Anesthesia Dogma

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Have you guys actually seen a wire embolus? I also used to think you shouldn't let go till I did an ICU rotation with this old school doc who was amazingly deft with CVL's. He ALWAYS lets go of the wire and claims it never moves an inch in or out when he isn't holding onto it. I mean its like what... 8 or so inches of wire sticking out beyond the skin - it would take some crazy venous pressure to suck it all the way in, right?

Ive seen one when I was an intern on SICU. It was placed in PACU and sure enough when we got the film back once she arrived in the ICU there it was. Not a fun conversation with the family. Why wouldnt you just maintain control of the wire. Its not like it slows you down.
 
Have you guys actually seen a wire embolus? I also used to think you shouldn't let go till I did an ICU rotation with this old school doc who was amazingly deft with CVL's. He ALWAYS lets go of the wire and claims it never moves an inch in or out when he isn't holding onto it. I mean its like what... 8 or so inches of wire sticking out beyond the skin - it would take some crazy venous pressure to suck it all the way in, right?

I am not sure I am following here:
are we talking about holding the end of the wire while advancing the catheter which you definitely should always do.
Or are we talking about holding the wire while it is sitting in the vessel before starting to insert the catheter which is really silly and is nothing more than an urban legend.
Here is how it goes:
You stick the vessel, thread the wire, take out the needle, you can let go of the wire to grab your catheter or introducer or scratch yourself if you need to, then when you start feeding the catheter over the wire you hold the wire at all times and feed it through the catheter until you see the end of the wire, then you hold that end and you don't let go of it while advancing the catheter, now you pull the wire.
 
here's mine: avoiding betadine/iodine/etc in people with shellfish allergy.

I hope this does not represent a "dogma" i'm allergic to shellfish and iodine/betadine. I had an episode of anaphylaxis when some shmuck decided that using iodine on me would be "okay" in light of the fact that i am allergic to shellfish and mollusks. Good work.😡
 
Have you guys actually seen a wire embolus?


I worked at a private hospital where residents rotated and there was a resident that did a line, the wire was sucked in or whatever, and he didn't say anything. The patient presented like 5 years later with some real problems and they discovered the wire.

Crazy eh?
 
I hope this does not represent a "dogma" i'm allergic to shellfish and iodine/betadine. I had an episode of anaphylaxis when some shmuck decided that using iodine on me would be "okay" in light of the fact that i am allergic to shellfish and mollusks. Good work.😡

How has shellfish allergy have anything to do with betadine? You cannot be allergic to a molecule (I2 in this case) you need a protein substrate.
Some people indeed develop reactions to betadine but this has nothing to do with shellfish allergy or even allergy to iv contrast agents.
 
I hope this does not represent a "dogma" i'm allergic to shellfish and iodine/betadine. I had an episode of anaphylaxis when some shmuck decided that using iodine on me would be "okay" in light of the fact that i am allergic to shellfish and mollusks. Good work.😡

Congrats, you're allergic to something in Betadine solution and something in shellfish and something in mollusks. The majority of people who are allergic (talking about significant IgE-mediated reactions) to crustaceans are not allergic to mollusks, or to fish. Or to Betadine!! Your "shmuck" did not do anything wrong.

Allergic individuals react to specific proteins present in whatever the trigger food is. In the case of crustaceans (shrimp, crab, lobster) this is a tropomyosin protein. This can be, but isn't necessarily, crossreactive with the protein that is found in mollusks. People which crustacean allergy have a higher incidence of mollusk allergy, but many people with crustacean allergies don't react at all to mollusks.

None of this has anything to do with iodine, which as was previously stated is an essential element found thoughout everyone's body, not a foreign protein. It is possible to have some type of adverse reaction to therapeutic doses of iodine, or a topical reaction to an iodine-containing prep solution such as Betadine, but these are not the IgE mediated anaphylactic reactions we're talking about.

