Hey all, this is just a short snippet, not a full blog post. As the 2012 Surviving Sepsis Guidelines were just released, I'm just making a few comments and directing you to Scott Weingart's great podcast on the guidelines.
Everyone who takes care of emergent/critical care sepsis patients needs to take 18 minutes of their life and go listen to Scott Weingart's new Practical Evidence podcast on the 2012 Surviving Sepsis guidelines here.
The whole document is 60 some pages, but the big highlights for me are:
Good:
1)Lactate clearance now included as measure of tissue perfusion - But there is also some BAD with this one (see below).
2)Norepinephrine is 1st choice vasopressor for all patients.
3)Epinephrine as 2nd vasopressor, followed by vasopressin (new does 0.03 units/min)
4)Dopamine pretty much gone - Yay!
5)Protective lung ventilation strategies for sepsis induced ARDS
Bad:
1)Still recommending use of CVP goal of 8-12 mmHg to guide fluid therapy. Haven't we beaten this dead horse enough. See here
2)Still recommends SCvO2 to monitor tissue perfusion. This is fine if you have a CVL, but they do not make mention of lactate clearance being non-inferior to SCvO2. Also discussed in previous post on CVL (linked above).
3)Recommends delaying antibiotics up to 45 mins to give BCx. Uh, isn't time to antibiotics our #1 goal?
4)No recommendation for U/S of IVC, but still recommend static markers (HR/BP) to guide fluid responsiveness.
Scott does a great job of going over all of this and more in his podcast. A summary of the guidelines is also found there.
Cheers,
@SocmobEM
Thursday, 24 January 2013
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:
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.
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.
Wednesday, 16 January 2013
How to make your own Cricothyrotomy Trainer
Who has done a cricothyrotomy?
Who thinks they would be comfortable doing a cric if asked? Without having a code brown first?
Though I have done a few tracheostomies (only three on live people), I've never done a cric on anyone. Furthermore, when it's time to cric, we need to be ready. Unfortunately, we can't practice on our fellow residents, cadavers are hard to come by, and industry made cric training devices are hundreds of dollars to purchase. How are we going to be ready to cric without any practice?
While there are many great videos out there showing how to perform a cric, they are usually performed on cadavers/simulators, which most of us do not have routine access to. In particular, Scott Weingart from EMCrit has a great quick n' dirty cric video which can be found here.
While Scott's video is awesome, there aren't any videos on how to make your own cric trainer, so I thought it would be nice to fill that gap. Below you'll find a video I've made showing the steps for making your own cric trainer.
This 2004 Anesthesiology article provides the basis for making the cric trainer. In this article, Varaday et al. compared use of a cric trainer made from a few standard operating room supplies (AKA Homemade) to expensive commercially available cric trainers. 20 anesthesia trainees practiced on the homemade device, while a second group of 20 trainees practiced on the commercial devices.
The study concluded, "trainees found the homemade model a useful substitute for practice of percutaneous techniques and teaching" and "both models were rated well, with similar scores. The homemade model is an easily assembled alternative to more expensive models"
The advantage of this cric trainer is being inexpensive, reusable and pretty realistic. I think the greatest value of this trainer will be for those who are required to teach cric's, especially for large numbers of residents/students. One set of ventilator tubing provides enough practice "trachea" for a large number (eg. > 10-20) of cric trainers, and the remaining materials are easily accessible.
If you are an individual resident/student looking to practice your skills, you'll just have to politely ask an anesthetist/OR staff to give you a few supplies. If you tell them the purpose of it, I doubt they'll have much problem with it.
Click the YouTube link if above video isn't working
Having now performed a few real life tracheostomies, I think this trainer is actually very good, and approximates the real thing quite well considering how easy and inexpensive it is to make.
You'll notice I made a few modifications from the trainer used in the article:
1 - If you only have single thickness vent tubing, reinforce the tubing and the skin with 2-3 pieces of iv tape. I find this definitely mimics reality a little better with regard to the difficulty of cutting the skin and trachea.
2 - I don't completely cover the trainer with tape as they do in the article. I find this is not totally necessary and allows you to rotate your vent tubing more easily to make a "fresh" trachea.
3 - I have not attached a bag here to act as lungs, but if you have an O2 source and jet insufflation equipment, attaching an old bag from the anesthesia cart will add to the realism.
That's all for today, watch for some upcoming toxicology myths that I'll be busting over the next few weeks.
P.S. I know today's blog was again a detour from busting up pseudoaxioms and dogma. Overall the SOCMOB blog will continue to focus on dispelling medical myths, but I'll also be incorporating more procedure videos, rants and interesting cases as well.
Happy cric-ing,
@SOCMOBEM
References:
Varaday SS et al. Anaesthesia. 2004 Oct;59(10):1012-5.
Sunday, 13 January 2013
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.
