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Anybody else see the case report in Aneshesiology? Maybe we should stock 100 ml in our crash cart.
intralipid for bupivacaine toxicity
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nimbus said:
Or give 100 cc's of propofol.
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Since the article came out, we've already put bottles of lipids in all our anesthesia block carts.UTSouthwestern said:
I never paid attention to the lipid content of propofol - don't know if that would do the same thing, plus I'm not sure giving 100cc of propofol to someone that has no blood pressure would be the best course of action.
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jwk said:
By the time you progressed to the point of considering using propofol, you would probably be best served going on pump. Barring that, use the propofol and have sticks of levophed and epi to push as well.
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The accompanying editorial specifically states that propofol should not be considered since it is a 1% emulsion and would have to be given in a quantity up to a gram in order to achieve the same amount of lipid. I recall a dog study from about a year ago that showed the same results with good rescue rates from bupiv toxicity with the lipid solution. Interesting stuff.
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Mman said:
Bolus infusion of 20% lipid emulsion, 1 ml/kg over 1 minute while continuing chest compressions.
This dose should be repeated every 3-5 minutes to a maximum of 3 ml/kg.
At the point of conversion to SR, an infusion of 20% intralipid at a rate of 0.25 ml/kg/min should be continued until HD recovery.
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How often are you guys getting bupivicaine toxcity that you guys have a plan in place for this event???
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can someone post the case report. I can't find my issue!!!!
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The patient was a 58y/o, 82kg, 170cm male who presented for arthroscopic repair of a torn rotator cuff in the right shoulder. His medical history was significant for coronary artery bypass graft surgery at age 43. He gave a history of angina upon exertion and occasionally at rest. He declined further preoperative cardiac workup but was considered by his cardiologist to be stable on medical therapy. This included nitroglycerine as needed, lisinopril, atenolol isosorbide mononitrate, and clopidogrel and enteric-coated aspirin, both of which had been discontinued 1 week previously. His preoperative electrocardiogram revealed a right bundle-branch block, a left anterior hemiblock, and evidence of an old anterior wall myocardial infarction.
The patient arrived at the operating room holding area, where standard monitors were applied. Blood pressure was 120/80, O2 sat 98%RA, and HR 60 bpm. Supplemental o2 was delivered at 3 l/min via a nasal cannula. A 20-gauge IV catheter was placed in the dorsum of his left hand, through which 2 mg midazolam and 50 µg fentanyl were administered. A 50-mm, 22-gauge Stimuplex® insulated needle was connected to a Stimuplex-DIG nerve stimulator, and the interscalene groove was identified at the level of C6. The brachial plexus was identified by eliciting biceps stimulation (0.1-ms duration, 2 Hz) at 0.34 mA, following which 40 ml local anesthetic solution (20 ml bupivacaine, 0.5%, and 20 ml mepivacaine, 1.5%) were injected slowly (over approximately 2.5 min) in 5-ml increments with gentle aspiration between doses. The patient was awake and conversant during the performance of the block. At no time was any blood aspirated, nor did he report pain or paresthesias.
Approximately 30 s after removal of the block needle, the patient became incoherent and then developed a tonicclonic seizure. Oxygen was delivered by a facemask attached to a self-inflating resuscitation bag while 50 mg propofol was injected intravenously. The seizure stopped, and spontaneous respirations resumed. Approximately 90 s later, the patient began to seize again; this time, 100 mg intravenous propofol was administered. The electrocardiogram showed asystole, and no pulse, by carotid or femoral palpation, or blood pressure was detectable. Advanced cardiac life support was immediately started. The trachea was intubated, and end-tidal carbon dioxide was detected with an EasyCapII . Tube position was confirmed by auscultation, after which chest compressions were immediately resumed. During the first 20 min of advanced cardiac life support, a total of 3 mg epinephrine, given in divided doses, 2 mg atropine, 300 mg amiodarone, and 40 U arginine vasopressin were administered. In addition, monophasic defibrillation was used at escalating energy levels200, 300, 360, and 360 J, according to the advanced cardiac life support protocol. Cardiac rhythms included ventricular tachycardia with a pulse, pulseless ventricular tachycardia that momentarily became ventricular fibrillation, and eventually asystole. The arrhythmias observed during most of the resuscitation period were pulseless ventricular tachycardia and asystole.