It is a MEDICAL MYTH (tragically, still propagated even within the medical community) that people with "shellfish allergy" should not be prepped with iodine/betadine or given IV contrast material for CT scans. It is true that people with asthma or ANY type of food allergy (shellfish, egg, milk, chocolate, etc) have an increased risk of anaphylactoid reaction to IV contrast but this is unrelated to iodine (occurs even with non-iodine-containing contrast dyes). All that that says is something we already know- people who are allergic to one thing are at higher risk for being allergic to more than one thing ("atopic" individuals).


From the Food Allergy & Anaphylaxis Network "Allergy to iodine, allergy to radiocontrast material (used in some lab procedures), and allergy to fish or shellfish are not related. If you have an allergy to fish or shellfish, you do not need to worry about cross reactions with radiocontrast material or iodine."
http://www.foodallergy.org/allergens/fish.html

Regarding the use of IV contrast in persons with shellfish allergy, from the American Academy of Allergy Asthma and Immunology:

Once a person has one contrast reaction they are at very high risk for more unless treated. The reactions do tend to be worse in people who are dehydrated (dried out) when they are given the contrast in their veins. These reactions are not caused by iodine and are not more common in people with shellfish or any other true allergy. They can be minimized by pretreatment with antihistamines and oral steroids and/or using non-ionic contrast material that, interestingly, still has iodine in it.


Imma start a medical MythBusters, fo sho.
 
The risk in sticking an appendage that's had a lymph node dissection is lymphangiitis (theoretically) not infiltration. I have a friend who used a BP cuff on the arm post mastectomy and this case resulted in chronic edema and a slamdunk lawsuit. I think she should have been worked up for an axillary vein thrombosis, but she wasn't.

putting a blood pressure cuff on an arm causing chronic edema is a "slam dunk" lawsuit? Seems like something far from a slam dunk to me.
 
Oh man, too many in my mind to name:

1. Masks in the OR are stupid unless there are prostheses going in, immunocompromised pts, high risks for infection, etc. Some studies have shown increased infection rates with OR personnel outside of surgeons who are wearing masks compared to those who do not wear them.

2. Toradol is a great analgesic. Bleeding risk is very minimally increased with a single post-surgical dose. No, it doesn't affect bone-healing in humans either. Fantastic drug.

3. Blocks on fractures do not "mask" compartment syndrome if patients are monitored competently.

4. Femoral blocks do not increase fall rates (this month's journal).

5. I see very, very few reasons not to pull an LMA deep. Why wake a person up with a supraglottic airway device?

6. Don't get me started on Beta Blockers and Poldermans fictitious studies.

7. You don't have to go "perfectly parallel to floor" when doing a subclavian central line (how I was taught). For starters, the patient should be in frikkin trendelenburg so it makes no sense.

8. Eye lube is silly. Just make sure the upper and lower eyelids are completely shut to prevent corneal abrasions.

9. Nasal trumpets are way underutilized.

10. Way too many blown 16G PIVs when an 18G would have been just fine.

11. Take the black box warning off of Droperidol already. No decreased rate of Torsades since the warning.

12. A single cc test dose of antibiotics is silly. It can still cause anaphylaxis and muscle relaxants cause anaphylaxis more frequently and I do not see test doses of those frequently if at all. Just get the abx in the patient because they absolutely do prevent SSIs.

13. Arterial lines and their thrombotic complications are under appreciated, if even acknowledged in many cases. I know it's a low rate but I've seen 3 surgical interventions for radial artery thromboses throughout my residency. So not unheard of. Don't just throw them in willy nilly. Have a good reason to place it.

14. Brachial arterial lines are not more dangerous than radial arterial lines. Put a pulse oximetry on the same hand.

15. You can do a lot more cases without muscle relaxant than most residents think.

Ha, some may disagree with the above. Could go on all night. Sitting in a vascularathon right now....which reminds me....

16. Studies have shown residents reading in the OR do not have higher complications than those who "pay attention".
 
Oh man, too many in my mind to name:



2. Toradol is a great analgesic. Bleeding risk is very minimally increased with a single post-surgical dose. No, it doesn't affect bone-healing in humans either. Fantastic drug.


