NSAIDs Part 1: Which one is best?

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I love NSAIDs!  Yup, love ‘em!

NSAIDs (Non-steroidal anti-inflammatory drugs) are some of the best analgesics available, plus they’re generally over the counter.  Despite their daily use for decades, NSAIDs remain sorely misunderstood.  I know they’re not a panacea, and they have some serious side effects in certain populations.   But for healthy patients without co-morbidities, they are pretty awesome painkillers, with no addictive potential (that I’m aware of).

Before we start, perform a Gedanken experiment if you will.  Not a true Gedanken Schrodinger’s Cat type experiment, but answer the following questions in your mind.

1) What is the best NSAID for analgesia?

2) Do oral or parenteral NSAIDs provide better pain relief?

Got your answers? Good.

Based on the conversations among staff, residents and nurses in the ED, oral or parenteral ketorolac (AKA: IM Toradol) is the strongest/bestest/most fantastic/awesome NSAID out there. 

WRONG!

I know that regardless of what I say from here on, some of you will stand by IM Toradol like a dying loved one. That’s okay, I understand.  It’s not your fault that you’ve been brainwashed into thinking this way.  Or maybe it’s anecdotal experience from years of practice, and I’m just a young pup who doesn’t know anything.

Just hear me out. 

What is the best NSAID for analgesia?

There isn’t one. 

They’re all the same when dosed appropriately. I cannot say it better than Grant Innes did in this 2005 review of ED pain medications.

“Although some agents have been advocated for specific indications (eg, indomethacin for gout), there is no compelling evidence that any one NSAID is superior to any other—for any indication. Consequently, NSAIDS should be selected based on convenience, cost, and availability rather than on theoretical efficacy advantages.”

Important to note are the dosing regimes for each NSAID, as they are more than often used in the ED:

Ibuprofen up to 800 mg QID

Naproxen up to 500 mg TID

Ketorolac up to 10 mg QID

Indomethacin up to 50 mg QID

*Edit: There is an important concept of ceiling effect with NSAIDs.  I left this out here, and it is very important so we'll discuss it in part two of the NSAID saga.  Thanks to reader @ETtube for pointing this out.

Other NSAID regimes are also found in this paper, but these are the most common ones in North America.

 

But what about IM toradol?  It always works for my patients.

I don't know but maybe these these guys know the answer.

That's right, Sanjay Arora and Mel Herbert from EM:RAP actually wrote a paper on this.  6 years ago!

I highly suggest you take 10 minutes of your day to read this great article in CJEM in 2007. The full text version is free as well.

Alternatively, I'll summarize it here.

1994 Wright et al.– Retrospective analysis of data that was collected by prior prospective survey. 

800 mg ibuprofen po vs. 60 mg ketorolac IM - NO DIFFERENCE in pain as rated by visual analogue scale (VAS)

1995 Turturro et al. – Prospective DBRCT (Double blind randomized controlled trial). 

800 mg ibuprofen vs. 60 mg ketorolac IM  - NO DIFFERENCE

1998 Neighbor and Puntillo – Prospective DBRCT. 800 mg ibuprofen vs. 60 mg ketorolac IM.  All patients had self-assessed pain between 5-8/10 on VAS. 

NO DIFFERENCE

*Funny thing about this study is the author’s name is spelled as Neighbour with a “U” in the text, but not in the references.  Funny because the Canadian CJEM autocorrect probably added the “U”.  Maybe funny just to me.*

They also cite two more trials comparing post-op pain with the same ibuprofen vs. ketorolac dosing, but at this point, you get the picture.

Finally, all of these studies compared 60 mg of ketorolac IM to 800 mg of ibuprofen.  Who actually gives 60 mg?  I've never seen it where I work, where 30 mg is the standard dose.  So, maybe ibuprofen is actually better than the 30 mg of IM ketorolac that we give.

Some of you may say, “I use the toradol for the placebo effect of an injection.  You can’t argue with that.” 

Sorry, someone studied that too.

This study by Schwartz et al. was a prospective DBRCT in which patients “were unknowingly given 800 mg oral ibuprofen in a flavoured drink and then given either a placebo IM injection or a placebo pill.”  No patient really received any IM medication in either group, and there was similarly no difference in the VAS between the two groups.  So IM for placebo effect only also appears unwarranted.  

