Hyperkalemia myths from EMLyceum

Hi all,

Short post today, as I just want to acknowledge the great work of another blog over at EMLyceum.

The myths of hyperkalemia management are many.  While I have discussed the uselessness of kayexalate in my introductory post, I was thinking about discussing ECG changes and the “textbook progression” so often cited with peaked T-waves, loss of PR, widening of QRS and so on.

However, I don’t think I could do a better job than EMLyceum has already done, so head over there and check it out.  Their website also has many other great posts, set in a question and answer style for teaching.

Kudos to them!

Cheers,

Chris Bond

@SOCMOBEM

The post Hyperkalemia myths from EMLyceum appeared first on SOCMOB Blog.

SOCMOB How To: Jet Insufflation and Bougie Assisted Cric

Hi all,

A few months back we looked at how to make your own cricothyrotomy trainer.  Easy and inexpensive, you can find the video here.

Today I’m adding two more procedure videos which demonstrate a simple jet insufflation setup, as well as the bougie-assisted cricothyrotomy.  Shout out to Darren Braude of EM:RAP and many other podcasts who this idea came from originally. You can find his paper here.

Combining these videos with the aforementioned cric trainer is useful for training large groups of medical students, paramedics and residents.  If you want to see other procedure videos, check out my videos page.  There are also loads of procedure videos over at GMEP.org.

First is the Macgyver’d jet insufflation setup, which requires only a BVM, 3 cc syringe, large bore (eg. short 14 gauge) iv cannula and 7.0 ETT adapter.  I think this technique would be feasible for a pediatric patient only, as there is quite a bit of airway resistance.  In an adult patient, I’m not sure that you could adequately oxygenate the patient doing this.

 

Here is the bougie assisted cric video.  Much simpler than a cric tray, all you require is a scalpel, bougie and 6.0 ETT.

 

If you like these videos, tweet about it.

Happy cric-ing!

Chris Bond

@socmobem

 

The post SOCMOB How To: Jet Insufflation and Bougie Assisted Cric appeared first on SOCMOB Blog.

Evidence Based Management of Acute Heart Failure: Forget LMNOP, think POND!

KimJong

Case:

Imagine you are an attending ED physician supervising a learner.

A 72 year old female presents to the ED with cough and shortness of breath worsening over a week.  She has a history of Afib, previous MI, diabetes and dyslipidemia.  She has recently been non-compliant with her meds and has been taking some ketorolac (damn you ketorolac) for her arthritis pain.  Tachycardic and hypertensive, the patient is in distress, but not about to die this second.

You’re medical student/resident assesses the patient and concludes the patient is suffering from acute decompensated heart failure (ADHF).

You ask what they would like to do, and it sounds something like this:

Lasix, morphine, nitroglycerin, oxygen, position (sit them upright).

The LMNOP mnemonic for acute CHF must be one of the all time most cited medical mnemonics. Most 1st and 2nd year medical students can rattle this one off without much difficulty (thanks a bunch, Toronto Notes!), but is LMNOP really all its cracked up to be?

LMNOP-CHFMeme

In this post, I’m going to propose we replace the old LMNOP acronym with “POND”.   It’s shorter, it’s a word, and it puts the interventions in their actual order of benefit, as opposed to LMNOP which starts with crappy lasix and morphine.

POND

Positive Pressure/Position

Oxygen

Nitrates

Diuretics (Lasix)

The primary reference for this post is this article by Paul Marik (He of the famous “Seven Mares” CVP article and central line infection meta-analysis.  See my post on CVLs here) and Mark Flemmer in the Journal of Intensive Care Medicine. I would highly suggest everyone read this article!

Let’s look at the old LMNOP mnemonic letter by letter.

L – Lasix (furosemide)

First, some critical ward pimping trivia: Why is lasix called lasix?

Because it lasts six hours.  (True of po lasix.  IV is more like 2 hours)

More important clinically relevant question:

What level of evidence is the use of diuretics in ADHF?

Level C – Expert opinion! 2006 Heart Failure Society of America (HFSA) guidelines.

In the words of Joe Lex, lasix is “GOBSAT” – Good ole’ boys sitting around a table.

The biggest study of lasix in ADHF comes from Peacock et al. who looked at the ADHERE (Acute Decompensated Heart Failure National Registry – A registry of over 100,000 patients treated for ADHF) data in 2009.  They found patients receiving <160 mg furosemide in the first 24 hours in hospital had significantly less decline in renal function, length of stay, and in-hospital mortality (OR 0.87, 95% CI 0.78-0.97 p=0.01) when compared with patients receiving > 160 mg in the first 24 hours.

In a smaller but cooler study of 110 patients, Cotter et al. randomized 110 patients with cardiogenic pulmonary edema to high dose nitrates vs. high dose lasix, and found much higher rates of mechanical ventilation (21 in lasix group vs. 7 in nitrate group, p=0.0041) and MI (19 in lasix group vs. 9 in nitrate group, p=0.047) in the lasix group.  Admittedly, the lasix dosing in this study was very high, but as a proof of principle, I think this article helps provide the leeway to get studies using less diuretics past ethics review boards.

Below is a quote from Marik’s paper in which he details why lasix is unlikely to be beneficial in heart failure.

“It has been erroneously suggested that diuretic-induced changes in preload increase ventricular performance by 2 mechanisms, namely (i) by shifting the ventricle to a “more optimal position on the descending limb on the Starling Curve” or (ii) by reducing LV size and thereby reducing systolic wall stress (afterload) by the LaPlace effect. However, high-dose loop diuretics have a number of adverse effects in patients with HF, which include direct activation of the RAAS, increased arginine vasopressin (AVP), increased norepinephrine levels, decreased glomerular filtration rate (GFR), increased systemic vascular resistance, and electrolyte disturbances.”

There are many more references in Marik’s paper supporting nitrates in place of diuresis, going as far back as 1983.

So, am I proposing we stop diuresing ADHF patients?  No. 

Lasix stays in the acronym, but based on the above data, you can see why it now moves to last place in the POND (D for Diuresis) acronym.  There are other interventions that will work more rapidly, effectively and have more benefit for the patient.

M – Morphine

While lasix is a slightly controversial therapy, morphine is downright dangerous.  We’ll keep this short and sweet.