5. I see very, very few reasons not to pull an LMA deep. Why wake a person up with a supraglottic airway device?


11. Take the black box warning off of Droperidol already. No decreased rate of Torsades since the warning.


15. You can do a lot more cases without muscle relaxant than most residents think.

Agree with most but these are of particular interest to me. Especially the Toradol one. I think it was victim of a smear campaign (renal failure from 1 single shot, bone healing impairment, bleeding, asthma...) because it just worked too well.
 
Agree with most but these are of particular interest to me. Especially the Toradol one. I think it was victim of a smear campaign (renal failure from 1 single shot, bone healing impairment, bleeding, asthma...) because it just worked too well.

Yeah, I'm not sure what the manufacturer of toradol did to some surgeon's wives/husbands, but I think it should be used more.

I forgot a few that are some of my favorites. This is a fantastic thread, btw.

1.) Outside of airway fire reasons, maintaining on 100% oxygen does not matter in patient outcome. In fact, could be the opposite. If I'm that worried about atelectasis, I'll just do a few vital capacity maneuvers at the end of the case. If I have restricted access to the airway i.e. prone cases, table turning, surgeries around the face, the patient is on 100%. That's a precious minute or so to salvage a compromised airway in a delicate position. I rarely if ever see turning down Fi02 to decrease atelectasis actually in turn increasing saturations. Some studies have shown high Fi02 significantly decreasing SSIs. Why does this not get more pub?

2.) Not allowing laboring patients clear liquid is cruel and unusual punishment.

3.) I think the saphenous field block around the head of the tibia is a little bit hocus pocus. Saw a stat one time where only 30% are successful. If I'm using the U/S for a popliteal, I try to locate it with ultrasound between the sartorius and vastus medialis.

4.) See it not infrequently- let's go turn on an inhalational agent then hyperventilate the patient to 25mm Hg ETC02. Umm, what are you trying to do exactly? Either attempt to decrease the ICP or don't.

5.) I'm a proponent of surprise drug tests on anesthesia personnel to get rid of arduous ways of tracking narcotics. Peeing in a cup once a month would be greatly favored by me over having to document multiple times in multiple cases every day how many narcs I am giving, wasting, and returning.

6.) Last but not least, there has not been a documented case of bacteremia with propofol since a preservative was added.
 
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If the nurse suggests that 100% O2 causes atelectasis, do you have the energy to explain that this is not really an issue?
 
I believe the data supporting oxygen for lowering SSI is with an FiO2 of 0.8 compared to 0.3. I also believe there is literature supporting the role of high FiO2 in increasing formation of free radicals and increasing pulmonary injury in sepsis/ards. I am not aware of any literature that suggests a nonhypoxic patient should be kept on 100% oxygen during a case.

What we do with the ventilator in the OR for 1-4 hours is almost irrelevant on a short term basis. It's the small change in long term outcome of 1000s of patients that we start to make a difference in. I suspect within 5-10 years it will be seen as standard of care to adapt ARDSnet protocol ventilation strategies of smaller tidal volumes and higher peep to nearly all patients in the OR undergoing controlled ventilation. Somebody is going to do the prospective trial and I bet it shows it's better for longterm pulmonary outcomes.

It personally irritates me to see somebody put the 5'3" 350 lb woman on 825 ml tidal volumes in the OR with a rate of 10 rather than turning the rate up and the volumes down. The fat person doesn't have bigger lungs, just a bigger minute ventilation requirement and adding stretch injury to her alveoli won't help her postop.
 
1 I believe the data supporting oxygen for lowering SSI is with an FiO2 of 0.8 compared to 0.3.

2 I suspect within 5-10 years it will be seen as standard of care to adapt ARDSnet protocol ventilation strategies of smaller tidal volumes and higher peep to nearly all patients in the OR undergoing controlled ventilation.

1 I don't. There is just as much data saying it is BS.

2 I would say that time came a few years ago. If you haven't switched you are outdated.
 
I believe the data supporting oxygen for lowering SSI is with an FiO2 of 0.8 compared to 0.3. I also believe there is literature supporting the role of high FiO2 in increasing formation of free radicals and increasing pulmonary injury in sepsis/ards. I am not aware of any literature that suggests a nonhypoxic patient should be kept on 100% oxygen during a case.

