally unproven theories.

we all should strive for what we think is best practice. the above thoughts are what i believe to be the best practice but i would never say that my strategy is "correct." we should be humble as we treat our patients--biology is SO complex that to think that you understand it is a deceit. our job as physicians and as anesthesiologists is to understand the physiology and the evolutionary purpose of the stress response, recognize that evolution (if you believe in that crocked theory) is far smarter than are we, and to, in light of this, utilize therapies that account for the patient's comorbidities (their CAD, their COPD) in helping them maintain a normal stress response.

the last thing i would say is that it is impossible for us to measure how our practice affects our patients. there was an excellent editorial in last months anesthesiology that discusses the downstream and delayed effects of our intraoperative management and should serve to remind us that we should do more than aim to get the patient to the PACU and sign the discharge sheet. things we do intraoperatively have wide-ranging and, importantly, difficult to measure effects. we should be conscientious of this fact and try to practice in such a fashion as to minimize these effects. it is entirely conceivable that there are some of us on this board who have practice patterns that actually harm patients (not necessarily in large, detectable ways). worse yet, it is entirely concievable that i'm one of these people. i don't think i am but i cannot prove it. it's impossible to measure. i am certain, however, that my cognizance of this fact allows me to approach the patient with a certain humility and respect that makes it far less likely.
 
Noyac said:
I missed it. Who called cop a douchebag?
Click to expand...
it was a mistake. i was acknowledging the contentiousness of the volume issue by noting that the two games people (not me) love to play in the hospital are (1) what's the volume status? and (2) who's the douche bag? for example,

"what did cardiology say? diurese? no, no, no. he's dry--give volume. that guy's a douche bag!"

for the record, i don't play that game because i'm smart enough to know that it's almost impossible to know anything about a patient's physiologic status, in general (about volume, specifically), with enough certainty as to insult a colleague.
 
coprolalia said:
Loblaw and Noyac,

I respect your guy's opinions. But, please do not send the wrong message here. Positioning is probably the most important preventive measure for AION, and I make it a habit to place my patients in slight "head up" while they are prone.

My experience, antithetical to Loblaw's, is that people are far too unwilling to pull the trigger on giving blood for often the nebulous and nefarious reasons he elucidates in his post. Again, if the patient has proved to you they need blood (the ultimate colloid), give it. That's my opinion.

Noyac, I actually - literally - have the APSF article on AION right in front of me now. This was translated to a practice advisory by the ASA. Here it is online:



http://www.apsf.org/resource_center/newsletter/2006/summer/ASApub.html

This is the current state of practice for this incredibly rare complication. Nowhere does it say to run a pressor. However, if the HCT is low and the patient is acting like they need blood, why wouldn't you give it? I'm not talking about willy-nilly transfusion here, but most of the patients who are multi-level and are going to need blood at some point during the procedure. If you're going to argue with that, you're being intellectually dishonest.

I respect what you guys are saying, but I can tell you that running a pressor will probably only mask hypotension and make the numbers look good, and will not prevent chemosis, as well as be likely to get you behind during the case. We're talking about an inherently bloody procedure with a large exposure and massive insensible losses.

Now, UTSW's suggestions are something that I have done inconsistently and probably should revisit. Perhaps his institution has genius surgeons that barely scrape the patient's spine when doing these too. However, we have run Amicar at low dose doing these cases and, at least anecdotally, I didn't feel that this made a huge difference in blood loss. Again, chemosis is going to happen no matter what you do and, if you consider this a surrogate marker for optic disk swelling, probably the best solution is to put the patient slightly head-up and position your a-line at the level of the tragus.

Poor answer? No. Just a different answer than yours. Personally, I don't run a pressor until I'm convinced that the patient has had their fluid balance optimized, and this includes replacing blood cells when it's clear they need them.

I guess that makes me a douchebag.

-copro
Click to expand...

For my part of this discussion, I would agree with low dose amicar as being relatively non-contributary. This is why I have abandoned it from my practice and use only TA plus/minus DDAVP. You should revisit it and use cardiac bypass protocols.

Our surgeons are exceptional. They work with us and take our suggestions as we do theirs. Anyone doing scoliosis is going to aggressively manipulate and scrape the spine. They just know that it is better to addess bleeding immediately via cauterization, flow seal, evaseal, sludge, packing, etc. and we likewise pretreat our patients for these cases.
 
UTSouthwestern said:
For my part of this discussion, I would agree with low dose amicar as being relatively non-contributary. This is why I have abandoned it from my practice and use only TA plus/minus DDAVP. You should revisit it and use cardiac bypass protocols.

Our surgeons are exceptional. They work with us and take our suggestions as we do theirs. Anyone doing scoliosis is going to aggressively manipulate and scrape the spine. They just know that it is better to addess bleeding immediately via cauterization, flow seal, evaseal, sludge, packing, etc. and we likewise pretreat our patients for these cases.
Click to expand...