Again looking at the ADHERE registry data, morphine is an independent predictor of mortality (OR 4.84) and also carries an increased risk of intubation.  There is a reason morphine is a good drug for dyspnea in end-of-life care, it blunts the respiratory drive.  So don’t blunt the respiratory drive of your acutely ill heart failure patients. (Unless of course you want to palliate them, which is an appropriate conversation you should be having.)

N – Nitrates

Now were getting to the good stuff.  Nitrates are a mainstay of ADHF management, but unfortunately get way, way, way less love than lasix.  Whether it is spray, patch, tablet or infusion, getting nitro on board right away is a critical intervention for your heart failure patients.  To hear the virtues and practical use of nitrates espoused further, take a stroll down memory lane with EMCrit Podcast #1 by Mr. ED Critical Care, Scott Weingart. Holy crap, that was 4 years ago!

When looking at the literature, there are numerous articles referencing what are considered huge doses of iv nitrates, 200-400 mcg/min.  I find that practically, this is impossible if you ask a nurse to do it, as the rates are about 4x higher than what they are comfortable with.  The concept of a nitro infusion alone is unfortunately fraught with trepidation among many staff, including nurses, medical students, residents, etc. because of concerns about a precipitous drop in blood pressure.  However, many decompensated HF patients have a massive catecholamine surge, and have blood pressure to spare.  If you have a hypotensive HF patient, well, that kinda sucks.

As an example, earlier this year I had a nurse setup a nitro infusion, then I asked him to turn away while I blasted it at 200 mcg/min for a couple of minutes before turning it down.  Worked like magic, but there was no way the nurse would have done this for me.

I think the more practical way to do this is to spray 1-2 pumps of sublingual spray (400 mcg/spray) q5mins while setting up the infusion.  Nurses will have no problem doing this, and at that point you can start the infusion at a lower rate after your sublingual “boluses”.

O – Oxygen

There are no randomized controlled trials studying oxygen vs. no oxygen for ADHF!

I think we’ll all agree that it’s probably a good idea :)

P – Position AND more importantly, Positive Pressure Ventilation

However, this does lead into the two P’s, Position (upright) and Positive Pressure Ventilation, where there is evidence for CPAP over standard oxygen therapy.

This 2008 Cochrane Review included 1071 patients and found that NIPPV significantly reduced hospital mortality (RR 0.6, 95% CI 0.45 to 0.84) and endotracheal intubation (RR 0.53, 95% CI 0.34 to 0.83) with numbers needed to treat of 13 and 8, respectively.

Those are ridiculous numbers, which is why CPAP is my #1 treatment for ADHF patients.  On my last CCU rotation, I was called every night about some crashing ward patient with hypoxemic respiratory failure from ADHF.  Every single time I would go to the ward, discuss code status, call a respiratory therapist and start CPAP.  Not one of those patients was intubated.  NIPPV rocks!

Note that CPAP is as good or better than BiPAP for heart failure because it is a problem of oxygenation.  BiPAP is only needed if there is concurrent hypercarbic respiratory failure, such as in combo CHF/COPD patients.

Note: As an aside, you should be aware that while hypoxia is bad, hyperoxia also has deleterious effects.  So, you don’t need to get that PaO2 up to 500 and blast those lungs with free radicals.

If you want to learn more about oxygen physiology, do a PubMed search for Daniel Davis from the University of San Diego.  You can also hear him discuss pulse oximetry lag on EMCrit episode 88 and the May 2012 EM:RAP podcast where he discusses hyperoxia in traumatic brain injury.

Bottom Line: Forget LMNOP, use POND instead!

Bond'sPond-Bellagio

Positive Pressure/Position

Oxygen

Nitrates

Diuretics (Lasix)

If you like POND, tweet the hell out of it!

Below is a table from Marik’s paper listing the evidence based beneficial and harmful therapies in ADHF.  There’s a lot more to discuss, particularly inotropes and beta-blockers, I’ll try to get to those in the future.

Cheers,

Chris

@socmobem

 

Pre-pub peer review by Brent Thoma (@boringem), Nadim Lalani (@ermentor), Danica Kindrachuk @Want2BeMD

 

References:

Marik PE, Flemmer M.  Narrative Review: The Management of Acute Decompensated Heart Failure. J Intensive Care Med. 2012 Nov-Dec;27(6):343-53

Cotter G, Metzkor E, Kaluski E, Faigenberg Z, Miller R, Simovitz A, Shaham O, Marghitay D, Koren M, Blatt A, Moshkovitz Y, Zaidenstein R, Golik A.Randomised trial of high-dose isosorbide dinitrate plus low-dose furosemide versus high-dose furosemide plus low-dose isosorbide dinitrate in severe pulmonary oedema. Lancet. 1998 Feb 7;351(9100):389-93.

Peacock WF, Costanzo MR, De MT, et al. Impact of intravenous loop diuretics on outcomes of patients hospitalized with acute decompensated heart failure: insights from the ADHERE registry. Cardiology. 2009;113(5):12–19.

Vital FMR, Saconato H, Ladeira MT, Sen A, Hawkes CA, Soares B, Burns KEA, Atallah ÁN. Non-invasive positive pressure ventilation (CPAP or bilevel NPPV) for cardiogenic pulmonary edema. Cochrane Database of Systematic Reviews 2008, Issue 3. Art. No.: CD005351. DOI: 10.1002/14651858.CD005351.pub2.

 

EMCrit Podcast #1 http://emcrit.org/podcasts/scape/

 

EMCrit Podcast #88 http://emcrit.org/podcasts/oxygen-physiology/

 

EM:RAP May 2012 http://www.emrap.org/episode/2012/may/airwaycorner

 

 

The post Evidence Based Management of Acute Heart Failure: Forget LMNOP, think POND! appeared first on SOCMOB Blog.

Eleven Madison Park with Mr. and Mrs. EMCrit

Happy Easter everyone.

Today I’m cross-posting a restaurant review of Eleven Madison Park in NYC, from my other blog over at licencetoeat.wordpress.com.  The FOAMed connection is that the dinner was with Scott Weingart of the EMCrit podcast.

Warning: This is primarily a food post, though there is one important piece of info about Scott’s job that was very enlightening for me, the concept of an ED/ICU.  Otherwise, there really isn’t much medicine info here, more of that to come in the future.  If you are looking for my “How to” videos, click here.