After 20 min, at which time plans were being made to institute cardiopulmonary bypass, the administration of a lipid emulsion was suggested, and 100 ml of 20% Intralipid was given through the peripheral intravenous catheter. Cardiac compressions continued, and a defibrillation shock at 360 J was given. Within seconds, a single sinus beat appeared on the electrocardiogram, and 1 mg atropine and 1 mg epinephrine were administered. Within 15 s, while external chest compressions were continued, the cardiac rhythm returned to sinus at a rate of 90 beats/min. The blood pressure and pulse became detectable. An infusion of lipid emulsion was started and continued at 0.5 ml · kg-1 · min-1 over the following 2 h and then discontinued. The patient remained in sinus rhythm. He was weaned from mechanical ventilation, and his trachea was extubated, approximately 2.5 h later. He was awake and responsive, and had right upper extremity weakness consistent with a brachial plexus block. No neurologic sequelae were sustained, and he was subsequently transferred to a monitored setting for overnight observation. There was no evidence of complications secondary to the administration of intralipid (i.e., pancreatitis) during the following 2 weeks.
Because the patient had a cardiac arrest after which he had increased levels of cardiac enzymes, he agreed to undergo cardiac catheterization. This revealed total occlusion of the right coronary artery and a left ventricular ejection fraction of 32%. As a consequence, an automatic implantable cardiac defibrillator was inserted without any complications, and the patient was discharged home.
Discussion
Bupivacaine was first synthesized in 1963 and since that time has had many applications, including infiltration anesthesia, regional nerve blocks, and neuraxial anesthesia. In addition to its local anesthetic effects, it is a potent depressant of electrical conduction, which predisposes the heart to reentry types of arrhythmias.4 Weinberg et al.1 made the observation that intravenous lipid infusions not only increase the dose of bupivacaine required to produce asystole in rats but also improve survival in rats resuscitated after receiving intravenous bolus doses of bupivacaine. They then applied this observation to dogs, as a model of a species closer in size to humans, and found that lipid infusions during resuscitation from bupivacaine-induced cardiac arrests improved survival. Specifically, 12 dogs were given 10 mg/kg bupivacaine. All of the dogs developed circulatory collapse, and internal cardiac massage was delivered. Six of these dogs received 20% lipid infusion and 6 received saline as a 4-ml/kg bolus given over 2 min, followed by a continuous infusion of 0.5 ml · kg-1 · min-1. All of the dogs treated with the intralipid solution were successfully resuscitated, whereas none of the saline-treated animals survived. Weinberg, et al offered two possible hypotheses for their findings. Either the lipid emulsion creates a lipid phase that extracts the lipid-soluble bupivacaine molecules from the aqueous plasma phase (and therefore out of the tissue), or alternatively, the lipid infusion diffuses directly into tissue and interacts with bupivacaine at that level. Although the potential utility of lipid emulsions for cardiac resuscitation after a bupivacaine-induced cardiac arrest in humans has been discussed in the literature, its actual use has not been previously described.