Thanks for your input, UT. I always value your opinion, and it's nice to see you back here posting. I did a ton of spines in residency and, quite frankly, our surgeons who did the multilevel scoli's sucked. We, as a rule, gave blood because they just couldn't control the bleeding. I haven't done a spine yet in my PP gig, but we have ortho spine guys that do these regularly and it's only a matter of time.

I have a couple of questions...

(1) Do you load then run the TXA just like in a cardiac case? Or, do you simply start the infusion after induction? The reason why I ask is because it seems like the "load" dose is mainly because you're going on pump in a cardiac case, and it may not be necessary here. Also, do you always give the 0.3/kg dose of desmo as a rule, or do you "wait and see" how much oozing there is at the site? I don't see a disadvantage, necessarily, of doing this pre-emptively, except that it is an ortho procedure (ultimately) and you're going to put the patient more into a pro-coagulation state by doing this (i.e., possibly increasing DVT/PE potential, etc.).

(2) Do you guys extubate in the OR? Or, do you go to the unit with the tube in? It seems the rule here is that the patients, especially for like the T6-L3 cases (etc.) that take 7+ hours to do inevitably go tubed to the unit secondary to "swelling" issues around the tube. Almost ineluctably, they get put on propofol and fentanyl sedation post-op and it seems to me that this may further contribute to hypotension, even at the relatively low doses they run in the units (which is another issue that annoys the crap out of me... but that's a separate discussion). It seems that if you guys have minimal fluid shifts, it would be prudent just to pull the tube in the OR and allow the patient a normal intermediate-care post-op.

If you have the time, I'd appreciate your input.

-copro
 
Wow,
I wish I had the patience or the attention span to read all these very lengthy and detailed fine posts!
On the other hand here is my humble opinion from a very practical point of view:
Most of the time patients having spine surgery become hypotensive because we give them high doses of whatever anesthetics we are using to avoid movement especially when no muscle relaxant is being used (for monitoring of motor evoked potentials).
So if we agree that most likely the hypotension is caused by more vasodilation than cardiac depression (since this is what our anesthetics do) then we need a medication that corrects the vasodilation and the best drug we have to do that is phenylephrine.
Now you guys can resume your lengthy posts and I apologize for the interruption.
 
FWIW The Lee of Lee et al on the POVL literature runs phenylephrine from the get go to maintain blood pressure (MAP) within 20-30% of baseline. She prefers 20% for sicker patients, but lets us go to 30% with healthier patients.

We try to match fluid losses and keep HBG >8 for all comers and >10 for cardiac patients.

We do not routinely use antifibrinolytics or desmopressin or cell saver.

Our surgeons are of the ignore it and hope it clots vein.

We routinely extubate after 6-8 hour cases unless there is significant edema and no cuff leak.

- pod
 
Last edited:
coprolalia said:
Thanks for your input, UT. I always value your opinion, and it's nice to see you back here posting. I did a ton of spines in residency and, quite frankly, our surgeons who did the multilevel scoli's sucked. We, as a rule, gave blood because they just couldn't control the bleeding. I haven't done a spine yet in my PP gig, but we have ortho spine guys that do these regularly and it's only a matter of time.

I have a couple of questions...

(1) Do you load then run the TXA just like in a cardiac case? Or, do you simply start the infusion after induction? The reason why I ask is because it seems like the "load" dose is mainly because you're going on pump in a cardiac case, and it may not be necessary here. Also, do you always give the 0.3/kg dose of desmo as a rule, or do you "wait and see" how much oozing there is at the site? I don't see a disadvantage, necessarily, of doing this pre-emptively, except that it is an ortho procedure (ultimately) and you're going to put the patient more into a pro-coagulation state by doing this (i.e., possibly increasing DVT/PE potential, etc.).

(2) Do you guys extubate in the OR? Or, do you go to the unit with the tube in? It seems the rule here is that the patients, especially for like the T6-L3 cases (etc.) that take 7+ hours to do inevitably go tubed to the unit secondary to "swelling" issues around the tube. Almost ineluctably, they get put on propofol and fentanyl sedation post-op and it seems to me that this may further contribute to hypotension, even at the relatively low doses they run in the units (which is another issue that annoys the crap out of me... but that's a separate discussion). It seems that if you guys have minimal fluid shifts, it would be prudent just to pull the tube in the OR and allow the patient a normal intermediate-care post-op.

If you have the time, I'd appreciate your input.

-copro
Click to expand...

Had a long reply eaten up by the maintenance work of the website this afternoon.

In summary, good questions.