Eleven Madison Park

Feb. 26, 2013

11 Madison Avenue, New York – www.elevenmadisonpark.com

eleven-madison-park-sign

When we initially decided to go on our NYC culinary adventure, Camille and I emailed Scott Weingart, the only person we knew in New York. In addition to being a famous medicine podcaster over at EMCrit, Scott is also a big time foodie. A little known fact is that Scott did a few years of culinary school prior to medicine. We first met Scott in Las Vegas at Essentials of EM, when we went out to Lotus of Siam with Scott and a slew of other famous bloggers/podcasters. He is a hilarious and down to earth dude who likes to have a good time, eat great food, and make dirty jokes. Pretty much the same as us.

 

Dinner at Lotus of Siam, Las Vegas with a bunch of funny ass people. Left side (front to back): Rob Orman of ERCast, Me (SOCMOB), Rob Ryan, Cliff Reid of Resus.me, Jan Trojanowski. Right side (front to back): Scott Weingart of EMCrit, ZDoggMD, Michelle, Leon Gussow of The Poison Review, Chris Nickson of LITFL, Michelle Lin of Academic Life in EM.
Dinner at Lotus of Siam, Las Vegas with a bunch of funny ass people. Left side (front to back): Rob Orman of ERCast, Me (SOCMOB), Rob Bryant, Cliff Reid of Resus.me, Jan Trojanowski. Right side (front to back): Scott Weingart of EMCrit, ZDoggMD, Michelle, Leon Gussow of The Poison Review, Chris Nickson of LITFL, Michelle Lin of Academic Life in EM. Still not sure how I got invited to this dinner. Thanks ZDogg.

On this occasion we had the pleasure of meeting his wife, who is a double boarded Pediatrician and Peds Anesthetist. In keeping with the typical anesthetist, she is a little calmer and less ADD than Scott, and overall just a super nice person.

Before we get to the food, here’s one quick fact that blew my mind when Scott told me.  In all of his podcasts, Scott talks about doing some crazy stuff, particularly intensive care type things that most ED docs don’t even consider.  The reason he is able to “bring the upstairs care, downstairs” is because he actually works in a short stay ICU that is within the ED.  This is a completely foreign concept for me, and most Canadian EM physicians, as we don’t have ED/ICUs in Canada (at least not that I am aware of).  Essentially, Scott has 8 beds for critically ill patients (eg. trauma, sepsis, etc.) and only sees those patients during a shift.  He is not responsible for department flow and seeing lower acuity patients, so he gets to manage the sickest patients all the time.  It’s basically the dream EM job. In Canada, ED/ICU means you work part time in the ED and part time in the ICU, which is entirely different.  After learning this, everything he talks about in the podcasts made a whole lot more sense.  I’m not sure, but maybe I am the only one who didn’t realize what Scott meant by ED/ICU.

That’s the end of the medical talk, now this is going to be all about the food.

 

After discussing a few possible restaurants, we decided on Eleven Madison Park (EMP), one of three Michelin 3-star restaurants on this trip, along with Per Se (review here) and Jean-Georges.

IMG_1756
Stumpy

First some background on EMP. Situated on the main floor of the Metropolitan Life North Building, EMP has a massive amount of space (much of it kitchen) because the Met Life building was originally intended to be 100 stories tall. Designed by Corbett and Waid in the 1920s, the Met Life building would have been the world’s tallest building at the time, were it not for the stock market crash of 1929. Looking at it from the outside, you can see the original intent to be a monstrosity towering over Manhattan. Unfortunately, it looks a little stumpy next to the South Met Life Tower.

Fleury1996
1996 Fleury Champagne

To start the evening we had a bottle of 1996 Fleury Champagne. Fleury is a biodynamic producer making a small amount of predominantly Pinot Noir Champagne. Coming from the legendary 1996 vintage, this 80% Pinot Noir and 20% Chardonnay Cuvee was fantastic with baked apple, lemon, toast and cinnamon on the nose. There was also an oxidative quality on the nose and palate, somewhat like the 1986 Krug Clos de Mesnil we had at Richard’s birthday. The most striking characteristic was the intense acidity, almost at the level of an extra brut. Fermented in stainless steel, this was like pure malic acid, which gave it a medium-plus finish. In a good spot right now, this versatile Champagne could be paired with anything from fish to pork.

Onto the food.

A primary theme of our menu at EMP was “New York”. How novel.

We would both start and finish the meal with a traditional NYC snack, the black and white cookie. Typically, the “half and half” is a sweet cookie composed of half vanilla fondant and half chocolate fondant. In this meal, we would begin with a savory black and white cookie, and complete the meal with the sweet version.

EMP-CheddarCookie
Photo courtesy Fooder from the Ramblings and Gamblings Blog

Cheddar – Savory Black and White Cookie with Apple

A delicate cookie with ample cheddar flavor and soft crunch, these were filled with crab apple chutney. Having had the Per Se gruyere gougere a few days earlier, I wished for a bit more richness and depth of flavour. Akin to a glorified Goldfish cracker, this was a decent palate cleanser to begin the meal.

EMP-Oyster2

Oyster – Sorrel, Buckwheat, and Mignonette

The next course was presented beautifully, a Duxbury oyster topped with Champagne vinegar mignonette, puffed buckwheat and sorrel. While a lovely presentation, this dish was a total miss for Camille and I, for different reasons. Camille’s oyster was too heavy on the mignonette, while mine was ridiculously over peppered. In both cases, the entire mouthful was overwhelmed by a single flavour, acid for Camille and black pepper for me. In hindsight, this was the single biggest miss of any dish during the trip, which encompassed well over 100 individual dishes during the 7 days. Harsh words to be sure, but this dish really failed due to its lack of balance.

EMP-Shrimp
Photo courtesy Ramblings and Gamblings

Shrimp – Marinated with Olive Oil, Horseradish, and Fennel

Next up was a taste of sweet Maine shrimp, with fennel and horseradish used to highlight the natural flavour of the shrimp. Creamy and rich, the shrimp was good, though a bit gelatinous in texture from having multiple pieces so close together. Reminiscent of a Chinese shrimp dumpling in texture, if you like those, you would enjoy this. For me a good, but not great dish.

At this point you’re probably like “Wow, this meal sucked”! In hindsight, the first three courses were pretty weak, though it would improve from here.