What we do with the ventilator in the OR for 1-4 hours is almost irrelevant on a short term basis. It's the small change in long term outcome of 1000s of patients that we start to make a difference in. I suspect within 5-10 years it will be seen as standard of care to adapt ARDSnet protocol ventilation strategies of smaller tidal volumes and higher peep to nearly all patients in the OR undergoing controlled ventilation. Somebody is going to do the prospective trial and I bet it shows it's better for longterm pulmonary outcomes.

It personally irritates me to see somebody put the 5'3" 350 lb woman on 825 ml tidal volumes in the OR with a rate of 10 rather than turning the rate up and the volumes down. The fat person doesn't have bigger lungs, just a bigger minute ventilation requirement and adding stretch injury to her alveoli won't help her postop.

Your statement of literature supporting 100% oxygen is lacking is true, but that's not what the dogma is about. I'm not talking about why patients SHOULD be on 100%. I'm talking about dogma that dictates that patients should NOT be placed on 100% oxygen. Likewise, I am unaware of any literature concluding adverse outcomes in non-critically ill patients kept on 100% oxygen intra-operatively. Without evidence, there is nothing. And evidence would just require simple retrospective analysis. Still, studies are incredibly lacking. We can talk about theories and what we think would happen, but without evidence, there is nothing.

Also, oxygen toxicity is thought to take quite a long time to occur before you start seeing radical formation and damage. Even when the big papers and evidence for oxygen toxicity came out 40-50 years ago, it was accepted that it took much more than 2-3 hours for toxicity to take effect. So I think the toxicity argument is better applied to critically ill patients in the ICU. I think it's misguided to apply it to arguments for intraoperative events in non-critically ill patients. There is just no evidence.
 
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If the nurse suggests that 100% O2 causes atelectasis, do you have the energy to explain that this is not really an issue?


I think where this comes into play is during induction and intubation. You can knock out something like 15% of your lung volume with diffusion atalectasis. This translates to less time until desaturation. Could just have the patient cough in the mask a few times after you know the A-a gradient has leveled out.
 
Oh man, too many in my mind to name:

6. Don't get me started on Beta Blockers and Poldermans fictitious studies.

Now a SCIP quality measure for isolated CABG in patients on beta blockers. Thankfully, the life saving 5mg bolus of Esmolol qualifies.


8. Eye lube is silly. Just make sure the upper and lower eyelids are completely shut to prevent corneal abrasions.

I used to feel this way when I lived in Seattle. I quickly changed my tune when I moved to a much drier climate here in Montana.

9. Nasal trumpets are way underutilized.

Absolutely. Now if I could just get the damn PACU nurses to leave them in. It's seems like the first thing they want to do after applying monitors is pull the nasal trumpet. Then, once things calm down from the transfer I invariably see them holding jaw thrust. Arrgh.

11. Take the black box warning off of Droperidol already. No decreased rate of Torsades since the warning.

Haldol 0.5 mg IM. Discovered this once droperidol became impossible to get and wish I had discovered it earlier. Equally effective. Far superior side effect profile. Frequently smooths out wakeup a bit on short cases. I give it right after induction.

-pod
 
2 I would say that time came a few years ago. If you haven't switched you are outdated.

Whatever you think about when the time came, it is not even remotely considered standard of care at this point nor do we have any practice guidelines from the ASA suggesting it should be so.

I'm saying I think that will change in the near future.
 
Periopdoc,

Nice tidbit on the haldol. Thanks for that. I'm going to give that a whirl in the future. I'm 3 months from being under my own liability in private practice. I need to soak up these tidbits.
 
One of my favorites at my institution: Having the patient tilt his/her head all the freaking way back on the doughnut ("Tilt your chin ALLLLLLL THE WAY BACK sir... Look at the wall behind me...") while pre-oxygenating. I'd say > 50% of attendings I regularly work with do this and I just can't think of any particular reason why. The patient stays in that position for 1 or 2 breaths at most, then they get tired, or forget entirely, and turn their head back to neutral and the attending yells at them to do it all over again. Seems like such a waste of time and energy.

