spinal for urology

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midazme

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do you all have any thoughts for keeping pts still after doing neuraxial anesthesia? i did a urology case today (orchoidectomy) and the pt was doing fine with a spinal and low dose propofol gtt. about thirty minutes in, he starts to move a little, and the surgeon (who had waffled on his anesthesia request) starts bitching about spinals. the case went fine, but i was curious what, if anything, you all do to prevent the pts from moving when using regional techniques?

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no easy way around this. the gut instinct is to deepen your patient and that is usually not the right answer...if you keep running into surgeons who arent comfortable with regional then thats typically when you abandon it, just because you dont want the hassle (or they dont want the hassle)
 
do you all have any thoughts for keeping pts still after doing neuraxial anesthesia? i did a urology case today (orchoidectomy) and the pt was doing fine with a spinal and low dose propofol gtt. about thirty minutes in, he starts to move a little, and the surgeon (who had waffled on his anesthesia request) starts bitching about spinals. the case went fine, but i was curious what, if anything, you all do to prevent the pts from moving when using regional techniques?

what else did you give? patients start moving around when they get disinhibited and forget where they are or what they are doing...i'm usually pretty heavy handed with the opioids and light with the benzos/pfol. patients are pretty calm with this approach and are not so disinhibited/disoriented that they get unruly. did a knee scope with local from the surgeons on a guy the other day and gave 400 mcgs of fentanyl (titrated 50 q 5-10 minutes) and ran p'fol at 25-50 mcg/kg/min...
 
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what else did you give? patients start moving around when they get disinhibited and forget where they are or what they are doing...i'm usually pretty heavy handed with the opioids and light with the benzos/pfol. patients are pretty calm with this approach and are not so disinhibited/disoriented that they get unruly. did a knee scope with local from the surgeons on a guy the other day and gave 400 mcgs of fentanyl (titrated 50 q 5-10 minutes) and ran p'fol at 25-50 mcg/kg/min...


I agree entirely with the comment about disinhibition. I seemed to have settled on the fentanyl heavy technique as well.

I do the block or spinal with just enough midazolam that they are slurring their speech and then hold off on Benzos. I keep giving 25mcg of Fentanyl every time I see their respiratory rate above 8. Sometimes this ends up being a huge dose of opoid. I usually don't even use a propofol drip.
 
I often find myself placing LMA's instead of the 'big MAC' or short spinal, unless of course the patient has severe pulmonary disease that warrants a regional technique. Is giving a huge load of narcotic and benzo better than a quick induction and inhaled anesthetic? If the argument is to avoid going to PACU, then get your PACU nurses on board with understanding discharge criteria for ambulatory surgery.
 
I've run into this issue as well. I've noticed that this "delirium" often accompanies tachycardia suggesting that the patient is in stage 2 anesthesia. I've had good results with reducing the propofol gtt.
 
I agree entirely with the comment about disinhibition. I seemed to have settled on the fentanyl heavy technique as well.

I do the block or spinal with just enough midazolam that they are slurring their speech and then hold off on Benzos. I keep giving 25mcg of Fentanyl every time I see their respiratory rate above 8. Sometimes this ends up being a huge dose of opoid. I usually don't even use a propofol drip.

Why do you need that much?
 
thanks for the advice.

FWIW, i used 2mg midazolam (1 mg in preop, 1 mg 5 mins later in OR) and 150 of fentanyl.

my initial thought was that the pt became disinhibited with the propofol gtt, and after i deepened him he began to obstruct a little, though he was still breathing. at this point i was facing the choice of supporting his airway until he lightened with some chin lift/jaw thrust, or deepening him further and putting in an LMA. i chose option A and it worked out.
 
thanks for the advice.

FWIW, i used 2mg midazolam (1 mg in preop, 1 mg 5 mins later in OR) and 150 of fentanyl.

my initial thought was that the pt became disinhibited with the propofol gtt, and after i deepened him he began to obstruct a little, though he was still breathing. at this point i was facing the choice of supporting his airway until he lightened with some chin lift/jaw thrust, or deepening him further and putting in an LMA. i chose option A and it worked out.

A lot of people will routinely give midazolam for every case. I almost never do unless a patient gives me a sense that they are anxious. I think that it interferes with my wake-ups. This is experiential, but I just don't think it adds that much, unless its for sedation or for an anxious patient.
 
I've run into this issue as well. I've noticed that this "delirium" often accompanies tachycardia suggesting that the patient is in stage 2 anesthesia. I've had good results with reducing the propofol gtt.

I don't know how to ask this question without sounding like an idiot, but I thought stage 2 was a phenomenon more or less exclusive to volatile anesthetics, and was not seen when using IV anesthetics like propofol (and not merely because the awake-->asleep and asleep-->awake transition is so much faster with IV anesthetics). Am I wrong?