When conventional algorithms for CPR were unsuccessful, a member of the code team suggested the use of a lipid emulsion, and arranged for the pharmacy to immediately dispatch a dose, through the pneumatic tube system at our institution. While it would have been preferable to infuse the lipid via a central venous catheter, the initial absence of such access necessitated the use of the peripheral intravenous line. Although recommendations for specific doses of intralipid have been suggested, we chose to administer 100 ml of a 20% lipid emulsion. While this is in excess of the suggested initial bolus of 1 ml/kg,5 we wanted to ensure that an adequate volume of lipid would reach the central circulation during cardiac compressions. Immediately after this administration, 1 mg each of atropine and epinephrine were administered, and sinus rhythm returned, where similar efforts had been unsuccessful before infusion of the lipid emulsion. Our maintenance infusion of 0.5 ml · kg-1 · min-1 was consistent with those used in the canine experiments but likely excessive. The specific recommendations of Weinberg et al. entail the use of a bolus infusion of 20% lipid emulsion, 1 ml/kg over 1 min while continuing chest compressions. This dose could be repeated every 35 min to a maximum of 3 ml/kg. At the point of conversion to sinus rhythm, Weinberg recommends that an infusion of 20% intralipid, at a rate of 0.25 ml · kg-1 · min-1, should be continued until hemodynamic recovery. Fortunately, there was no deleterious effect from this dose of intralipid. Since this event, a 100-ml bag of 20% lipid emulsion has been made immediately available in all areas in which peripheral nerve blocks are performed at our institution.
Levsky and Miller recently reported CV collapse from a bupivacaine dose of less than 1.1 mg/kg administered during a lumbar sympathetic ganglion radiofrequency ablation in a patient who previously sustained nonQ-wave myocardial infarction and whose preoperative electrocardiogram showed first-degree atrioventricular block. Although our patient had significant cardiac risk factors, he had been evaluated preoperatively by his cardiologist, who deemed him to be medically optimized to undergo this surgical procedure. His preoperative electrocardiogram revealed both a right bundle-branch block and a left anterior hemiblock. A significant preoperative conduction deficit may predispose to the development of local anesthetic induced cardiac toxicity at lower mg/kg basis than expected, and although no recommendations currently exist, in this group of patients, the use of levo-isomeric local anesthetics may offer some advantage. We have added ropivacaine to our hospital formulary specifically for the use in patients with significant cardiac histories who are undergoing peripheral plexus blockade.
We report the first use of a lipid emulsion as part of the successful resuscitation efforts in a patient who most likely sustained a local anestheticinduced cardiac arrest. We concur with Picard who considers a lipid emulsion, like dantrolene, a crucial antidote (which is both inexpensive and has a long shelf life) that should be routinely kept in areas in which peripheral nerve blocks are being performed.
The patient arrived at the operating room holding area, where standard monitors were applied. Blood pressure was 120/80, O2 sat 98%RA, and HR 60 bpm. Supplemental o2 was delivered at 3 l/min via a nasal cannula. A 20-gauge IV catheter was placed in the dorsum of his left hand, through which 2 mg midazolam and 50 µg fentanyl were administered. A 50-mm, 22-gauge Stimuplex® insulated needle was connected to a Stimuplex-DIG nerve stimulator, and the interscalene groove was identified at the level of C6. The brachial plexus was identified by eliciting biceps stimulation (0.1-ms duration, 2 Hz) at 0.34 mA, following which 40 ml local anesthetic solution (20 ml bupivacaine, 0.5%, and 20 ml mepivacaine, 1.5%) were injected slowly (over approximately 2.5 min) in 5-ml increments with gentle aspiration between doses. The patient was awake and conversant during the performance of the block. At no time was any blood aspirated, nor did he report pain or paresthesias.