2002DielLabel
2002 Schlossgut Diel Dorsheimer Goldloch Riesling Kabinett

At this point we opened a Riesling alongside the Fleury, to pair with subsequent courses. At the suggestion of our Sommelier, I went with a 2002 Schlossgut Diel Dorsheimer Goldloch Riesling Kabinett. Pure kerosene on the nose initially, with honey and lemon notes, this was on the sweeter side for a Kabinett, and a bit lacking in acidity. Overall a solid wine, but more acidity would have added balance and improved it immensely. For the same price point, I should have gone with the 2002 Karthauserhof Kabinett, a far superior wine.

Note: The 2002 vintage in Germany is vastly underrated, and wines can be had at bargain prices from this vintage. The Germans are meticulous about their viticulture, and almost always make great wines, even in the toughest vintages.

EMP-SeaUrchin2

Sea Urchin – Custard with Apple Gelée and Scallop

This dish was light and balanced, the softness of the panna cotta and uni contrasting with the firmer scallop texture. Lemon juice and tart apple gelee provided acidity and brightened the fish flavour. While very good, this was nowhere near the caliber of a similar Uni dish we would have at Bouley later in the week.

EMP-ClamFoam

Clam – Surf Clam with Morcilla Sausage and Celery Root

The first “wow” course of the meal, the crumbled morcilla sausage provided depth and richness, while the light and airy celery root espuma was a perfect foil to the heavier sausage. There were also sweet tiny pieces of pear, celery root and chive to complement the clam. An excellent course.

EMP-Clam2 EMP-Clam3 EMP-Clam4 EMP-ClamChowder

Top left: Hot water poured over the rocks and kelp releasing the aroma of the ocean. Top right: Sliced raw whelk with shaved fennel, couscous, and lemon vinaigrette. Bottom left: Littleneck clam with radicchio and pear Bottom right: Clam chowder

Clam – Clambake with Whelk, Parker House Roll, and Chowder.

One of several elaborate multi-part courses of the dinner, this began with the great aroma of the hot water poured over the rocks to ignite the senses. The whelk (snail) was light and balanced by the freshness of lemon and fennel, with a slight crunch from the couscous. The radicchio and pear were a classic pairing to match with the clam, and again were fresh and vibrant. The best part was the clam chowder. Rich and deep, this was the essence of clam.

EMP-ParkerHouse
Photo courtesy Ramblings and Gamblings

Parker House rolls: Rich, buttery and delicious and topped with great finishing salt. Nuff said.

IMG_1622

Bread and Butter

The second bread course was a light, flaky roll paired with two different butters. The first was from the Chef’s favorite creamery, while the second contained some of the beef fat from out upcoming rib eye course. Both were superb.

IMG_1623

Scallop – Seared with Radish, Caviar, and Apple

Creme fraiche, caviar and scallop, how can you go wrong? This was an elegant presentation and had clean flavours with multiple textures of scallop (fresh and steamed). The apple and radish provided crunch, sweetness and heat. A well composed and balanced dish.

IMG_1624IMG_1625  IMG_1628

Carrot – Tartare with Rye Bread and Condiments

The next course would be another interactive and memorable one. A play on the traditional tartare course, lightly blanched carrots were ground tableside and served with a variety of garnishes including (from top left): apple mustard, sunflower seeds, pickled quail egg yolk, smoked bluefish, chives and broccoli flower, pickled mustard seed, grated horseradish, pickled apple, and Amagansett sea salt. There were also two squeeze bottles which contained spicy carrot and mustard oil, respectively.

Mixing all of the accompaniments with the carrot, this dish was a spectacular success, with huge depth of flavour and balance. The sweetness of the carrot was offset by the spicy oils and horseradish, acidity of the pickled apple and mustard seed, with all the flavours tempered by the rich egg yolk. This had all the components of a 5/5 dish, great flavour, originality and creativity, while simultaneously being visually impressive and interactive.

IMG_1629

Lobster – Poached with Citrus, Tarragon, and Daikon

Another beautifully presented course, the sweet lobster was elevated by subtle flavours of daikon radish, dehydrated citrus (grapefruit and blood orange) and tarragon. Licorice from the fennel, acidity from the citrus and a touch of heat from the daikon, this was a well executed and balanced dish.

ARPEPE1999

1999 AR. Pe. Pe Sassella Rocce Rosso Riserva

From Valtellina in the Northern province of Lombardy, this 100% Nebbiolo (known as Chiavannesca in Valtellina) was chosen to pair with the upcoming beef and cheese courses, though it would do fine with many fishes as well. Garnet in color, a traditional Nebbiolo nose of cherry, tar, and mushroom, this had racy acidity on the palate and improved over the evening. A great, less expensive alternative to Barolo/Barbaresco.

IMG_1631 IMG_1630

140 Day Aged Rib Eye

The piece de resistance of the meal at EMP, the 140 day aged rib eye was the oldest I’ve ever tried. Brought out two courses before it would be served, it was fascinating to see the extent of the mold development after almost 5 months of hanging. The mold extended at least 3/4 of an inch deep around the cap, and probably a good 1/4-1/2 inch around the bone. The marbling of the rib eye was impressive as well, though it has to be in order to be capable of dry aging for this long.

IMG_1632

Potato – Baked with Bonito Cream, Shallot, and Pike Roe

A contrast of textures, this course included smashed fingerling potatoes, a crispy russet skin and a potato cup. This was effectively still a fish course, with the strong Bonito cream and black shellfish sauce being tempered by the velvety potatoes. Another very good course.

IMG_1633

Beef – Beef Broth

The multi-part beef course began with beef broth made from the delicious 140 day aged rib eye. Deep, rich, and closer to a demi glace than a jus, this was unctuous and amazing. A perfect broth.

IMG_1634

Beef – Grilled with Mushrooms, Amaranth, and Bone Marrow

This was another of the standout courses at EMP, and typically we find beef courses to be overrated. The grilled beef was perfectly cooked over charcoal, and amazingly deep in flavour due to the extended dry aging. There was also an exquisitely tender morsel (beside the hen of woods mushroom in the photo) which may have come from the cap, though I’m not sure. It was sublime. The accompanying bone marrow was soft and rich, while the amaranth and black garlic were a crispy contrast. The Hen of Woods mushroom was charred nicely and the dish was reminiscent of the “burnt forest mushroom” course from Alinea last year.

