[paindoc]

My experience shows CRNAs are more likely to be involved in office anesthesia than MDs but perhaps this is a regional difference. A series of calls to surgeons I know that perform office procedures revealed the following:
4 give versed via RN in their office
4 utilize CRNAs for procedures (mainly plastic surgery)
1 uses a MDA

It is likely somewhere within the organization of CRNA$ that there are statistics being expounded that CRNA$ provide 2/3 or more of all office anesthetics, just as they make the same assertion for anesthesia throughout the US. Perhaps we should check inside the CRNA$' little black bag they take with them to the surgeon's offices.....I am sure the CRNA$ carry their own stock of dantrolene given that the surgeon's offices do not typically stock dantrolene. Or if they do not carry dantrolene with them, why would they jeopardize patient lives by giving an anesthetic without having dantrolene immediately available?

[wtbcrna]

Originally Posted by paindoc

My experience shows CRNAs are more likely to be involved in office anesthesia than MDs but perhaps this is a regional difference. A series of calls to surgeons I know that perform office procedures revealed the following:
4 give versed via RN in their office
4 utilize CRNAs for procedures (mainly plastic surgery)
1 uses a MDA

It is likely somewhere within the organization of CRNA$ that there are statistics being expounded that CRNA$ provide 2/3 or more of all office anesthetics, just as they make the same assertion for anesthesia throughout the US. Perhaps we should check inside the CRNA$' little black bag they take with them to the surgeon's offices.....I am sure the CRNA$ carry their own stock of dantrolene given that the surgeon's offices do not typically stock dantrolene. Or if they do not carry dantrolene with them, why would they jeopardize patient lives by giving an anesthetic without having dantrolene immediately available?

Paindoc,

I agree that it is more common for CRNAs to provide office based anesthesia. One of the best places to look for ancetdotal evidence of which provider works where the most is to just look on www.gaswork.com.
The simple fact is that if a provider is going to use MH triggering agents then they should stock the full 36 vials of dantrolene. There is no excuse in this country not to stock the full 36 vials of dantrolene. It doesn't matter if it is CRNA or an MDA the standards of care are the same.

By the way if CRNA=$ then an MDA=$$$

[jwk]

Originally Posted by paindoc

My experience shows CRNAs are more likely to be involved in office anesthesia than MDs but perhaps this is a regional difference. A series of calls to surgeons I know that perform office procedures revealed the following:
4 give versed via RN in their office
4 utilize CRNAs for procedures (mainly plastic surgery)
1 uses a MDA

It is likely somewhere within the organization of CRNA$ that there are statistics being expounded that CRNA$ provide 2/3 or more of all office anesthetics, just as they make the same assertion for anesthesia throughout the US. Perhaps we should check inside the CRNA$' little black bag they take with them to the surgeon's offices.....I am sure the CRNA$ carry their own stock of dantrolene given that the surgeon's offices do not typically stock dantrolene. Or if they do not carry dantrolene with them, why would they jeopardize patient lives by giving an anesthetic without having dantrolene immediately available?

Wow - n=8. No wait, n=5, because RN's giving versed in an office is NOT anesthesia. So by your own poorly designed and completed study, 20% of office anesthesia is administered by an anesthesiologist, and 80% by CRNA's.

[paindoc]