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.
Monday, 24 December 2012
Choosing your Battles: My Christmas Pearl of 2012
This blog post isn't about EBM or getting my hate on about antiquated dogma; it is about a useful pearl that I think can benefit all of my like-minded, avant-garde, #FOAMed friends out there. In particular, this is a piece of advice that the "young whippersnapper" types like myself should pay attention to.
Last week while at Tintinalli Rounds with one of my preceptors, we covered tons of material and talked EBM galore. It was a nerd alert to the extreme. While we were ranting about how "ridiculous" it is to give gravol to pediatric patients with gastro, and that ondansetron is the evidence based pediatric panacea, we paused for a serious discussion. As residents soon to enter practice, he gave us this advice.
"Choose your battles"
Having only graduated from residency a few years ago, this preceptor moved from a highly respected pediatric EM fellowship program to a pediatric EM department in its relative infancy. Upon arrival, he did what most of us would do in the same situation. He wanted change. And he didn't want a bit of change, he wanted a revolution. There was room for improvement everywhere, with everything.
However, he quickly realized that enthusiasm only goes so far, and knowledge translation can be a bitch.
Rather than revolutionize a new department and effectively ostracize himself in the process, he chose the battles that he wanted to fight. Every time he saw something in need of change, he asked himself, "is this a battle I want to fight?"
Ondansetron for pediatric gastroenteritis was a battle he wanted to fight, and there were a couple of others as well. By limiting himself to a few battles, he could effectively stimulate change, while keeping his new colleagues from beating him senseless.
(Oh fine, I keep mentioning the peds gastro thing so head over to theNNT for a summary of this if you're interested.)
He also made the point that while some of us are up to date and evidence based, that knowledge will never supplant the 20 years of experience that our older colleagues have. Rules and scores allow junior physicians to "catch up faster", effectively giving us some of the gestalt that thousands of hours of ER medicine have traditionally provided. So despite all of your book knowledge, respect your seniors/colleagues.
Another form of choosing your battles is what to do as learners desiring to challenge the status quo.
Here's a twitter conversation I saw today
The context here is that PPIs are not the miracle UGIB treatment that we once thought, and that Lauren, a FOAM loving medical student, tried unsuccessfully to convince someone (I'm guessing an attending) of this.
This is another form of choosing our battles. As junior learners/staff, we need to diplomatically approach these topics, and be selective as to how often we question the methods of our seniors. Nobody likes the learner (or colleague for that matter) who contradicts everything. I know I have probably been that annoying resident in the past, and thus ask myself "is this really worth it" before choosing a battle. Furthermore, if circumstances (eg. busy shift, non receptive preceptor) indicate I am about to run into a stone wall, sometimes it's better to just "abort mission" and try again at a better time/place.
For what it's worth, I think Lauren picked a great battle here, and her follow-up tweet to this is impressively mature. This is an excellent example of the attitude FOAM advocates should have, so take note.
To summarize, being young and enthusiastic about medical education, EBM and FOAM is awesome. But regardless of your medical profession (EMT, nurse, resident, etc.), if you are keen and on the FOAM bandwagon, you will be saying some crazy sounding things. If you are in a position to effect change, fantastic, but this is another situation where less may be more, and choosing your battles wisely is a lesson for us all.
It's been Christmas Day for 30 minutes now, so put in the Die Hard (or whatever your favorite Christmas movie is), and do not stand on the corner minding your own business. Bruce Willis was just minding his own business at Nakatomi Plaza and look what happened.
With that, I wish you all Happy Holidays (whatever you may celebrate) and a great 2013.
SOCMOBEM
Saturday, 8 December 2012
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:
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.
Friday, 23 November 2012
The Gaco Cycle (No educational content)
Two weeks ago, some of the EM residents and I were in Las Vegas for the Essentials of EM conference. It was a great time, with many highlights, one of which was the first night of drinking with Damjan, AKA the Serbian teddy bear. Damjan's (pronounced Dam-yin) mission was to get blind drunk ASAP after getting off the plane, so he proceeded to get 4 double tremclad-cokes (actually bourbon, but they tasted like paint thinner) in our first half hour at the Cosmopolitan.
At this point he decided it was time to play some poker, so we headed over to Planet Hollywood.
What happened next is best shown in diagram form.
Two hands and 10 minutes later, we were done.
In this variation of the Krebs cycle, 8 bourbon in leads to 2 cry as the product.
Next trip maybe we'll get to Gacolysis or Oxidative Damjanalation.
At this point he decided it was time to play some poker, so we headed over to Planet Hollywood.
What happened next is best shown in diagram form.
Two hands and 10 minutes later, we were done.
In this variation of the Krebs cycle, 8 bourbon in leads to 2 cry as the product.
Next trip maybe we'll get to Gacolysis or Oxidative Damjanalation.
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