1. We load the TA to quickly achieve an adequate level prior to the surgeons reaching the deeper, more vascular tissues. We also ask that they place 40-60 cc's of 0.5% bupivicaine with epi superficially as well as deeper to promote vasoconstriction of vessels in the path of dissection. DDAVP has one drawback in that the full effect may not be seen until 3-6 hours after being given. We therefore communicate with our surgeons before the case or the day before to determine the complexity of the case and the likelihood that DDAVP will be needed/useful. In primary scoliosis repairs in teens and young adults, who can tolerate lower Hct's and in which the cases are likely to be shorter (4-6 hours), DDAVP is likely not necessary. In complicated cases such as revisions with multiple SPO's and extension of hardware, repairs utilizing vertabrectomies/corpectomies, 3 part repairs (multilevel ALIF, thoracotomy for anterolateral fusion, T2-ilium PSF with instrumentation and SPO's), etc. and/or in patients with hereditary or medication mediated coagulopathy, DDAVP will be given from the start.

Proper use of full leg SCD's intraop and postop is a must in any of the cases. The risk of DVT/PE is there which is why we still select for appropriate use of DDAVP. This risk pales in comparison with multiple exposed bleeding sites causing an inflammatory reaction leading to massive hemorrhage, transfusion of multiple products, and/or DIC. Since adopting our protocols, we have seen a tremendous drop in blood product utilization and complications of and presence of massive hemorrhaging.

2. Positioning and fluid balance are essential to prevent airway swelling issues as well as PION, and in the 100 scoliosis cases we have done this year so far, only two have required postop ventilation, both due to preexisting severe COPD. Most of our patients are extubated in the OR, some on arrival to the ICU. As noted in a previous post on scoli cases, the utilization of an epidural and PCEA allows for a much smoother transition to extubation. After the patient has been spontaneously breathing for almost 30 min during closing and after the epidural has been loaded, I usually flip the patient supine, get a chest X-ray to check for line placement and look for obvious signs of fluid overload if present, then pull the tube. Most of my patients wake up with little to no pain with a properly loaded epidural and require little breakthrough IV treatment. Many are out of the ICU by the next day. Some require NO supplemental IV pain meds for the duration of their stay. It requires a balanced anesthetic to facilitate appropriate neuromonitoring (precedex, low volatile, narcotics, etc.), a surgeon that understands the benefits of efficiency and hemostasis, and repetition among us, the anesthesiologists, to be able to anticipate issues prior to their arrival.

Hopefully, we will have publications ready by next year once we are adequately powered to detail our protocols.
 
UTSouthwestern said:
Hopefully, we will have publications ready by next year once we are adequately powered to detail our protocols.
Click to expand...

Thanks...

For the rest of this thread, I re-read it and am reminded of that scene in Caddyshack where Al Czervik (Rodney Dangerfield) is in the pro-shop before teeing off and he comments on the hat the manakin is wearing... "Look at this hat. This is the worst looking hat I ever saw. What? When you buy this hat I bet you get a free bowl of soup."

He then turns to see Judge Smails (Ted Knight) already wearing the exact same hat. "Oh," he says, "but it looks good on you, though." And, you see him roll his eyes as he turns his head away.

Think about it.

-copro
 
coprolalia said:
Thanks...

For the rest of this thread, I re-read it and am reminded of that scene in Caddyshack where Al Czervik (Rodney Dangerfield) is in the pro-shop before teeing off and he comments on the hat the manakin is wearing... "Look at this hat. This is the worst looking hat I ever saw. What? When you buy this hat I bet you get a free bowl of soup."

He then turns to see Judge Smails (Ted Knight) already wearing the exact same hat. "Oh," he says, "but it looks good on you, though." And, you see him roll his eyes as he turns his head away.

Think about it.

-copro
Click to expand...


Which character are you, Rodney or Ted?
 
Southpaw said:
Hey Bob Loblaw...I'm a new resident. Post more....I've got a lot to learn from you. Your posts are chock full of valuable information. That is all.
Click to expand...

Loving the user name too, Bob. If you had a law blog, I'd read it for sure.

(That's an Arrested Development reference for those not in the know.)
 
Absolutely outstanding thread!! I thank everyone who contribuated to this post. I've learned a great deal from this disucussion. Thank you all !! 👍
 
You must log in or register to reply here.

Similar threads

P
Pain versus cardiac fellowship?
2 3 4 5
Replies
228
Views
18K
AKMD_1984
A
morri493
dopamine distrust
Replies
17
Views
2K
Twiggidy
Twiggidy
Y
Sugammadex Usage / Cost versus Benefit
Replies
40
Views
4K
deleted875186
D
G
Phenylephrine vs. Norepi in CHF Pt
Replies
49
Views
5K
T-burglar
T
JWebar
Sensory versus motor spinal anesthesia duration differences
Replies
1
Views
825
JWebar
JWebar
Top