Another: Sniffing position! Apparently dogs sniff in all manner of different ways, because it never fails that when I put a folded blanket or two underneath the doughnut to push the patient's head anteriorly and align the ears with the sternum, some clown comes and pulls them out just as I'm inducing. Of course when I put the blade in the mouth and take a look...epiglottis. I have to then crank their head to the ceiling and use my ETT hand to support the occiput just to get a reasonable view.
 
it never fails that when I put a folded blanket or two underneath the doughnut to push the patient's head anteriorly and align the ears with the sternum, some clown comes and pulls them out just as I'm inducing.

Who is the clown? The attending? The circulator?
 
One of my favorites at my institution: Having the patient tilt his/her head all the freaking way back on the doughnut ("Tilt your chin ALLLLLLL THE WAY BACK sir... Look at the wall behind me...") while pre-oxygenating. I'd say > 50% of attendings I regularly work with do this and I just can't think of any particular reason why. The patient stays in that position for 1 or 2 breaths at most, then they get tired, or forget entirely, and turn their head back to neutral and the attending yells at them to do it all over again. Seems like such a waste of time and energy.

Another: Sniffing position! Apparently dogs sniff in all manner of different ways, because it never fails that when I put a folded blanket or two underneath the doughnut to push the patient's head anteriorly and align the ears with the sternum, some clown comes and pulls them out just as I'm inducing. Of course when I put the blade in the mouth and take a look...epiglottis. I have to then crank their head to the ceiling and use my ETT hand to support the occiput just to get a reasonable view.

I have found putting the patient in reverse trendelenburg before tubing is one of the best ramps out there. Like throwing a hot dog down a hallway sometimes.
 
How about not putting ipsilateral IVs on patients who have had breast surgery for fear of arm swelling?

Seems to me that if make sure you place the IV in the vein rather than in the tissue then you should be OK.

I have always wondered about this. So are you telling me that in reality, it is ok to place IVs in arms on the same side as mastectomy with lymph node dissection? On the same note, how about arms with old dialysis AVF that are no longer in use. Are we still not allowed to measure BPs or attempt IVs? Please enlighten me on this someone.
 
What about giving midazolam to a patient on HAART? The prep/PACU nurses are always so gung-ho to bring this up, even though they have no idea why.
 
pretreatment of asthma with albuterol preinduction
 
I have always wondered about this. So are you telling me that in reality, it is ok to place IVs in arms on the same side as mastectomy with lymph node dissection? On the same note, how about arms with old dialysis AVF that are no longer in use. Are we still not allowed to measure BPs or attempt IVs? Please enlighten me on this someone.
If she had only the sentinel node(s) removed, it's ok to place the iv ipsilaterally. Was told this by one of our best breast cancer surgeons.

I personally try to follow the patient's preferences, unless I have no choice.

Same goes for the idiocy of giving antibiotics for every single stupid procedure in a patient with a prosthetic joint. I am just tired of arguing with idiots.
 
I believe the data supporting oxygen for lowering SSI is with an FiO2 of 0.8 compared to 0.3. I also believe there is literature supporting the role of high FiO2 in increasing formation of free radicals and increasing pulmonary injury in sepsis/ards. I am not aware of any literature that suggests a nonhypoxic patient should be kept on 100% oxygen during a case.

What we do with the ventilator in the OR for 1-4 hours is almost irrelevant on a short term basis. It's the small change in long term outcome of 1000s of patients that we start to make a difference in. I suspect within 5-10 years it will be seen as standard of care to adapt ARDSnet protocol ventilation strategies of smaller tidal volumes and higher peep to nearly all patients in the OR undergoing controlled ventilation. Somebody is going to do the prospective trial and I bet it shows it's better for longterm pulmonary outcomes.

It personally irritates me to see somebody put the 5'3" 350 lb woman on 825 ml tidal volumes in the OR with a rate of 10 rather than turning the rate up and the volumes down. The fat person doesn't have bigger lungs, just a bigger minute ventilation requirement and adding stretch injury to her alveoli won't help her postop.
There is good data to support lower tidal volumes with High resp rates in the OR as it does affect outcome.