Approximately 30 s after removal of the block needle, the patient became incoherent and then developed a tonicclonic seizure. Oxygen was delivered by a facemask attached to a self-inflating resuscitation bag while 50 mg propofol was injected intravenously. The seizure stopped, and spontaneous respirations resumed. Approximately 90 s later, the patient began to seize again; this time, 100 mg intravenous propofol was administered. The electrocardiogram showed asystole, and no pulse, by carotid or femoral palpation, or blood pressure was detectable. Advanced cardiac life support was immediately started. The trachea was intubated, and end-tidal carbon dioxide was detected with an EasyCapII . Tube position was confirmed by auscultation, after which chest compressions were immediately resumed. During the first 20 min of advanced cardiac life support, a total of 3 mg epinephrine, given in divided doses, 2 mg atropine, 300 mg amiodarone, and 40 U arginine vasopressin were administered. In addition, monophasic defibrillation was used at escalating energy levels200, 300, 360, and 360 J, according to the advanced cardiac life support protocol. Cardiac rhythms included ventricular tachycardia with a pulse, pulseless ventricular tachycardia that momentarily became ventricular fibrillation, and eventually asystole. The arrhythmias observed during most of the resuscitation period were pulseless ventricular tachycardia and asystole.
After 20 min, at which time plans were being made to institute cardiopulmonary bypass, the administration of a lipid emulsion was suggested, and 100 ml of 20% Intralipid was given through the peripheral intravenous catheter. Cardiac compressions continued, and a defibrillation shock at 360 J was given. Within seconds, a single sinus beat appeared on the electrocardiogram, and 1 mg atropine and 1 mg epinephrine were administered. Within 15 s, while external chest compressions were continued, the cardiac rhythm returned to sinus at a rate of 90 beats/min. The blood pressure and pulse became detectable. An infusion of lipid emulsion was started and continued at 0.5 ml · kg-1 · min-1 over the following 2 h and then discontinued. The patient remained in sinus rhythm. He was weaned from mechanical ventilation, and his trachea was extubated, approximately 2.5 h later. He was awake and responsive, and had right upper extremity weakness consistent with a brachial plexus block. No neurologic sequelae were sustained, and he was subsequently transferred to a monitored setting for overnight observation. There was no evidence of complications secondary to the administration of intralipid (i.e., pancreatitis) during the following 2 weeks.
Because the patient had a cardiac arrest after which he had increased levels of cardiac enzymes, he agreed to undergo cardiac catheterization. This revealed total occlusion of the right coronary artery and a left ventricular ejection fraction of 32%. As a consequence, an automatic implantable cardiac defibrillator was inserted without any complications, and the patient was discharged home.
Discussion
Bupivacaine was first synthesized in 1963 and since that time has had many applications, including infiltration anesthesia, regional nerve blocks, and neuraxial anesthesia. In addition to its local anesthetic effects, it is a potent depressant of electrical conduction, which predisposes the heart to reentry types of arrhythmias.4 Weinberg et al.1 made the observation that intravenous lipid infusions not only increase the dose of bupivacaine required to produce asystole in rats but also improve survival in rats resuscitated after receiving intravenous bolus doses of bupivacaine. They then applied this observation to dogs, as a model of a species closer in size to humans, and found that lipid infusions during resuscitation from bupivacaine-induced cardiac arrests improved survival. Specifically, 12 dogs were given 10 mg/kg bupivacaine. All of the dogs developed circulatory collapse, and internal cardiac massage was delivered. Six of these dogs received 20% lipid infusion and 6 received saline as a 4-ml/kg bolus given over 2 min, followed by a continuous infusion of 0.5 ml · kg-1 · min-1. All of the dogs treated with the intralipid solution were successfully resuscitated, whereas none of the saline-treated animals survived. Weinberg, et al offered two possible hypotheses for their findings. Either the lipid emulsion creates a lipid phase that extracts the lipid-soluble bupivacaine molecules from the aqueous plasma phase (and therefore out of the tissue), or alternatively, the lipid infusion diffuses directly into tissue and interacts with bupivacaine at that level. Although the potential utility of lipid emulsions for cardiac resuscitation after a bupivacaine-induced cardiac arrest in humans has been discussed in the literature, its actual use has not been previously described.