In determining whether dantrolene should be stocked, perhaps it would be advantageous to examine a risk analysis based on the specific agents used. For example, propofol has now been proven not to trigger MH unless the amounts given are 100 fold greater than those used in clinical practice. (Anaesth Intensive Care. 2007 Dec;35(6):894-8.). Similarly, midazolam was found to have no effect on MH susceptible tissues (Can Anaesth Soc J. 1984 Jul;31(4):377-81. Effects of midazolam on directly stimulated muscle biopsies from control and malignant hyperthermia positive patients.). Based on rabbit studies, opiates, lidocaine, and non-depolarizing muscle relaxants were demonstrated not to trigger calcium release, and were therefore deemed safe, while ketamine and SCH were potentiators of calcium release and therefore were not safe in MH. (J Anesth. 1989 Mar 1;3(1):1-9. Effects of anesthetic and related agents on calcium-induced calcium release from sarcoplasmic reticulum isolated from rabbit skeletal muscle.) Inhalational agents have almost uniformly demonstrated activation of MH.
Therefore, in an office setting in which no inhalational agents, SCH, or ketamine are to be used, one may conclude based on clinical experiential evidence and basic science studies that MH will not be induced by other available agents used in MAC or general anesthesia. Propofol, midazolam, lidocaine, and opiates are not triggering agents, therefore dantrolene should not be necessary to have immediately available during the use of these agents to induce amnesia/analgesia/anesthesia. In cases where SCH, ketamine, or inhalational agents are employed, dantrolene should be stocked and immediately available as a standard of care.

[wtbcrna]

Originally Posted by paindoc

In determining whether dantrolene should be stocked, perhaps it would be advantageous to examine a risk analysis based on the specific agents used. For example, propofol has now been proven not to trigger MH unless the amounts given are 100 fold greater than those used in clinical practice. (Anaesth Intensive Care. 2007 Dec;35(6):894-8.). Similarly, midazolam was found to have no effect on MH susceptible tissues (Can Anaesth Soc J. 1984 Jul;31(4):377-81. Effects of midazolam on directly stimulated muscle biopsies from control and malignant hyperthermia positive patients.). Based on rabbit studies, opiates, lidocaine, and non-depolarizing muscle relaxants were demonstrated not to trigger calcium release, and were therefore deemed safe, while ketamine and SCH were potentiators of calcium release and therefore were not safe in MH. (J Anesth. 1989 Mar 1;3(1):1-9. Effects of anesthetic and related agents on calcium-induced calcium release from sarcoplasmic reticulum isolated from rabbit skeletal muscle.) Inhalational agents have almost uniformly demonstrated activation of MH.
Therefore, in an office setting in which no inhalational agents, SCH, or ketamine are to be used, one may conclude based on clinical experiential evidence and basic science studies that MH will not be induced by other available agents used in MAC or general anesthesia. Propofol, midazolam, lidocaine, and opiates are not triggering agents, therefore dantrolene should not be necessary to have immediately available during the use of these agents to induce amnesia/analgesia/anesthesia. In cases where SCH, ketamine, or inhalational agents are employed, dantrolene should be stocked and immediately available as a standard of care.

Interesting I can find no references to ketamine being a triggering agent in any of my books or notes. Ketamine is actually listed as a safe agent. I checked Clinical Anesthisology 4th ed, Nagelhout 3rd ed, and my notes from Dr. Sheila Muldoon one the head researchers in MH/head of the MH testing center at USUHS.

Malignant Hyperthermia Trigger and Safe Anesthetic Agents (from Dr. Muldoon)

Trigger Agents
Inhaled Anesthetics
Halothane
Isoflurane
Enflurane
Sevoflurane
Desflurane

Muscle Relaxants
Depolarizing (succinylcholine)

Intravenous Anesthetics
None

Safe Agents

Inhaled Anesthetics
N2O
Xenon

Intravenous Anesthetics
Barbiturates
Propofol
Ketamine

Muscle Relaxants
Nondepolarizing (all)

Local Anesthetics
All

Narcotics
Benzodiazepines

[deepz]

Originally Posted by paindoc

.......propofol has now been proven not to trigger MH ... (Anaesth Intensive Care. 2007 Dec;35(6):894-8.).....

A single study, while indicative, does not constitute 'proof' of anything per se.