Also, that study design is kick ass!

Treatment bottom line: 

There is no difference between NSAIDs when it comes to pain control.  Just use an adequate dose of whichever you choose.   

IM ketorolac still has a role in vomiting patients or those unable to take po meds, but don’t kid yourself that it’s a “stronger” medication.  It’s not.

Despite all of this, I agree that some NSAIDs work better for certain people?  Why is this?

Watch for parts 2 and 3 of the NSAID discussion, where we'll talk about this and much more.  

*Personal disclosure: I use ibuprofen almost exclusively, but also use Naproxen, as the BID (can go TID) dosing regimen generally means patients will be more compliant and hopefully have better pain control for a greater duration.  When we discuss side effect profiles in the coming weeks, you'll see why I don't use ketorolac.

Cheers,

SOCMOBEM

References:

Innes GD, Zed PJ, Emerg Med Clin North Am. 2005 May;23(2):433-65, ix-x. 

Arora S, Wagner JG, Herbert M. CJEM. 2007 Jan;9(1):30-2. 

Schwartz NA, et al. Acad Emerg Med. 2000 Aug;7(8):857-61. 

Thiamine Before Glucose will not cause Wernicke's Encephalopathy

If there's one area of medicine that suffers from more dogma than any other, it's toxicology.  

I'm not razzing tox, I love tox.  But management in toxicology usually = throw kitchen sink at patient, followed by a case report that concludes the last intervention done just prior to the patient improving is a new treatment for that toxicity. One of the biggest researchers I've published with once told me, "I don't do case reports, that's not real evidence based medicine".

Over the next few weeks we're going debunk a few of the best tox myths.

Before we get into myth #1, if you do not know about Leon Gussow's blog at The Poison Review, you should check it out here.


The other day, a fellow EM resident asked me about one of my favorite toxicology related myths. 

Will giving glucose before thiamine cause acute development or worsening of Wernicke's encephalopathy?

Like most medical dogma, this teaching can be traced back to case reports/series and a few animal studies.  This article from Schabelman and Kuo in JEM 2012 reviews the literature on this topic, and concludes that while prolonged (at least >24 hours and usually longer) administration of glucose without thiamine may worsen Wernicke's, there is no evidence for the near instantaneous development of Wernicke's that we are taught in medical school. 

Reading some of the studies that form the basis of this concept is both enlightening and entertaining.  One of the two studies that forms the basis of the Thiamine teaching comes from Drenick et al. in the NEJM, 1966. 

In this case report, a morbidly obese man (180 cm, 335 lbs.) was starved for just under two months (Feb.25 to April 20th), on a 500 calorie per day diet with no vitamin supplementation.  They measured daily thiamine in the urine and found it to be absent by 30 days.  There were 4 others originally in the study who also had absent thiamine by 30 days.  

The obese male developed nausea and required withdrawal from the study on April 20th, at which point they re-fed him with only glucose and orange juice for 13 days! Over that period, he developed worsening symptoms of Wernicke's encephalopathy, and upon administration of thiamine, his symptoms resolve over a period of days.  

The study that is most often cited regarding this myth is a 1981 article by Watson et al.  This case series looked at 4 patients who were given between 24 hours and 5 days of glucose without thiamine and developed partial/complete Wernicke's.  These resolved either partially or fully with the administration of thiamine. 

Finally, you may want to read this 1952 study by Phillips et al, if only to see what a crazy study design and lack of ethics looks like.  The study design here could be called random case series, observational study or high school science project.  They looked at 9 alcoholic patients with 6th nerve palsies other Wernicke's symptoms (presumably, as this was pre-CT head era, these patients may have had chronic SDH for all we know) and then fed them glucose only diets for days.  After a few days of getting worse, they'd start supplementing various quantities of thiamine, and some patients improved.

Bottom line: Giving glucose prior to thiamine will not precipitate an acute Wernicke's encephalopathy.  Prolonged administration (at least > 24 hours) of glucose only diets may worsen symptoms, but can then be reversed by giving thiamine.

Over the next few weeks, the site will be moving, so please bear with me.