EMP-BraisedOxtail EMP-BraisedOxtail2

Beef – Braised Oxtail with Foie Gras and Potato

The final part of the beef course was similarly excellent. The ultimate custard, this was a perfect dish of deep oxtail, rich foie gras and topped with potato foam. I could eat a vat of this.

IMG_1635 IMG_1636 IMG_1637 IMG_1639

Greensward – Pretzel, Mustard, and Grapes

Another playful course, we were next presented with a picnic basket containing everything we would need for our “Picnic in Central Park”. The cheese was a soft, nutty, cow’s milk with a washed rind. There was also a pretzel bread, mustard, grapes and a craft beer from Ithaca Brewery. The beer was a high acid, “food beer”, much like the Jolly Pumpkin or Jose Andres ales, and paired awesomely with the bread, cheese and mustard.

IMG_1640

Malt – Egg Cream with Vanilla and Seltzer

Another New York tradition, this was our first experience with egg cream, a carbonated vanilla drink. This was good, but nothing special.

IMG_1641

Maple – Bourbon Barrel Aged with Milk and Shaved Ice

The first of two plated desserts, this was like the French-Canadian tradition of shaved ice with maple syrup. Except that was picked up with popsicle sticks instead of a spoon. The bourbon gave it a little extra oak and spiciness, and this was a delicious, if somewhat nostalgic course.

IMG_1644

Earl Grey – Sheep’s Milk Cheesecake, Honey, and Lemon

This was a well balanced dessert with a rich but not overly heavy cheesecake, loads of bergamot from the Earl Grey, and some nice acidity from the lemon and creme fraiche. Very enjoyable.

IMG_1645Magic Trick – Chocolate

At this point our server came out with a deck of cards and performed a magic trick, in which we selected a point in the deck and she then flipped four cards, each with an ingredient symbol upon it. They lifted an upside down cup previously placed on our table to reveal the exact chocolates we had selected (different for each person). The server did a good job from the illusion standpoint, though Camille didn’t listen to her spiel at all, and watched for the obligate deck switch during the trick. Overall, I thought it was well done, and about as good an incorporation of magic as could be expected.

The chocolate itself had a thin crispy outside and creamy hazelnut center.

IMG_1647 IMG_1649

Tea ServiceOolong

Quite simply, this was the best tea service we’ve ever had.

EMP offers a tableside Manhattan cart to begin the meal, and optional tableside coffee/tea at the end. Being major tea lovers, we opted for an Oolong from The Pursuit of Tea.

This was served Gongfu cha style, with a rinse followed by three steepings. We asked for a fourth steeping, preferring the delicate flavors of later steepings. A separate server came to do the tea service, he was caring, meticulous, and timed each steeping.

It was a high quality Oolong with medium oxidation and still fairly green. The first two steepings were earthy, spicy and had good astringency/tannin, while the third and fourth steepings were subtle, with delicate floral notes and virtually devoid of tannin. A fantastic tea service, something we should adopt at home.

IMG_1650

Pretzel – Chocolate covered with sea salt

The penultimate dessert was a large chocolate pretzel. We love pretzels, and these were great.

EMP-ChocolateCookie

Chocolate – Sweet Black and White Cookie with Apricot

The final dessert brought us back to where we started, with a sweet black and white cookie. This time a butter cookie filled with apricot chutney, these were more enjoyable than the savory version at the start of the meal.

EMP-AppleBrandy

Apple Brandy Eau de Vie

If you need an after dinner drink, their Eau de Vie is complimentary.

The EMP-Alinea Connection

In September 2012, Alinea and Eleven Madison Park traded locations for 1 week each. A crazy idea, it was apparently conceived by Chefs Grant Achatz of Alinea and Daniel Humm of EMP over a few drinks one night. And thus, Grant Achatz brought his team to EMP and Daniel Humm’s staff traveled to Chicago. Video footage of this monumental event can be seen here on YouTube.

This meal had a definite Alinea feel to it, particularly with the interactive courses, opening of boxes and baskets to see what was inside, and the presentation/flavors of the rib eye and clam dishes. I am not sure if these were conceived before or after the Alinea exchange, but in any case, they were the highlights of the meal at EMP. I am curious what techniques were adopted over at Alinea.

After our dinner, Camille and I toured the EMP kitchen and had a nice 5-10 minute chat with the Chef de Cuisine. The most notable things about EMP’s kitchen were:

1)It is massive. Being the base floor of a proposed 100 storey building allows for a huge amount of space.

2)The atmosphere is happy. Most kitchens of this caliber are very business-like. At Per Se and Alinea, the kitchens are nearly silent, save for the voice of one person at a time. EMP actually had a few people talking, joking, and they seemed to be genuinely enjoying themselves.

The Chef de Cuisine gave us some insight into the EMP/Alinea exchange, and apparently the kitchen environment at Alinea is just a tad more militant than it is at EMP. That’s putting it mildly. If you read Achatz’s autobiography, I think you’ll get a sense of how things run at Alinea.

Service

Overall excellent.

Only gripe was that they did not tell us what was in the course a few times because we were talking amongst ourselves. This is a matter of personal preference, but I like to be gently interrupted when a course arrives so that I can hear the details. A few times they just put it down and walked off, without waiting for even a second for us to stop talking. Eventually we decided to shut ourselves up whenever they came with a new course.

Overall

EMP had several spectacular courses, and has the potential to be a 5/5 meal. The carrot tartare, clam espuma and rib eye courses were memorable and were “wow” dishes in conception and execution. The playfulness and interaction also added to the overall experience. Unfortunately, the first 4 courses underperformed, and the oyster with mignonentte was a huge miss. Because of this, based on this meal, EMP does not fall into the pantheon of our greatest meals, and I’m unsure that I would re-visit on my next NYC trip.

Special thanks to Fooder from Chowhound and ramblingsandgamblings.blogspot.com for many of the pictures for this dinner. You can read his take on the same meal at his blog, linked above. It was very dark in EMP, and some of my photos did not turn out that great.

If you made it this far, thanks for reading, we’ll be back to our regularly scheduled #FOAMed shortly.