When conventional algorithms for CPR were unsuccessful, a member of the code team suggested the use of a lipid emulsion, and arranged for the pharmacy to immediately dispatch a dose, through the pneumatic tube system at our institution. While it would have been preferable to infuse the lipid via a central venous catheter, the initial absence of such access necessitated the use of the peripheral intravenous line. Although recommendations for specific doses of intralipid have been suggested, we chose to administer 100 ml of a 20% lipid emulsion. While this is in excess of the suggested initial bolus of 1 ml/kg,5 we wanted to ensure that an adequate volume of lipid would reach the central circulation during cardiac compressions. Immediately after this administration, 1 mg each of atropine and epinephrine were administered, and sinus rhythm returned, where similar efforts had been unsuccessful before infusion of the lipid emulsion. Our maintenance infusion of 0.5 ml · kg-1 · min-1 was consistent with those used in the canine experiments but likely excessive. The specific recommendations of Weinberg et al. entail the use of a bolus infusion of 20% lipid emulsion, 1 ml/kg over 1 min while continuing chest compressions. This dose could be repeated every 35 min to a maximum of 3 ml/kg. At the point of conversion to sinus rhythm, Weinberg recommends that an infusion of 20% intralipid, at a rate of 0.25 ml · kg-1 · min-1, should be continued until hemodynamic recovery. Fortunately, there was no deleterious effect from this dose of intralipid. Since this event, a 100-ml bag of 20% lipid emulsion has been made immediately available in all areas in which peripheral nerve blocks are performed at our institution.
Levsky and Miller recently reported CV collapse from a bupivacaine dose of less than 1.1 mg/kg administered during a lumbar sympathetic ganglion radiofrequency ablation in a patient who previously sustained nonQ-wave myocardial infarction and whose preoperative electrocardiogram showed first-degree atrioventricular block. Although our patient had significant cardiac risk factors, he had been evaluated preoperatively by his cardiologist, who deemed him to be medically optimized to undergo this surgical procedure. His preoperative electrocardiogram revealed both a right bundle-branch block and a left anterior hemiblock. A significant preoperative conduction deficit may predispose to the development of local anesthetic induced cardiac toxicity at lower mg/kg basis than expected, and although no recommendations currently exist, in this group of patients, the use of levo-isomeric local anesthetics may offer some advantage. We have added ropivacaine to our hospital formulary specifically for the use in patients with significant cardiac histories who are undergoing peripheral plexus blockade.
We report the first use of a lipid emulsion as part of the successful resuscitation efforts in a patient who most likely sustained a local anestheticinduced cardiac arrest. We concur with Picard who considers a lipid emulsion, like dantrolene, a crucial antidote (which is both inexpensive and has a long shelf life) that should be routinely kept in areas in which peripheral nerve blocks are being performed.
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militarymd said:How often are you guys getting bupivicaine toxcity that you guys have a plan in place for this event???
Never seen one, but I stayed at a Holiday Inn last night and read the article in the medical library after seeing the post here.
But my facility doesn't do much regional anyways so this is not exactly a shocker.
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jwk said:
Yep. No intralipid available at the pharmacies of any of the hospitals I work at, although plenty is available in the cafeterias.
UTSouthwestern said:
This is an interesting thread....but, I'm too tired to contribute significantly right now...a very looooong day!
But...no intralipid anywhere in the hospital - no Intralipid, no Liposyn, NO lipid emulsions? Doesn't your hospital(s) do intravenous nutritional support. What do they use for the fat content of an NPO pt? Just curious.
Then, I do have questions about how they said they got the stuff....I will admit, I didn't read the whole thread very carefully, but I will. Lipid emulsions must be in glass or in a specialized plastic container (non PVC) since the lipid will emulisfy the plasticizer (phthalates) of regular IV bags & tubings. That's why they need special tubings (not for resucitation, obviously.....) but for long term use...they'd need to be transferred to a special bag, if the pharmacy only purchased 500ml) which will decrease its shelf life. They do come in small sizes - 50, 100, 250, 500ml containers...so a small container is a possibility for OR use.