[paindoc]

Proof is defined by both basic science and clinical science. There are many papers in the clincal realm that specify propofol does not trigger MH. The basic science paper proves what the clinical science cannot due to lack of sufficient numbers enrolled in clinical trials. Evidence based medicine is a process in which proof is offered through examination of ALL literature, levels I-V NASS or Cochrane levels A-D or one of many other systems. All literature is evaluated, then those with the highest scientific merit are given deference over others. In this realms, the proponderance of evidence is that there is unequivocal proof propofol does not trigger MH. The basic science study is but one of many, but demonstrates through the process of EBM (or in the case of CRNAs, I suppose it would technically be called EBN), how basic science (sorely lacking in the AANA Journal) can provide definitive evidence.
With ketamine, there is conflicting evidence, in far more definitive sources than the level V "opinion" of some professor (level V evidence is completely discounted by most EBM systems when there is more definitive evidence available) . One of the negative association papers is Masui. 1998 Nov;47(11):1296-301. [Effect of ketamine on the Ca(2+)-related functions of skinned skeletal muscle fibers from the guinea pigs]. Nevertheless, the overall level of evidence based on clinical studies for ketamine falls into the inconclusive category due to a lack of studies being published on the subject by CRNAs and anesthesiologists. (Why have you guys not published any studies on this?)

[foraneman]

Originally Posted by paindoc

It is likely somewhere within the organization of CRNA$ that there are statistics being expounded that CRNA$ provide 2/3 or more of all office anesthetics, just as they make the same assertion for anesthesia throughout the US. Perhaps we should check inside the CRNA$' little black bag they take with them to the surgeon's offices.....I am sure the CRNA$ carry their own stock of dantrolene given that the surgeon's offices do not typically stock dantrolene. Or if they do not carry dantrolene with them, why would they jeopardize patient lives by giving an anesthetic without having dantrolene immediately available?

You began your comments in this thread by assuming a CRNA had failed to properly care for a patient. You were wrong. You proposed that MDA practice in surgeon's offices was a rarity. You were wrong. Now, you resort to childish rhetoric and symbolism (CRNA$) which again singles out CRNAs and makes assumptions and accusations which are based on nothing other than your personal bias. You have NO idea what occurs in office surgery centers thruought the country and you frankly do not care. Your interest lies in attacking the practice of CRNAs whenever possible, regardless of facts or scientific basis. Your credibility, as such is nil. Falsus in uno, falsus in omnibus.

[wtbcrna]

Originally Posted by paindoc

Proof is defined by both basic science and clinical science. There are many papers in the clincal realm that specify propofol does not trigger MH. The basic science paper proves what the clinical science cannot due to lack of sufficient numbers enrolled in clinical trials. Evidence based medicine is a process in which proof is offered through examination of ALL literature, levels I-V NASS or Cochrane levels A-D or one of many other systems. All literature is evaluated, then those with the highest scientific merit are given deference over others. In this realms, the proponderance of evidence is that there is unequivocal proof propofol does not trigger MH. The basic science study is but one of many, but demonstrates through the process of EBM (or in the case of CRNAs, I suppose it would technically be called EBN), how basic science (sorely lacking in the AANA Journal) can provide definitive evidence.
With ketamine, there is conflicting evidence, in far more definitive sources than the level V "opinion" of some professor (level V evidence is completely discounted by most EBM systems when there is more definitive evidence available) . One of the negative association papers is Masui. 1998 Nov;47(11):1296-301. [Effect of ketamine on the Ca(2+)-related functions of skinned skeletal muscle fibers from the guinea pigs]. Nevertheless, the overall level of evidence based on clinical studies for ketamine falls into the inconclusive category due to a lack of studies being published on the subject by CRNAs and anesthesiologists. (Why have you guys not published any studies on this?)

Just two things: 1. When nurses are talking about evidence based research it is EBP (evidenced based practice). We use the term EBP, because it shows that we are open to all research not just research done by people w/ MD or DO behind their names. 2. I will assume there is no reason to do research on ketamine at this point, if one of the U.S.'s biggest MH research facility & faculty don't see a need to do further research on ketamine then what is the point (It wasn't even mentioned as potentially controversial by Dr. Muldoon during her lectures on MH). The research is overwhelming in favor that ketamine is safe to use just like all other known IV anesthetics for MH patients.

FYI: The biggest push for MH research right now is finding a genetic test for MH susceptible patient vs. muscle biopsy, and several of my classmates are involved in that research for their SRNA research project.