Also, as there is so much great FOAM mythbusting going on out there, you may start to notice more short posts that collate already great FOAM resources.

Finally, there may be some guest bloggers coming on board in the near future, so you can look forward to an increased volume of posts here at SOCMOB.

Cheers,

@SocmobEM

References:

Schabelman E, Kuo D. J Emerg Med. 2012 Apr;42(4):488-94. doi: 10.1016/j.jemermed.2011.05.076. Epub 2011 Nov 21.

Drenick et al. N Engl J Med 1966; 274:937-939

Watson AJ, Walker JF, Tomkin GH, Finn MM, Keogh JA. Acute Wernickes encephalopathy precipitated by glucose loading. Ir J Med Sci 1981;150:301–3.

Phillips GB, Victor M, Adams RD, Davidson CS. A study of the nutritional defect in Wernicke’s syndrome; the effect of a purified diet, thiamine, and other vitamins on the clinical manifestations. J Clin Invest 1952;31:859–71.

Drinking the PPI Hate-O-Rade

Hi all, sorry about the extended hiatus.  I was away after Christmas for about 12 days and have been getting back in the swing of things over the past week.  

Since the break, one great new blog that has popped up on the FOAMed landscape is the boringem blog, started by Brent Thoma, one of the other ER residents in Saskatoon.  You can check it out here.

Also, look for a new blog section for med ed. videos in the near future.  I'll start it out with a cardiology parody I made back as a med student.  Watch for a How To video on making a homemade cricothyrotomy trainer soon.

Onto the blog.

Proton pump inhibitors (PPIs) have been taking a beating in the FOAM arena lately, with a large portion of the credit going to David Newman of SmartEM and theNNT.  Just before Christmas, theSGEM blog did an excellent blog post and podcast on this topic as well.  The links above will allow you to review the common misconceptions surrounding PPIs, as well as the evidence to support this. 

Briefly, PPIs have been thought of as a panacea over the past decade, with the 80 and 8 bolus + infusion protocol thought of as the cure for all UGIBs.  Unfortunately, this 2010 Cochrane systematic review on PPIs for UGIB showed no reduction in mortality at 30 days, nor did it show any reduction in rebleed rates or requirement for surgery at 30 days.  Transfusion requirements and hospital LOS could not be analyzed, but there is no good, reproducible evidence that these outcomes are improved either. 

At this point, it seems pretty obvious that I'm not too keen on the empiric use of PPIs for UGIB.  Unfortunately, there's one reason we will not win this battle with gastroenterologists any time soon.  Need for endoscopic intervention.  This RCT by Lau et al. showed that despite no reduction in other significant outcomes, there was a decreased need for endoscopic therapy (28% vs. 19%, p <0.007).

As ER physicians, we do not admit or scope our UGIB patients.  We resuscitate, stabilize and refer for endoscopy.  Despite the fact that there is no change in major outcomes (eg. mortality, rebleeding and surgery), a faster endoscopy requiring less intervention remains a significant outcome for the physician performing it.  For that reason, I find it difficult to believe this battle will be won by ER physicians any time in the near future.  I would love to be proven wrong.

My question to readers is if you have discussed this with your GI docs, and what reasoning they are using for the PPI infusions?  Please post in the comments if you have.

However, I think it remains important for med students, residents and nurses to understand that the PPI infusion is not the most critical intervention in the course of the UGIB patient. 

Bottom Line: PPIs do not reduce 30 day mortality, rebleed rates or surgery requirements at 30 days.  However, because of reduced need for endoscopic intervention and the prolonged period required for knowledge translation, their empiric use will continue for the foreseeable future.

Cheers,

SOCMOBEM

References:

Cochrane Database Syst Rev. 2010 Jul 7;7:CD005415. Review. PubMed PMID: 20614440

N Engl J Med. 2007 Apr 19;356(16):1631-40.

Evidence Based Laceration Repair

First, a huge thanks to everyone who has been visiting the site, tweeting and spreading the #FOAMed love.  FOAM is all about word of mouth, and having others spread the word drives me to put up more posts.  Second, if you have comments or suggestions to improve the blog, questions for me, or myths you'd like to see busted, please tweet or email.  I'm always looking for new ideas.