A glass container will not normally go safely by pneumatic tube - it breaks. I gotta wonder - did a tech take it to the OR - or did the pharmacist just go to the ICU to get one??? But...who cares really!
And yes....propofol is a 10% lipid emulsion (1.1Kcal/ml) & we consider that when calculating fat calories in a pt who is on a propofol infusion (which is a very bad thing economically!). Both 10 & 20% lipid emulsions are isotonic so don't require a central line.....they do very well with a peripheral line - they just have lots of drug interactions.......
Like someone else said.....an interesting thing to think about...I'll have to do that later....
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sdn1977 said:
None readily available for the OR. Of course the hospitals do IV nuitritional support. However, when a patient experienced bupi toxicity in one of the hospitals last year, no intralipid could be obtained, so the anesthesiologist pushed a huge load of propofol into the patient, followed by a stick of levophed, and some epi. Patient was rescued, but not before a CT surgeon had started a sternotomy incision for CPB and direct compression of the heart. The patient sued everyone involved, including the techs.
UTSouthwestern said:
Do you have an OR pharmacist? Where was she (or he
). That is their job - to get you what you need FAST! It can easily be stored in pyxis - do you have that? for access 24/7 by anybody with a code - I assume all MDs (DO's too)/RNs/techs.....
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sdn1977 said:Do you have an OR pharmacist? Where was she (or he
Half of the hospitals have an on site OR pharmacist. Others have a satellite pharmacy nearby. Three hospitals have non-pharmacist accessible pyxises (pyxi?), the rest have pharmacist and designated OR staff-only accessible pyxises. I'm sure they could get some intralipid from the main pharmacy (maybe not at the smaller hospitals, but at least the big ones), but timing is the key. If it's going to take more than ten minutes to get there, then you likely have either crashed onto bypass (yes in the private practice world, you can actually crash onto bypass in 5 minutes), have stabilized the patient such that the intralipid is no longer emergently needed, the patient has died, or you have used propofol.
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UTSouthwestern said:
You must really have all your ducks lined up for this kind of performance. Where I work we have one heart room and one rarely used backup room. Who knows where the cardiac surgeon and perfusionist may be at any given time. Best case scenario without prior warning is probably 30 minutes here.
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UTSouthwestern said:
If you have no alternative and the patient is essentially dead, I agree you could try giving a gram or two of propofol to someone already in cardiovascular collapse. But you better be prepared to chase it with a lot of inotropes and vasopressors as in your example.
Intralipid would be a better choice choice because it would not cause the degree of direct myocardial depression and vasodilation that propofol would. Why not just keep it around. Even the most rinky dink surgicenter stocks dantrolene even though it's rarely used.
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militarymd said:How often are you guys getting bupivicaine toxcity that you guys have a plan in place for this event???
You don't generally expect to see MH, yet hopefully you have a plan in place to deal with it if it occurs.
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5 minutes to get on bypass? Our block room is at least 3 minutes away from the bypass machine!!! And that's if you're good at maneuvering corners with the 1500 lb OR bed. 5 minutes? 5?
jwk said:
If this were brought before our P&T....it should be stored on the block cart & OR pyxis (pyxis is both plural & singular
) - not on the crash cart! The reason is crash carts are standard throughout the hospital - yes - the one in radiology looks just like the one in OB-GYN, peds, ortho, etc.. - thats so the people who need to find stuff can find stuff fast (nurses, rt, & yes - pharmacists). Intralipid, altho, cheap, is not necessary everywhere - just some prominient places & it should be readily availble there. So....it should be wherever anesthesia should find a need for it - perhaps the 50 or 100ml (originally designed for neonate/pedi TPN) on each anesthesia cart to get tx started (altho - in my experience, room there is scarce). Remember....pharmacists are responsible for keeping ALL the medications in date EVERYWHERE! Just think how much is stocked in some places??? That's why we have pyxis - they are on a routine check so everything stays in date. Can you imagine how often a bottle of intralipid would outdate in the radiology crash cart - its bad enough with epi.