In all the TIVAs and MACs I've done, I don't think I've ever really noted a hyperexcitable period during emergence that I would have called "stage 2", in contrast to nearly 100% of patients emerging from volatiles. And I can't recall ever thinking that my sedated but disinhibited moderate-heavy MAC patient was wiggling because they were in stage 2.
 
I don't know how to ask this question without sounding like an idiot, but I thought stage 2 was a phenomenon more or less exclusive to volatile anesthetics, and was not seen when using IV anesthetics like propofol (and not merely because the awake-->asleep and asleep-->awake transition is so much faster with IV anesthetics). Am I wrong?

In all the TIVAs and MACs I've done, I don't think I've ever really noted a hyperexcitable period during emergence that I would have called "stage 2", in contrast to nearly 100% of patients emerging from volatiles. And I can't recall ever thinking that my sedated but disinhibited moderate-heavy MAC patient was wiggling because they were in stage 2.

Although Guedel's classification of the stages of anesthesia was described in patients undergoing ether anesthesia, it has also been described in patients anesthetized with inhalational and intravenous agents. In fact, some proponents of BIS monitoring feel that it has replaced Guedel's classification. BIS monitoring is probably used more frequently in intravenous than inhalation anesthesia.

I agree that the stages are rarely associated with intravenous agents because they are generally administered as part of a balanced anesthetic +/- a muscle relaxant. In the case of propofol, if bolused, it rapidly redistributes so the transition through the stages is not evident.

Guedel's classification also applies to the induction of anesthesia, not only emergence. Patients receiving infusions may indeed progress through stages of anesthesia depending on how their anesthetic is titrated. Progressing from stage 1 to stage 2 is a spectrum. I've personally seen increased heart rate, irregular respirations and agitation in patients receiving propofol infusions that looks the same clinically as kiddos emerging from a sevoflurane anesthetic. I've HEARD horror stories about emesis occurring during propofol infusions. Although there are many reasons why this may have occurred, this would also be consistent (although not exclusive) to stage 2.
 
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I don't know how to ask this question without sounding like an idiot, but I thought stage 2 was a phenomenon more or less exclusive to volatile anesthetics, and was not seen when using IV anesthetics like propofol (and not merely because the awake-->asleep and asleep-->awake transition is so much faster with IV anesthetics). Am I wrong?

In all the TIVAs and MACs I've done, I don't think I've ever really noted a hyperexcitable period during emergence that I would have called "stage 2", in contrast to nearly 100% of patients emerging from volatiles. And I can't recall ever thinking that my sedated but disinhibited moderate-heavy MAC patient was wiggling because they were in stage 2.

I tend to agree. The only time I have ever seen stage 2 is with volatiles, never with IV agents.
 
I often find myself placing LMA's instead of the 'big MAC' or short spinal, unless of course the patient has severe pulmonary disease that warrants a regional technique. Is giving a huge load of narcotic and benzo better than a quick induction and inhaled anesthetic? If the argument is to avoid going to PACU, then get your PACU nurses on board with understanding discharge criteria for ambulatory surgery.

I employ RA to avoid some of the drawbacks of GA. Hitting a patient with large amounts of benzos and narcotics defeats the purpose . If there is a risk of injury to the patient or surgeon I will reassess my level of sedation. Let's face it, a patient who is breathing spontaneously and is not relaxed may move.

You don't want to hurt a patient trying to cater to a surgeons' unrealistic expectations.

Cambie
 
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I employ RA to avoid some of the drawbacks of GA. Hitting a patient with large amounts of bezos and narcotics defeats the purpose . If there is a risk of injury to the patient or surgeon I will reassess my level of sedation. Let's face it, a patient who is breathing spontaneously and is not relaxed may move.

You don't want to hurt a patient trying to cater to a surgeons' unrealistic expectations.

Cambie

good point all around
 
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I tend to agree. The only time I have ever seen stage 2 is with volatiles, never with IV agents.

I think in this thread we're talking about 2 different entities, which are, proper stage 2 anesthesia, vs., disinhibition that can occur with low-moderate IV sedatives/hypnotics.
 
Also something to think about when using spinal for other urology procedures (TURP, cysto ect) - the obturator nerve isn't blocked by spinal so during the surgery it can be tickled and cause the pt to move even though they may be quite sedated.

Anyone try precedex? I've been trying to use it more for sedation and have found it quite useful some of the times. Seems that drug is really hit or complete miss.
 
Also something to think about when using spinal for other urology procedures (TURP, cysto ect) - the obturator nerve isn't blocked by spinal so during the surgery it can be tickled and cause the pt to move even though they may be quite sedated.