As to 100 percent Fio2 the best available evidence suggests an FI02 of 60 percent or less. This is what the mayo Clinic recommends as well. I'm aware of the study utilizing fio2 of 0.80 but it could not be duplicated. I see little evidence for the any benefit of fio2 beyond 0.60 in your standard patient not requiring extra oxygenation to maintain saturation
 
http://www.nejm.org/doi/full/10.1056/NEJMoa1301082

http://www.ncbi.nlm.nih.gov/pubmed/22156334


There is some weak evidence that an Fio2 of 0.80 may reduce the risk of SSI in patients undergoing colorectal surgery. This study has been used by proponents of high Fio2 to justify the routine practice of 0.80-.99 Fio2 in every patient for every case. Of course, the vast majority of healthy ASA1-2 patients won't suffer any consequences from this high fio2 but neither with they get much benefit ( small reduction in nausea). The subgroup we should be concerned about is the high risk surgical patient. In that subgroup caution is advisable and the best practice based upon evidence from the ICU is keep the fio2 down.
 
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The use of 100% FiO2 before tracheal extubation promotes atelectasis, which may be followed by significant complications such as pneumonia and in patients undergoing cardiopulmonary bypass may exacerbate lung injury manifested by a significant decrease in oxygenation and increased levels of bronchial tree cytokines [2,3]. Similarly, Zoremba et al. showed that perioperative saturation is significantly better in the first 24 hours in moderately obese adults undergoing minor peripheral surgeries if lower than 100% FiO2 is used, and in their study 80% oxygen was employed. The mechanisms of atelectasis in the perioperative period are complex, and it seems that use of lower than 100% FiO2 and perhaps a recruitment maneuver prior to extubation may be considered in order to resolve or at least partly improve the atelectasis that can develop in the postoperative period [4,5].
 
pretreatment of asthma with albuterol preinduction

why?

I have exercise induced asthma. If I go out running I'm wheezing and hacking up loogies within 1-2 miles. If I take 2 puffs of albuterol first, I can go till exhaustion without wheezing.

Do you not think albuterol works or do you find it harmful in some way?
 
why?

I have exercise induced asthma. If I go out running I'm wheezing and hacking up loogies within 1-2 miles. If I take 2 puffs of albuterol first, I can go till exhaustion without wheezing.

Do you not think albuterol works or do you find it harmful in some way?

I'm on the camp that thinks prophylactic preop albuterol is unnecessary. Does albuterol work?>Yes. Do I like to do unnecessary things?>No

Patients with real asthma are on long acting dilators and steroids. I see no reason to administer dilators for "mild asthma" when the patient is properly anesthetized.

"Asthmatic" patients are dime a dozen. However, in many years of practice, without administering any dilators, I have only had a handful of bronchospasms.

You have to understand that nowadays everybody is "especial", everybody has asthma, allergies, ADHD, autism......

It's all BS.
 
I'm on the camp that thinks prophylactic preop albuterol is unnecessary. Does albuterol work?>Yes. Do I like to do unnecessary things?>No

Patients with real asthma are on long acting dilators and steroids. I see no reason to administer dilators for "mild asthma" when the patient is properly anesthetized.

"Asthmatic" patients are dime a dozen. However, in many years of practice, without administering any dilators, I have only had a handful of bronchospasms.

You have to understand that nowadays everybody is "especial", everybody has asthma, allergies, ADHD, autism......

It's all BS.
You forgot that nowadays everybody has fibromyalgia, chronic fatigue and taking Oxycontin for chronic back pain.
 
I'm on the camp that thinks prophylactic preop albuterol is unnecessary. Does albuterol work?>Yes. Do I like to do unnecessary things?>No

Patients with real asthma are on long acting dilators and steroids. I see no reason to administer dilators for "mild asthma" when the patient is properly anesthetized.

"Asthmatic" patients are dime a dozen. However, in many years of practice, without administering any dilators, I have only had a handful of bronchospasms.

You have to understand that nowadays everybody is "especial", everybody has asthma, allergies, ADHD, autism......

It's all BS.

Does anybody give preop albuterol to somebody with mild asthma? I give it people with severe asthma or COPD. Helps decrease chance of severe bronchospasm after intubation in my anecdotal experience and has no real downside.
 