But...this is an example of a need which has been identified by a service (OR) which needs to be communicated readily to another service (pharmacy). Altho 500ml of Intralipid 10% costs about $12 (don't know the cost for the lesser qtys - we aren't a tertiary pedi facility) the cost is inconsequential to the outcome alternatives. Just get your chief of service to call the director of pharmacy - its done!
btw...UT - there is NO non-pharmacist accessible pyxis anywhere. Who do you think stocks the pyxis???? Pharmacy (well - mostly pharmacy techs..but when they aren't there - pharmacists have to do it, altho we don't like it) We have a universal code to all the pyxis machines on all services - so call us......most of the stuff in pyxis is also in the OR pharmacy which is faster than having to get a nurse to figure out what the actual name is they are suppposed to look for (not to disparage nurses - they just aren't familiar with unusual names - like you asking for Dantrium, but its in pyxis under dantrolene, also...perhaps no Intralipid - its lipid emulsion). Call us - we're easy & fast - what a great combination
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the ucsf moffitt-long hospitals have stocked intralipid on all block carts for over a year, and it has been used at least once since then.
sdn1977 said:If this were brought before our P&T....it should be stored on the block cart & OR pyxis (pyxis is both plural & singular
Intralipid, altho, cheap, is not necessary everywhere - just some prominient places & it should be readily availble there. So....it should be wherever anesthesia should find a need for it - perhaps the 50 or 100ml (originally designed for neonate/pedi TPN) on each anesthesia cart to get tx started (altho - in my experience, room there is scarce). Remember....pharmacists are responsible for keeping ALL the medications in date EVERYWHERE! Just think how much is stocked in some places??? That's why we have pyxis - they are on a routine check so everything stays in date. Can you imagine how often a bottle of intralipid would outdate in the radiology crash cart - its bad enough with epi.
But...this is an example of a need which has been identified by a service (OR) which needs to be communicated readily to another service (pharmacy). Altho 500ml of Intralipid 10% costs about $12 (don't know the cost for the lesser qtys - we aren't a tertiary pedi facility) the cost is inconsequential to the outcome alternatives. Just get your chief of service to call the director of pharmacy - its done!
btw...UT - there is NO non-pharmacist accessible pyxis anywhere. Who do you think stocks the pyxis???? Pharmacy (well - mostly pharmacy techs..but when they aren't there - pharmacists have to do it, altho we don't like it) We have a universal code to all the pyxis machines on all services - so call us......most of the stuff in pyxis is also in the OR pharmacy which is faster than having to get a nurse to figure out what the actual name is they are suppposed to look for (not to disparage nurses - they just aren't familiar with unusual names - like you asking for Dantrium, but its in pyxis under dantrolene, also...perhaps no Intralipid - its lipid emulsion). Call us - we're easy & fast - what a great combination
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xjohns1 said:
Used with success??
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nimbus said:
Dantrolene is easily stored very long term as a powder.
Our main hospitals have at least 2 fully equipped, ready to go heart rooms, usually three or more cardiac surgeons in house either operating on in office, with perfusionists always on call. If the **** hits the fan, it's nice to know that you can call one of those guys. These guys are also blindingly fast and efficient. They have to be to turn a profit with heart surgery.
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How does Dandrolene work in this situation
Thx
Thx
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It doesn't - it's being used as an example of a drug that HAS to be available, even if you never have occasion to use it.dhb said:
The biggest differerence is cost. Intralipid is cheap - dantrolene is not. Plus, if I had to guess, local anesthetic toxicity is far more common than MH, an even more important reason to have the lipids readily available.
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jwk said:
Personal anecdote
I've seen 3 patients trigger with MH.
I've seen 1 case of bupivicaine toxicity ...a kid after a caudal.
but I suspect you are right about which is more common.
Why not just use Ropivicaine?