The obturator nerve isn't blocked by spinal (which typically will get to a T8 or above level for uro cases)?
 
The obturator nerve isn't blocked by spinal (which typically will get to a T8 or above level for uro cases)?

No it isn't -- or at least the reflex isn't. It's in one of the common textbooks. I forget which one. You may even be able to Google it.

That having been said, I have yet to have a problem with the obturator reflex. But then again maybe I just haven't done enough cases. 🙂

Here, found something for you: "The obturator reflex is not abolished by spinal anesthesia, it can be suppressed only by a selective obturator nerve block." from http://www.nysora.com/peripheral_ne...or_techniques/3095-Obturator-Nerve-Block.html under Clinical Pearl under Indications.

As I said I read it in a textbook first, but NYSORA's website is a close second.
 
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Interesting. It says I edited at 11:18 PM. I am in Central Time Zone and it is shows 9:18 PM. What kind of time zone does SDN operate in?
 
Bah... maybe it is the cardiac anesthesiologist in me, but I like my patients sound asleep with a well secured airway. I have never been sorry that I chose that avenue, but I have certainly regreted and sweated the non-GA route on multiple occasions. Thankfully most of my clientele really don't like the idea of being awake for surgery either.

My favorite is when a surgeon requests sedation/mac/whatever non GA option for the über sick patient with pulmonary disease and severe pulm htn. Sorry buddy, your patient is much safer with a GA with all variables controlled.

Spinals are for c-sections for moms who are motivated to be awake to see their babies immediately upon delivery, otherwise they should get a nice nap too.

- pod
 
No it isn't -- or at least the reflex isn't. It's in one of the common textbooks. I forget which one. You may even be able to Google it.

That having been said, I have yet to have a problem with the obturator reflex. But then again maybe I just haven't done enough cases. 🙂

Here, found something for you: "The obturator reflex is not abolished by spinal anesthesia, it can be suppressed only by a selective obturator nerve block." from http://www.nysora.com/peripheral_ne...or_techniques/3095-Obturator-Nerve-Block.html under Clinical Pearl under Indications.

As I said I read it in a textbook first, but NYSORA's website is a close second.

i believe this is incorrect. the spinal obturator (L2,3,4) REFLEX is definitely abolished by a successful SAB.

however, the obturator courses in close proximity to the lateral walls of the bladder, and direct stimulation leads to adduction, and possibly perforation. if you want to be safe, the obturator has to be blocked DISTAL to the bladder walls (or at them, transvesicular), or the patient has to be paralyzed.
 
i believe this is incorrect. the spinal obturator (L2,3,4) REFLEX is definitely abolished by a successful SAB.

however, the obturator courses in close proximity to the lateral walls of the bladder, and direct stimulation leads to adduction, and possibly perforation. if you want to be safe, the obturator has to be blocked DISTAL to the bladder walls (or at them, transvesicular), or the patient has to be paralyzed.

+1.

The nerve is blocked at the spinal level, but its neuromuscular junction is intact, so if you stimulate it distal to the block (as slavin points out, it passes close to the bladder), you'll get contraction that makes it look like the patient is moving.
 
Bah... maybe it is the cardiac anesthesiologist in me, but I like my patients sound asleep with a well secured airway. I have never been sorry that I chose that avenue, but I have certainly regreted and sweated the non-GA route on multiple occasions. Thankfully most of my clientele really don't like the idea of being awake for surgery either.

My favorite is when a surgeon requests sedation/mac/whatever non GA option for the über sick patient with pulmonary disease and severe pulm htn. Sorry buddy, your patient is much safer with a GA with all variables controlled.

Spinals are for c-sections for moms who are motivated to be awake to see their babies immediately upon delivery, otherwise they should get a nice nap too.

- pod


I do spinals all the time for urology procedures on little old folks. As long as it is safe, I believe it is probably the best anesthetic choice for them when you take into account the risk of postoperative cognitive dysfunction after general anesthesia.

I mean if you are 85 years old and have no contraindication to a spinal (and have a spine that I can actually navigate through), why take the chance of messing with your brain? Some elderly patients have major congitive setbacks after even short general anesthetics that can affect them the rest of their life.
 
Although postoperative cognitive dysfunction (POCD) in the elderly is a real problem (a much bigger problem in cardiac surgery), there is no evidence that regional techniques reduce the risk. In fact the evidence is pretty clear that the rates of POCD are the same whether a general or regional technique is employed.



Evidence-based clinical update: General anesthesia and the risk of delirium and postoperative cognitive dysfunction - Gregory L. Bryson and Anna Wyand

A meta-analysis of the 18 RCTs of the effect of regional vs GA on POCD and delirium.