Cheers,

Chris

The post Eleven Madison Park with Mr. and Mrs. EMCrit appeared first on SOCMOB Blog.

SOCMOB How To: Make an atomizer device

It’s time for another video.  Today I’ll be showing you how to MacGyver your own atomizer for intranasal and orotracheal drug administration.  Shout outs to fellow USask FOAMite Dr. Nadim Lalani (@ERMentor) and Dr. Whit Fisher for the idea behind this one.  Today’s video is a modification of the design outlined by Whit Fisher here.   For more of my “How To” videos, check out the videos page here or GMEP.org.

The intranasal (IN) route of drug administration is becoming ever more popular, specifically in pediatrics and awake intubations. This PK SMACC Talk video from Italian Valerio Pisano Brasca (His blog is here), who has a much cooler name than me, is a good 6 minute overview on the types of medications and doses that can be used via the intranasal route.  Some of the big ones are fentanyl, ketamine, and midazolam.  Administering these drugs without intranasally is useful for procedures and pain in children, and could also be used before establishing IV access as well.  Another drug that can be given IN is naloxone, useful for your narcotized post-op patients on the ward, and drug users in the ED.

What I like most about the atomizer is that you can effectively deliver topical anesthetics to the posterior oropharynx and have the patient hold it themselves for elective intubations.  Rather than stick something in their mouth, the patient or a parent could do it for them.

To test this out, I tried it on myself with 2% lidodan and it did a pretty good job of decreasing my gag reflex.  Definitely to the point that I could easily get a MAD back there to spray the cords.  A common question is “why not just use a nebulizer”?  I’ve tried the nebulized 4% lidocaine for topicalizing the airway, and I find most patients say that it just coats their tongue and inner cheeks, while not actually getting their oropharynx.  The atomizer does a much better job of this.

Onto the video.  If it’s not working, check the YouTube link here.

 

Questions and comments on how to improve are always appreciated.

Cheers,

Chris

@SOCMOBEM

 

Post written by Chris Bond.  Peer reviewed by Nadim Lalani (@ERMentor)

 

 

The post SOCMOB How To: Make an atomizer device appeared first on SOCMOB Blog.

NSAIDs Part 3: Gastrointestinal Side Effects and Toxicity

In part 1 of our discussion on NSAIDs, we discussed the equal efficacy of various NSAIDs, while in part 2, we looked at the concept of an analgesic ceiling effect when using NSAIDs.

Congrats to all of those who identified the ceiling in part 2 as the Chihuly work at the Bellagio in Las Vegas.  Damon Tedford (@DamonTedford) wins the sammich for being the first to get the correct answer.

Today we’ll look at the side effect profiles of different NSAIDs.  While all NSAIDs are created equal with regards to analgesia, this is not the case for their side effect profiles.  Some NSAIDs are definitely more toxic than others.

While NSAIDs are a great bunch of analgesics, they unfortunately have GI, renal, and cardiac side effects.   For young, healthy patients, the upper GI complications (UGICs) are the most common side effect, as their renal/cardio complications are better tolerated.  In the over 60 population, those with pre-existing cardiac/renal disease, and a few other groups, the renal and cardiac complications are also often seen.

So which NSAIDs are most dangerous?

Golden-poison-frog P. terribilis (No joke, it’s actual species name is terribilis)

If this frog were an NSAID, which one would it be?

If you guessed ketorolac, nice work.

This 2010 systematic review looks at the relative risk for upper GI bleeding/perforation for both traditional and non-traditional (ie: coxib) NSAIDs.  It should be noted that NSAIDs increase the risk of lower GI bleeding as well, despite UGICs being most commonly discussed in the literature.

 

NSAIDtoxicityhttp://link.springer.com/article/10.1007/s00296-011-2263-6/fulltext.html

 

As you can see, the traditional NSAIDs fall into 3 rough categories for UGIG: low-risk, intermediate risk and high-risk. (Pooled RRs in parentheses)

Low risk

Ibuprofen (2.23)

Intermediate risk

Diclofenac (3.61)

Naproxen (4.6)

Indomethacin (5.12)

High risk

Ketorolac (14.54)

 

In addition to being no better for pain, ketorolac is also way nastier than other NSAIDs.  Depending upon the paper you read, you’ll find slightly different numbers, but the relative risk of traditional NSAIDs will pretty much always fall into these 3 groups.

An important caveat to these numbers is that they are pooled RRs between low dose and high dose NSAIDs.  All NSAIDs have much greater toxicity at higher doses.

Here is an example from a paper looking at UGICs with traditional NSAIDs.

The odds ratios for UGICs with Ibuprofen at:

Dose (mg/day)                        OR:

<1200                                        1.1 (95% CI 0.6-2.0)

1200-1799                                 1.8 (0.8-3.7)

>1800                                        4.6 (0.9-22.3)

Thus, 400 mg QID and 600 mg QID of ibuprofen have the same analgesic effect, but a total daily dose of 2400 mg is associated with more side effects than 1600 mg.

With ketorolac, risk similarly increases, but the complication rate is already so high (RR 20 at <20 mg/day) in this 2001 study, why would you even want to prescribe it in the first place.  For those wondering about risk when given parenterally, the RR for IM ketorolac is even greater than PO (28.3 vs. 20) in the same study.

 

So who will get the bleed?  In this great 2012 review article from Conaghan, the risk factors for UGIC are:

*Elderly (Age >60)

*History of PUD (especially if complicated by bleed/perforation)

*Multiple NSAID use

Concomitant ASA, steroids, anticoagulants or SSRIs

Concurrent H. pylori infection

Smoking

*denotes major risk factor

 

But I want to prescribe my patient some NSAIDs for their pain.  Can I prevent these side effects?

Fortunately you can.  Both misoprostol and PPIs will significantly reduce side effects of traditional NSAIDs, while H2 blockers will not.  This has been studied in the ARAMIS cohort study, where it was found that the RR for UGICs when misoprostol or omeprazole was added was 0.6, while the RR was 1.4 with H2 blockers.

Bottom line:

Different NSAIDs all produce similar levels of analgesia, but some are much worse than others when it comes to side effects.  There is no need to prescribe NSAIDs above their dose ceiling, as it endangers the patient without providing any benefit.  Be aware of risk factors for UGICs (esp. age >60, previous ulcer and multiple NSAIDs) and always consider prescribing a PPI when giving out an NSAID.