Also, a shout out to a new podcast I've found recently.  The SGEM (Skeptics Guide to Emergency Medicine) podcast is based out of Ontario, Canada, and takes a similar approach to topics as I do.  Episode 9 covers some of the wound management myths I'm about to deal with, and a few others I've left out.  It can be found on iTunes or on their website http://thesgem.com/

Onto the blog.

Case: A 25 year old female presents to the ED with a 3 cm laceration to the dorsum of her forearm.  It is superficial, entering only the hypodermis.  It is easily approximated, not over a joint, and under no tension.  Before reading on, mentally go through the steps of how you would manage this wound. (eg. cleaning, prepping, suture material, dressing) Got it?  Read on.

No procedure in medicine contains as many ancient, dogmatic teachings as laceration repair.  Considering this is something we do and teach every day, it's critical that we have an evidence based approach.

In this post, I will present the thinking that goes through my head as I prepare to close a wound.

NB. Throughout this post, we are talking about uncomplicated lacerations/wounds ie: no fracture, foreign body, tendon injury, bone injury, joint injury, immunosuppression, anti-coagulation, etc.

The reason behind all of the laceration repair dogma can be summarized in one word, infection.  

We've all seen someone prepare a simple cut as if it were an open abdomen in the OR.  Why?  Not so long ago, surgeons began using sterile technique in the OR; this was critical for reducing post-op infection rates.  Naturally, that meticulous preparation was then passed down to ED physicians as lore.  

But lets think about this for a minute.  There are millions of lacerations every year, and we see a miniscule number of them in the ED.  The rest are managed at home with water, some paper towel and maybe a band-aid.  That's certainly not sterile technique.  So why aren't our departments overrun with wound infections from people who cut themselves and didn't waste 4 green huck towels, a bottle of chlorhexidine, a sterile kidney basin, and countless other tools?  Because clean wounds rarely get infected. 

Preparing wounds with sterile technique and meticulous detail is not only unnecessary from an infectious standpoint, it's time consuming.  As a medical student and resident, laceration repair is great.  It's fun, you get to work with your hands, sit down, take a mental break.  Overall, as a presenting complaint, laceration is about as good as it gets.  As I get closer to the realm of being a staff physician, I view lacerations differently, in much the same way as I look at insertion of lines and tubes (see previous blogs).  Properly repairing a laceration remains the most important element, but efficiency and managing department flow are also critical.  Furthermore, I don't want to waste my patient's time by having them unnecessarily return to the ED for follow-up, suture removal, or complications of the procedure.

Onto the pseudoaxioms.

1)Wounds must be cleaned with fancy solutions.      NO!

    VS.     


We usually clean lacerations with tap water at home, so why do we need sterile water/saline or chlorhexidine in the ED? 

Thankfully, this has been studied.

First, forget antiseptics.  There is little, if any evidence that chlorhexidine or other antiseptics reduce rates of infection.  Conversely, chlorhexidine and povidone-iodine solutions are more likely damage normal cells and slow healing.  These are skin cleansers, for external use only.

So the real choice is between tap water and sterile saline/water.

This Cochrane Review last updated in 2010 included 11 quasi-randomized studies, 3 of which were RCTs.  In adults, tap water is at least as good, if not better, than sterile saline for preventing infectious complications.  In children, there was similarly no difference between tap water and sterile saline. 

I think my favorite part of this review is the authors conclusion that there is no evidence that cleansing a wound is better than not cleansing it.  Now that would be a kick ass RCT!  Even if it passed ethics, I think you'd need a used car salesman to consent the patients for the no cleansing group.

This prospective RCT done in 2007 also compared sterile saline with tap water.  Though the study had several problems, one thing it made clear was the cost savings of using tap water in place of sterile saline, a syringe and splash guard would be ~$65.6 million annually in the U.S.  That's huge!

Disclaimer: If you don't have a clean tap water source, this likely doesn't apply, but you could still be using boiled and cooled distilled water in place of the more expensive alternatives.  

When I clean a wound in the ED, especially if it's an upper extremitiy, I will anesthetize, walk the patient over to the sink, and wash their hand under running water for a few minutes. The volume difference is huge, and it takes virtually no time at all.