Conclusion: Available randomized controlled trials suggest that there is no significant difference in the incidence of delirium or POCD when general anesthesia and regional anesthesia are compared.



Does anaesthesia cause postoperative cognitive dysfunction? A randomised study of regional versus general anaesthesia in 438 elderly patients. - Rasmussen et al

Conclusion: No significant difference was found in the incidence of cognitive dysfunction 3 months after either general or regional anaesthesia in elderly patients. Thus, there seems to be no causative relationship between general anaesthesia and long-term POCD. Regional anaesthesia may decrease mortality and the incidence of POCD early after surgery.



Cognitive effects after epidural vs general anesthesia in older adults. A randomized trial. - Williams-Russo et al

Conclusion: The type of anesthesia, general or epidural, does not affect the magnitude or pattern of postoperative cognitive dysfunction or the incidence of major cardiovascular complications in older adults undergoing elective total knee replacement. This is the largest trial of the effects of general vs regional anesthesia on cerebral function reported to date, with more than 99% power to detect a clinically significant difference on any of the neuropsychological tests.

- pod
 
That stuff is all quite old in the world of POCD, the majority of the important work in the field has only come out within the last few years. I'm too lazy to dig up articles (while on call at 3 AM), but I believe that most experts in the field would agree that a spinal with minimal to no sedation provides a lower risk of POCD compared to a general anesthetic in an elderly patient.

Conceptually, it has to.
 
Two of the studies I cited present level 1 evidence that the modality of anesthesia does not influence the incidence of POCD. The other was a meta-analysis of the RCTs that directly compared modalities. No difference resulting from modality was demonstrable. To date, there is no level 1 evidence that refutes these findings.

The largest and most robust in vivo study of the problem is the International Study of Postoperative Cognitive Dysfunction (ISPOCD). 1218 patients from 11 countries undergoing a variety of non-cardiac procedures. The findings...

Risk factors for early POCD at the 7 day test: increasing age, increasing duration of anaesthesia, little education, second operation, postoperative infections and respiratory complications.

Risk factors for long-term POCD after 3 months: age and the use of benzodiazepines before surgery.

Negative findings I: no relation between different degrees of durations of hypoxaemia or hypotension or a combination of hypoxaemia and hypotension and early or late POCD was found.

Negative findings II: no relation was found between ASA physical status, history of lung disease, heart disease, peripheral ischaemia, hypertension, head injury, stroke, atrial fibrillation, delirium, cardiovascular complications, diagnosis of cancer, long-term stay in an intensive-care unit, major drug groups, anaesthetic technique, post-operative pain treatment, smoking, alcohol consumption, blood loss, perioperative fluids given, type of operation and sex.


A priori randomization of 438 of these patients looked specifically at the question of modality. The results were published in 2003, the Rasmussen study that I cited.

...there seems to be no causative relationship between general anaesthesia and long-term POCD. Regional anaesthesia may decrease mortality and the incidence of POCD early after surgery.


While our understanding of some of the basic mechanisms of POCD has increased over "the last few years", there hasn't been another large scale study of the problem in vivo. The findings over the last few years lend theoretical support to the idea that general anesthesia may in fact be more culpable than regional, but there is no data to directly support that supposition. There is data to directly refute it. Even in this age of rapid data acquisition and publication, ten-year-old data is hardly outdated.

I think we all understand the risks of intuitive evidence i.e. "Conceptually, it has to."


- pod
 
To quote from the 2006 meta-analysis by Bryson and Wyand.

Outcomes for POCD were identified from 16 trials that enrolled 2,708 patients (1,313 regional anesthesia; 1,395 general anesthesia).

...consistent Level 1 evidence indicates that exposure to general anesthesia is not significantly associated with POCD.

Conclusion
Available randomized controlled trials suggest that there is no significant difference in the incidence of delirium or POCD when general anesthesia and regional anesthesia are compared.


Then there is the 2002 report from Johnson et al. (Postoperative cognitive dysfunction in middle-aged patients) that claimed an association between POCD and epidural analgesia. It has been appropriately criticized for the post hoc nature of the analysis.


It appears that, as of Oct 2007, the ASA concurs with the statements I have made and the information that I have provided.

- pod
 
Also something to think about when using spinal for other urology procedures (TURP, cysto ect) - the obturator nerve isn't blocked by spinal so during the surgery it can be tickled and cause the pt to move even though they may be quite sedated.

Anyone try precedex? I've been trying to use it more for sedation and have found it quite useful some of the times. Seems that drug is really hit or complete miss.


I think precedex would be ideal for these patients with spinals...IF they were inpatients. Unfortunately the precedex sticks around for a while and if it's an outpaitent they have to be "watched" for a while in the pacu. Do they REALLY need to be watched? Probably not, but that's our current protocol at my hospital.
 
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