Does anybody give preop albuterol to somebody with mild asthma? I give it people with severe asthma or COPD. Helps decrease chance of severe bronchospasm after intubation in my anecdotal experience and has no real downside.
Unlike the "purists" on this forum or academia I'm pretty liberal with the use of Albuterol prep.

"Did you take your inhaler this morning? How often do you use your inhaler? What types of inhalers do you use at home? What induces your asthma or airway disease?"

If I don't like the answer to any of these questions the patients gets a preop treatment. I'm also VERY liberal with Solumedrol IV prior to induction as it can save your arse at the end of the case or in PACU.


http://www.cfp.ca/content/57/10/1134.full

I've done several literature searches on the issue ao spare me the lecture...please. One interesting thing I did come across was the use of decadron (10-12 mg) instead of solumedrol for asthma. Perhaps, all I need to do is up the dose of decadron?
 
Asthma – Does the steroid matter?
Posted on July 30, 2012 by sgschauer
Adults and children present to emergency departments on a regular basis with exacerbation of their condition for a variety of reason. Anecdotally, the standard treatment for run-of-the-mill asthma is nebs followed by a 5 day prednisone burst. However, does it really matter which steroid we use? And would the use of another steroid have advantages over the classical “gold standard” treatment? Here we will explore some literature that may help change your current practices.

Butler et al. prospectively conducted phone interviews following prescriptions of 161 children discharged from a pediatric emergency department regarding adherence to the prescribed regimen. They were able to follow up almost 94% of the discharged patients. They found that prescription fill rates were over 98%. However, they found slightly more than 1 in 3 caregivers reported not following the complete medication regimen. Most of them cited concerns about possible side-effects as the reason for not adhering to the regimen.

Lindenauer et al. retrospectively reviewed the charts of over 73,000 patients that were admitted for COPD exacerbation to a non-ICU bed. Co-founding factors were controlled among the two groups: high-dose IV steroids, low-dose oral steroids. They defined a treatment failure as mechanical ventilation more than 24 hours after admission, in-hospital death, or re-admission within 30 days for COPD. They found that low-dose oral steroids were not inferior to high-dose IV steroids. While this study focused on COPD, the general pathophysiology of COPD and asthma share a lot in common, including most of the treatment modalities. The take-home point here is that high-dose steroids are probably unnecessary, and IV steroids confer no benefit over oral regimens.

So, let’s take a look at some alternate medication regimens. Kravitz et al. did an RCT of 2 days of dexamethasone versus 5 days of prednisone for adults with acute asthma exacerbation. 200 patients were randomized to 50mg of prednisone for 5 days or 16 mg of dexamethasone for 2 days. They found that 90% of the dexamethasone group reported resuming normal daily activities at the 3 day mark compared to only 80% in the prednisone group. Additionally, they found the bounce-back rate to be the same between the two groups.

Now that we see that dexamethasone in adults is actually more effective in symptom relief than prednisone in adults, how does it perform in children?

Qureshi et al. randomized children 2 to 18 years of age with acute asthma exacerbation presenting to a pediatric emergency department to 5 days of prednisone at 2mg/kg (max 60mg) versus 2 days of dexamethasone at 0.6mg/kg (max 16mg). Hospitalization rates, relapse rates, and 10-day symptom persistence were equivalent in both groups. However, more parents reported non-adherence in the prednisone group (4% vs 0.4%) and more missed days of school (20% vs 13%).

Altamimi et al. randomized children ages 2 to 16 years old to a single dose of dexamethasone 0.6mg/kg (max 18mg) in the ED or 5 days of prednisone at 1mg/kg (max 30mg) twice daily for 5 days. Mean days to patient baseline by way of a standardized Patient Self Assessment Scoring system were equivalent in both groups.