Bottom line: Tap water is just as good, if not better than sterile saline for irrigating simple wounds in the ED.

2)Glove selection



After I've cleaned my patient's hand in tap water, should I grab some sterile gloves to sew them up?  Maybe the patients love to see me snap on those fancy gloves that come from their own, individually sealed bag.

Bottom Line: Clean gloves are just fine.  
The best data on this comes from a 2004 study by Perelman et al. in Annals of EM.  This Canadian study was a prospective RCT, and looked at 816 patients over the age of 1 year with simple lacerations.  They found the infection rate for sterile vs non-sterile gloves was 6.1% and 4.4%, respectively with no significant statistical difference.  

Again, the cost difference between using sterile and non-sterile gloves is massive when we consider how often they are used on a daily basis.  

I will admit that in cases that require a significant amount of suturing or I want an optimal cosmetic result, (eg. facial lacs) I will use sterile gloves because they provide a much better feel than the non-sterile ones.  Go ahead and call me a hypocrite.  

3)All lacerations must be sutured using non-absorbable suture.

First, there is evidence that not all lacerations < 2 cm even require suturing in the first place.  But let's say that we do decide to close this laceration, how will we do it?

Who asks for prolene, ethilon or another non-absorbable suture when they repair lacerations?  What about vicryl rapide, fast chromic gut or another absorbable suture?  Does anyone ask for glue?

Has anyone heard this: Don't use absorbable sutures or glue, they'll get a nasty scar! 

Let's look at the evidence.

First let's take the scenario of the 3 year old child with a non-gaping facial laceration after running into a coffee table.  I'm sure many of us have gone through the joy of anesthetizing this child and suturing them while a nurse holds them in a death grip.  All the while, the parents are looking on horrified and never wanting to return to the hospital.  

 

While rotating through the Alberta Children's Hospital (AKA Lego-land with an ICU), I was exposed to all the awesome ways of repairing lacs in kids.  The children would have topical maxilene or lidocaine applied at triage and we would sometimes give intranasal midazolam as well.  Suffice it to say, this place is pretty much heaven as far as peds EM is concerned, and laceration repair was all happiness and roses.  Unfortunately, most of our EDs do not have these luxuries, but we do have one awesome thing.  Glue!

Again we have some Canadians to thank for this Cochrane Review looking at tissue adhesives vs. standard wound closure for laceration repair.  Eleven studies compared a tissue adhesive with standard wound closure. No significant difference was found for cosmesis at any time point examined. As would be expected, pain scores and procedure time significantly favoured tissue adhesives.  However, there was a statistically significant increased rate of wound dehiscence favouring standard wound care, with a NNH of 40.   

But what about gaping lacerations where glue won't work?

Traditionally we are taught to always use non-absorbable sutures, as they are stronger, less prone to infection, etc.  Having been sutured up several times as a child, I recall fearing the return visit for suture removal even more than the initial visit to get sewn up.  When a child is bleeding everywhere, the pain is bearable, but pulling out the scissors and forceps in front of a completely well child creates unnecessary fear.

Can we avoid this return visit without compromising cosmesis?  Yes.

This 2004 paper by Karounis et al. looked at pediatric patients (0 to 18 years) with traumatic lacerations.  It showed no differences in early or late cosmesis, wound dehiscence or need for scar revision when comparing absorbable and non-absorbable suture.  In fact, all of the outcomes showed a trend toward benefit in the absorbable suture group.  (I know, trends don't mean squat in EBM)
The main weakness of this study was the extremely high loss to follow-up of 34%.  However, this is a very common weakness of laceration repair studies, and getting good follow-up in these types of studies seems impossible.

Another study from 2008 looked at fast absorbing catgut suture vs. nylon in 88 pediatric patients.  Again there were no differences in cosmesis, infection rate, dehiscence, keloid formation or parental satisfaction.  This paper also suffered from a lack of follow-up (though it was equal in both groups).

Bottom Line: For non-gaping lacerations, glue is where it's at.  For gaping lacerations in children, absorbable suture is at least as good as non-absorbable. 
The savings on patient/parental trauma and time are huge. 