I know cost is more but with one incident like UT described your cost savings just went down the hopper...
I would think from a medico-legal standpoint you would be further protected by showing you made an effort, at a not insignificant cost to your facility, to prevent these occurrences, not just plan to treat them when they occur.
I know cost is more but with one incident like UT described your cost savings just went down the hopper...
I would think from a medico-legal standpoint you would be further protected by showing you made an effort, at a not insignificant cost to your facility, to prevent these occurrences, not just plan to treat them when they occur.
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fval28 said:
Ropivacaine, like bupivacaine, is also a lipophilic amide local anesthetic. It can also cause irreversible cardiac arrest albeit at higher doses. I would not recommend doing bier blocks with it.
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fval28 said:
I am not disagreeing with the above statement but there are people out there using 0.2% Ropivicaine for beir blocks. It lasts longer and once the tourniquet is down the extremity remains numb for a period of time unlike Lidocaine.
Just passing on information.
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Noyac said:
tell me how to do this.......and any references?
Noyac said:
Thanks Noyac,
Do you have any references for this? I would be interested in learning more about the practice- I assume the tourniquet needs to remain up for 15-20 min at least or is it longer with the ropivicaine?
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militarymd said:
I'll present them as soon as I can find them. It was about 4 yrs ago.
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Noyac said:
Its gonna try some searchin'. All I saw so far were bier blocks with bupivicaine.
Noyac said:Its gonna try some searchin'. All I saw so far were bier blocks with bupivicaine.
There actually was a study done in 1999 - reported in Anesthesia & Analgesia - I'm not familiar with the term bier blocks - but this was a comparison of ropivacaine & lidocaine using a double cuff technique of regional analgesia.....they concluded that ropivacaine provided longer sensory blockade & fewer CNS side effects (thats it in a nutshell - obviously...more detail in the study itself!) Does that reference help? Its pretty old......
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sdn1977 said:
Thats it. You ROCK.
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OK so here are some articles for you guys;
http://www.ncbi.nlm.nih.gov/entrez/...=Display&dopt=pubmed_pubmed&from_uid=16547088
http://www.ncbi.nlm.nih.gov/entrez/...=Display&dopt=pubmed_pubmed&from_uid=16547088
My med school bud is a gas attending at UVM. Just about 8 weeks ago, at their surgery center, about 20 min from main hospital...the husband of one of the anes residents was undergoig an interscalene block for a scope shoulder. Attending gas doc is doing the block when the pt arrests. obviously an intravascular placement. pt goes into wide complex arrest. CPR, 911, ambulance ride to main hospital with chest compressions. pt goes on bypass. reverts to SR after a length of time i do not know...pt is discharged i think 4-5 days later with no real neuro deficit. about 45 minute arrest time with intubation immediately and cpr immed.
I feel bupivicaine provides a much better block, but i have since been using ropivicaine bacause of this. that is one luck pt, and one even luckier attending....would have absolute shat myself....go figure, one of your own residents husband.....
the intralipid is interesting...may hae to include that on the crash cart...have one colleague that uses epi in his shoulder blocks...i do not, and had an MI at time of block in pt.....otherwise, no comps from regional that I am aware of in the year i have been here.........
on a side note. in a 10 or hospital, with a fair amt of ortho. all of the blocks we did only accumulated to about 55k in extra reimbursement total.....
I feel bupivicaine provides a much better block, but i have since been using ropivicaine bacause of this. that is one luck pt, and one even luckier attending....would have absolute shat myself....go figure, one of your own residents husband.....
the intralipid is interesting...may hae to include that on the crash cart...have one colleague that uses epi in his shoulder blocks...i do not, and had an MI at time of block in pt.....otherwise, no comps from regional that I am aware of in the year i have been here.........
on a side note. in a 10 or hospital, with a fair amt of ortho. all of the blocks we did only accumulated to about 55k in extra reimbursement total.....
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