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.
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