Note: Although I didn't cover staples, they are likely as good as sutures for repairing scalp lacerations.  There are small studies comparing them, but no large RCTs.

4)After closing the wound you should apply a topical antibiotic such as polysporin/neosporin.

This one may be my biggest peeve of all, as somehow the marketing of topical antibiotics that are primarily effective against Gram -ve bacteria has resulted in physicians regularly recommending these to patients.  For this, we have to go to the Dermatology literature.  This peeve comes from doing 6 weeks of dermatology electives, several of which were spent with someone who only did patch testing for contact dermatitis.

It is true that a clean, moist, covered wound will heal faster than an uncovered, dirty wound.  However, all of the dermatology literature points toward non-antibiotic containing petroleum based lubricants being equally efficacious to neomycin (Neosporin), bacitracin and polymixin B (both in Polysporin) containing ones.  Furthermore, neomycin is the number one contact allergen in patch testing at a whopping 11% of the U.S. population.  Bacitracin is not far behind at 8% of the population.
Fortunately Neosporin is no longer sold in Canada, but it is the bane of American dermatologists.

Bottom Line: Use Vaseline, Aquaphor or other petrolatum based gel for wounds, and stop creating allergies.


Summary:

1)Tap water is as good as sterile saline

2)Clean gloves are fine

3)Glue and absorbable sutures provide the same cosmetic results as non-absorbable ones, particularly for facial lacerations.

4)Use non-antibiotic, petrolatum based gels to cover wounds, not poly/neosporin.

You now have all the evidence you need to manage simple lacerations in 5-10 minutes, without putting your patients at increased risk of infection, giving them an ugly scar, or causing a contact dermatitis.

Until next time, I'll be getting up in people's faces, not minding my own business.  I'm way less likely to get stabbed that way.  

Happy sewing.

SOCMOBEM


References:

Cleaning Wounds:

Fernandez R, Griffiths R. Water for wound cleansing. Cochrane Database of Systematic Reviews 2008, Issue 1. Art. No.: CD003861. DOI: 10.1002/14651858.CD003861.pub2. 

Moscati RM et al. Acad Emerg Med 2007; 14:404–410

Gloves:

Perelman VS et al. Ann Emerg Med. 2004 Mar;43(3):362-70.

Suture and glue:

Farion KJ, Russell KF, Osmond MH, Hartling L, Klassen TP, Durec T, Vandermeer B. Tissue adhesives for traumatic lacerations in children and adults. Cochrane Database of Systematic Reviews 2002, Issue 3. Art. No.: CD003326. DOI: 10.1002/14651858.CD003326. 

Karounis H et al. A Randomized, Controlled Trial Comparing Long-term Cosmetic Outcomes of Traumatic Pediatric Lacerations Repaired with Absorbable Plain Gut Versus Nonabsorbable Nylon Sutures Acad Emerg Med July 2004; 730-735

Luck RP et al. Pediatr Emerg Care. 2008 Mar;24(3):137-42.

 

Welcome to SOCMOB!

THE INTRO

 

"You're not going to use lidocaine with epi for that ring block, are you?"

"Whoa, that potassium is 7, go get some Kayexalate."

"Calcium in a digoxin overdose, you'll kill them!"

Do any of the above sound familiar to you?  I hope so!

I'll venture to guess that many of you have heard injecting the "fingers, toes, ears, nose or hose" with epinephrine will cause your patient's bits to start falling off.  Or that Kayexalate will "exchange that potassium" and fix hyperkalemia. And if you give an amp of calcium to a dig toxic patient, their heart will turn to stone!

What is this all about?  

 

David Newman of the NNT and SMART EM fame said it best in this article from Annals of EM in 2007:

"Although axioms are universally accepted principles or rules, pseudoaxioms, like pseudoscience, are false principles or rules often handed down from generation to generation of medical providers and
accepted without serious challenge or investigation."

As medical trainees, whether we are nurses, paramedics, residents, or any other health care provider, we are bombarded with information at every opportunity.  Often, it is the simple question, "Why?", that befuddles us or our preceptors the most.  We often respond with correct, evidence based answers.  But just as often, we give answers like "that is how we've always done it" or "Rosen's, Tintinalli's or (insert other textbook) says so?  It is at times like these that we must go back and look at why humans, and not computers, practice medicine.  