Take home point: One to two days of oral dexamethasone is equal to, if not better, than a prednisone course. Additionally, treating patients with dexamethasone is likely to result in higher rates of medication adherence. In short, next time you treat a patient acute asthma consider 1-2 days of oral dexamethasone instead
 
Glucocorticoids

Early administration (within one hour) of glucocorticoids in the treatment of acute reactive airway disease results in fewer hospital admissions and a lower rate of relapse after ED discharge.97-99 Therefore, steroids should be administered to all asthmatics whose acute exacerbation is not relieved by one nebulized bronchodilator aerosol and given urgently to those who appear in moderate to severe distress.

While the exact mechanism of action is unclear, one theory proposes a reduction of airway inflammation, as well as restoration of β-adrenergic responsiveness in the constricted airways. Accepted dosage regimens in adults include prednisone (40-60 mg PO), a 60-125 mg intravenous bolus of methylprednisolone, or a 60-125 mg intramuscular dose of methylprednisolone. No clear benefit has been demonstrated by using “high-dose” steroids (> 80 mg/d of methylprednisolone) for those patients requiring hospitalization for their exacerbation, 100 though it is commonplace for adult patients to receive 120 mg of methylprednisolone in the ED.

Oral, intravenous, and intramuscular routes of administration of steroids share equal efficacy and have an onset of action of approximately four hours.98,101 In prolonged ED stays or ED observation units, steroids should be re-administered every 6-8 hours, whether they are given orally or intravenously. In one study, 125 mg of intravenous methylprednisolone increased PEFR and percent-predicted PEFR over time compared to placebo.102 However, because no well-designed trial has demonstrated a “head to head” superiority of one route over another, oral administration is the preferred route, particularly in children and even in moderately ill asthmatics if they are able to tolerate the drug (i.e., they do not regurgitate it within the hour).

Intramuscular steroids have also been well studied in the treatment of asthma. Studies on the use of intramuscular “depo” steroids show they are as effective as a seven- to 10- day course of oral prednisone.103 Side effects are rare.

In one randomized study, a single intramuscular injection (approximately 1.7 mg/kg) of dexamethasone acetate (Decadron, Dexasone, Dexone, Hexadrol) was as effective as a five-day course of oral prednisone (approximately 2 mg/kg/day) in children with mild-to-moderate asthma exacerbations. In a similar study involving adults, a single 40 mg dose of intramuscular triamcinolone diacetate (Aristocort, Kenalog, Aristospan) proved equivalent to prednisone (40 mg/d PO for 5 days) after ED treatment of mild-to moderate exacerbations of asthma.104 Intramuscular methylprednisolone sodium acetate (Depo-Medrol) is therapeutically equivalent to an eight-day course of oral prednisone.105Inhaled corticosteroids are currently under investigation for the treatment of the acute exacerbation and may be beneficial for asthmatics who have a more severe exacerbation.101,106,107 Home use of inhaled budesonide and oral prednisone is equally effective in patients discharged from the ED after treatment with systemic corticosteroids for a severe acute exacerbation of asthma.

In one study, patients randomized to receive either inhaled budesonide (Turbuhaler) 600 mcg QID (3 puffs QID) or prednisone 40 mg each morning for 7-10 days showed no difference in relapse rates.108However, combining inhaled with oral steroids does not consistently provide an additive effect.109 In one study, the addition of high-dose inhaled flunisolide to standard therapy (including oral steroids) did not benefit inner-city patients with acute asthma in the first 24 days after ED discharge.110 Other studies have confirmed this finding.111On the flip side, however, Rowe et al did show improved outcomes in patients who were prescribed inhaled corticosteroids at the time of discharge.112 In this study, patients with acute asthma who were discharged from the ED were prescribed inhaled budesonide (1600 mcg/d) or placebo added to a fixed course of oral prednisone. Those who received the inhaled budesonide had fewer relapses, fewer asthma symptoms, a decreased need for inhaled β-agonists, and reported an improved quality of life over the next 21 days.
 
I also give IV steroids preop if I'm worried about the possibility of severe bronchospasm during the case.
 
For a change I agree with Blade's statements...
There is nothing wrong with giving Albuterol to an asthmatic who is about to have a foreign body inserted in the airway, despite the lack of literature supporting the prophylactic use.
And the reason why Dexamethasone is better than Solumedrol is because Dexamethasone has more glucocorticoid properties which makes it a more potent anti inflammatory.
 
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