Cheers,

Chris

@SocmobEM

 

References

ARAMIS Study: Singh G Am J Ther. 2000 Mar;7(2):115-21.

García Rodríguez LA, Hernández-Díaz S. Epidemiology. 2001 Sep;12(5):570-6.

Conaghan PG, Rheumatol Int. 2012 Jun;32(6):1491-502. doi: 10.1007/s00296-011-2263-6. Epub 2011 Dec 23. Review.

Lewis, S. C., Langman, M. J. S., Laporte, J.-R., Matthews, J. N. S., Rawlins, M. D. and Wiholm, B.-E. (2002), Dose–response relationships between individual nonaspirin nonsteroidal anti-inflammatory drugs (NANSAIDs) and serious upper gastrointestinal bleeding: a meta-analysis based on individual patient data. British Journal of Clinical Pharmacology, 54: 320–326. doi: 10.1046/j.1365-2125.2002.01636.x

Massó González, E. L., Patrignani, P., Tacconelli, S. and Rodríguez, L. A. G. (2010), Variability among nonsteroidal antiinflammatory drugs in risk of upper gastrointestinal bleeding. Arthritis & Rheumatism, 62: 1592–1601. doi: 10.1002/art.27412

 

 

 

The post NSAIDs Part 3: Gastrointestinal Side Effects and Toxicity appeared first on SOCMOB Blog.

SOCMOB How To: Make Your Own End-Tidal CO2 Detector

Hey SOCMOBBERS,

The ASA now recommends that all procedural sedations (not conscious sedations!) be done with quantitative waveform capnography. While I understand it’s not feasible in some places, capnography is a hugely valuable tool, and detects apnea long before the pulse ox reading drops.

Where I work, there are no fancy nasal prongs or face masks with built in CO2 detectors, so in order to get a capnograph, some improvisation is needed.

An anesthesia resident helped me with this idea, as did Minh Le Cong’s great 4 minute video on MacGyvering an ETCO2 detector on the SMACC website (link below).  Thanks to both Kyle Raab and Minh for the idea.

For all the Saskatchewan docs and other ED people out there, this video shows you how to make a Microstream Sidestream ETCO2 detector work with your face mask or non-rebreather device.  I receive no payment from, nor do I have any affiliation with this product, it’s simply what is available in our ED.

Over the next while I’ll be releasing more “SOCMOB How To” videos.  Click here to go straight to YouTube video or if it isn’t working below.  Enjoy!

 

If you enjoyed this video, like it, tweet it, etc. and spread the #FOAMed.  If you didn’t like it, send me suggestions on how to improve.

Here are the links for Minh Le Cong’s video, as well as his great PHARM (Pre Hospital and Retrieval Medicine) website/podcast.

In other news, SOCMOB has joined forces with BoringEM, ERmentor and Want2BeMD in a University of Saskatchewan FOAM collaborative.  Check out all of their great FOAM here.

Cheers,

Chris Bond

@SocmobEM

The post SOCMOB How To: Make Your Own End-Tidal CO2 Detector appeared first on SOCMOB Blog.

SMACC 2013

Hey SOCMOBBERS,

Welcome to the new WordPress site.  It took a while, but we’ve finally made it.  Part 3 of the NSAID discussion will be out in the next few days (it keeps getting longer), as will some new videos on how to Macgyver some equipment in the ER.  In the meantime, sign up for the new RSS feeds, or follow by twitter/email.

I wanted to give a massive shout out to the SMACC 2013 Conference currently going down in Sydney.  This is the first annual Social Media and Critical Care Conference and is basically a #FOAMed nerd’s wet dream.  It was organized by the master educators behind www.lifeinthefastlane.com

If you’ve been living under a rock, you can follow all the great FOAM on Twitter, hashtag #SMACC2013, or on their website here.

Here’s an example of the awesomeness that’s going on down under, thanks to Cliff Reid of the Resus.me blog.

Rocketamine

The post SMACC 2013 appeared first on SOCMOB Blog.

NSAIDs part 2: The Ceiling Effect

Sorry readers.  I've been slacking off on vacation in NYC, eating too much and blogging about food more than medicine.  Tonight at dinner with Mr. EMCrit, Scott called me out a bit for insufficient content.  Also, one of my readers has some rounds coming up soon, and needs to talk NSAIDs.  With that in mind, here's part 2 of the NSAID saga.

In part 1 on NSAIDs, we looked at NSAID equivalency for analgesia and the myth that is  ketorolac (Toradol).  

Hat tip to readers Moshe and Elisha (@ETtube on twitter) for pointing out the concept of the ceiling effect with NSAIDs.  I did not mention this in part 1, and will discuss it today.
There's a great talk by Larry Raney on the Free Emergency Talks website that discusses NSAIDs and the ceiling effect.  You can find it here.  As an aside, the Free Emergency Talks website is run by Joe Lex, one of the great EM educators, and has a thousands of talks from any conference you can think of. 

What is the ceiling effect?

* Free sammich to the first reader who tells me where this ceiling is. (Sammich will be good when it goes in the mail, but I can't guarantee quality on arrival.  Might make it a cockroach and twinkie sammich to prevent spoilage.)

The ceiling effect is the concept that there is a maximum level of analgesia that can be reached with a dose of medication, and beyond that dose, you get no more analgesia.  

In addition, you continue to get more side effects That double sucks!

Tylenol and NSAIDs classically fall into the category of analgesics with a ceiling, while opiates have no ceiling.  This is why we can bomb in loads of fentanyl or morphine, but you don't see us pounding patients with ibuprofen.

If you look at the doses of NSAIDs listed in part 1, you'll see some pretty whopping doses.  
Aside from the ceiling of anti-inflammatory dosing, there is also the concept of a second ceiling for acute pain?

Two ceilings?  Yup, two ceilings.

The ceiling dose for acute pain with ibuprofen is 400 mg po.

The higher ibuprofen dose ceiling of 800 mg I mentioned in part 1 is the anti-inflammatory ceiling of the NSAID and comes from the rheumatology literature.   I apologize if I confused anyone with this.  One key to understanding the NSAID literature is that it generally comes from 3 patient groups: rheumatologic disease, post-operative pain and dental pain.  The latter two are probably both representative of pain we see in ED patients, ie: acute, non-inflammatory pain.