Medicine is a field based in Science, and prides itself on the powers of observation, logic and reasoning.  Over thousands of years, observation has served us extremely well, but in the past few decades, there has truly been a paradigm shift.  Evidence based medicine.  More recently, Free Open Access Medical Education or Med-ucation (FOAM) has spread like wildfire, and we are able to share information in real time, across the globe.  Rather than wait months or years for an NEJM article to be published and disseminated across the country, we can now tweet critical appraisals of articles that came out yesterday.  

Combining EBM and FOAM, medicine is in a golden era, not because of the superior technologies and techniques we have available, but because we can instantly re-examine the evidence for a particular topic through an online search.  Just tweet it to a friend, and the discussion begins.

Let's take a look at the pseudoaxioms mentioned above.  Since it's an intro blog, I've chosen three that have been reviewed beautifully by some of the super-geniuses in the EM world.  

First, the purported dangers of injecting epinephrine into digits.  

This was still (and maybe still is) published in Toronto Notes when I began medical school in 2006. For Canadian med students/residents, Toronto Notes is kind of like a bible for our end of medical school licensing exam.  In addition to the paper linked above, David Newman gave an amazing lecture on pseudoaxioms for USC Grand Rounds in Nov. 2011.  It can be found in the itunes store if you search "USC Emergency Medicine."  

Bottom line:  Don't put your finger in hot boric acid!   A common theme that arises from papers advocating against the use of epinephrine was the surgeons sending their patients home with instructions to keep their wounds clean by immersing them in "hot boric acid".  Sometimes, the patients were still partially or fully anesthetized, and thus could not feel the temperature or severity of the burns being caused by the acid.  

In his lecture, Dr. Newman also covers some other great ED myths including; septal hematomas, treatment of strep throat and others.  Well worth a listen.

Second up is the use of Kayexalate or sodium polystyrene sulfonate for treatment of acute hyperkalemia.  There is a brilliant podcast over at the emcrit site that is a must-listen for anyone who has ever used Kayexalate.  Have a listen, then do yourself a favor and look up the two 1961 NEJM references and have a read.  Great stuff!

Bottom line: Kayexalate is no more effective than placebo in reducing potassium for treatment of acute hyperkalemia.  The drug was approved by the FDA in 1958, yet it was 3 years before a study was required to be done on it.  This study is a must read, as it contained 10 patients, 5 of whom received sorbitol+resin, 3 received sorbitol only and 2 received sorbitol+resin as an enema.  The sorbitol only group had a non-statistically greater reduction in serum potassium (6.3 to 4.6) than the sorbitol+resin group (6.6 to 5.2).  They state "sorbitol alone is as effective as a combination of resin and sorbitol in removing potassium, or more so. However, sorbitol alone necessitated a greater volume of debilitating diarrhea. In either case the predictability of the fall in serum potassium was impressive." A second study supporting the use of Kayexalate was in the same issue of NEJM, and was an uncontrolled, 32 patient trial with NO CONTROL GROUP.  Yup, times have changed.

Recently, there have been multiple case reports of intestinal ischemia/colonic necrosis with Kayexalate, one of which can be found here.  Safety and effectiveness are reviewed by Sterns et al. here.  So when I show up with my K of 8, no Kayexalate for me please.

Finally, digoxin toxicity.  As a cardiac poison that's been in use for hundreds of years, the literature on this is a lot of fun to read.  There are countless articles that start with sentences like "Over the past year I have seen four cases of poisoning with foxglove", which is how articles were written back in the day.  Along with this body of mostly observational literature comes many conclusions based on case reports, including the concept of the "stone heart".  This refers to cardiac arrest precipitated by giving calcium to hyperkalemic patients.  Amit Maini of ED Trauma Critical Care does a great job of reviewing this here.

Bottom line: Calcium is unlikely to cause any harm in acute digoxin toxicity, and even less likely in chronic toxicity.

Inspired by the great reviews above, I'll do my best to analyze other medical dogma, and separate the axioms from the pseudoaxioms.

Please send me your questions, comments and ideas for future topics using the contact page, comments or on twitter @socmobem

Cheers!