This is the reason why meta-analyses of NSAID efficacy are a challenge; the indications, duration of therapy, dose, etc. are completely different.   In some studies, you are looking at patients with chronic inflammatory conditions on long term therapy.  These patients may need higher dose NSAIDs for their anti-inflammatory effects.  In other studies, it is single dose or short-term NSAIDs where analgesic ceiling will be 400 mg.

You can see how lumping all of these studies together in a review would misconstrue pretty much any endpoint.

Let's now look at the two main studies supporting the 400 mg ceiling dose of ibuprofen and 10 mg ceiling dose of ketorolac.

In contrast to the usual scenario in which old research = bad research (or a HSSP: High School Science Project), there are papers from 1978 and 1986 looking at the ibuprofen ceiling effect.  

The first, by Winter et al. in 1978 looked at 510 post oral surgery patients who had 1 or more extractions, impactions and even a few with alveolectomies. That all sounds pretty painful!  They compared five treatments: ibuprofen 400 mg, ibuprofen 800 mg, ASA 650 mg, Darvon 65 mg and placebo.  Both ibuprofen groups had similar reduction in pain scores and were better than the other 3 treatment arms.  The study was done with pooled data from two separate dentists; in one group 400 mg ibuprofen seemed slightly more effective, while 800 mg seemed slightly more effective in the other.  However, there are no data to support any statistically significant difference between ibuprofen groups in the article.

The second article, by Laska et al. in 1986 was a double blind parallel group study with 200 patients post oral surgery compared doses of 400 mg , 600 mg and 800 mg of ibuprofen.  There was no evidence of a dose response efficacy difference between 400, 600 and 800 mg.

Considering that dental pain hurts like hell, I'm inclined to believe these studies are sufficiently representative of ED patients with most injuries.  *As an aside, learn to do dental blocks, they are invaluable to patients.

With regards to ketorolac, this double blind RCT from Staquet in 1989 compared 10 mg, 30 mg and 90 mg IM ketorolac with placebo in 128 patients with cancer pain.  Again, no difference was found between the 3 ketorolac dosing regimens, with all being much superior to placebo.

Other similar studies have been done and show 10 mg is probably the ceiling dose of ketorolac both orally and parenterally.  

In the next parts of the NSAID saga, we'll discuss side effects profiles of various NSAIDs, and NSAID hodgepodge such as effect on fracture healing, use in renal colic and more.

Cheers,

SOCMOBEM  


References:

Winter et al. Oral Surg Oral Med Oral Pathol. 1978 Feb;45(2):159-66.
 
Laska et al. Clin Pharmacol Ther. 1986 Jul;40(1):1-7.

Staquet MJ J Clin Pharmacol. 1989 Nov;29(11):1031-6.

NSAIDs part 2: The Ceiling Effect

Sorry readers.  I’ve been slacking off on vacation in NYC, eating too much and blogging about food more than medicine.  Tonight at dinner with Mr. EMCrit, Scott called me out a bit for insufficient content.  Also, one of my readers has some rounds coming up soon, and needs to talk NSAIDs.  With that in mind, here’s part 2 of the NSAID saga.

In part 1 on NSAIDs, we looked at NSAID equivalency for analgesia and the myth that is  ketorolac (Toradol).  

Hat tip to readers Moshe and Elisha (@ETtube on twitter) for pointing out the concept of the ceiling effect with NSAIDs.  I did not mention this in part 1, and will discuss it today.
There’s a great talk by Larry Raney on the Free Emergency Talks website that discusses NSAIDs and the ceiling effect.  You can find it here.  As an aside, the Free Emergency Talks website is run by Joe Lex, one of the great EM educators, and has a thousands of talks from any conference you can think of.

What is the ceiling effect?

* Free sammich to the first reader who tells me where this ceiling is. (Sammich will be good when it goes in the mail, but I can’t guarantee quality on arrival.  Might make it a cockroach and twinkie sammich to prevent spoilage.)

The ceiling effect is the concept that there is a maximum level of analgesia that can be reached with a dose of medication, and beyond that dose, you get no more analgesia.

In addition, you continue to get more side effects That double sucks!

Tylenol and NSAIDs classically fall into the category of analgesics with a ceiling, while opiates have no ceiling.  This is why we can bomb in loads of fentanyl or morphine, but you don’t see us pounding patients with ibuprofen.

If you look at the doses of NSAIDs listed in part 1, you’ll see some pretty whopping doses.
Aside from the ceiling of anti-inflammatory dosing, there is also the concept of a second ceiling for acute pain?

Two ceilings?  Yup, two ceilings.

The ceiling dose for acute pain with ibuprofen is 400 mg po.

The higher ibuprofen dose ceiling of 800 mg I mentioned in part 1 is the anti-inflammatory ceiling of the NSAID and comes from the rheumatology literature.   I apologize if I confused anyone with this.  One key to understanding the NSAID literature is that it generally comes from 3 patient groups: rheumatologic disease, post-operative pain and dental pain.  The latter two are probably both representative of pain we see in ED patients, ie: acute, non-inflammatory pain.

This is the reason why meta-analyses of NSAID efficacy are a challenge; the indications, duration of therapy, dose, etc. are completely different.   In some studies, you are looking at patients with chronic inflammatory conditions on long term therapy.  These patients may need higher dose NSAIDs for their anti-inflammatory effects.  In other studies, it is single dose or short-term NSAIDs where analgesic ceiling will be 400 mg.

You can see how lumping all of these studies together in a review would misconstrue pretty much any endpoint.

Let’s now look at the two main studies supporting the 400 mg ceiling dose of ibuprofen and 10 mg ceiling dose of ketorolac.

In contrast to the usual scenario in which old research = bad research (or a HSSP: High School Science Project), there are papers from 1978 and 1986 looking at the ibuprofen ceiling effect.

The first, by Winter et al. in 1978 looked at 510 post oral surgery patients who had 1 or more extractions, impactions and even a few with alveolectomies. That all sounds pretty painful!  They compared five treatments: ibuprofen 400 mg, ibuprofen 800 mg, ASA 650 mg, Darvon 65 mg and placebo.  Both ibuprofen groups had similar reduction in pain scores and were better than the other 3 treatment arms.  The study was done with pooled data from two separate dentists; in one group 400 mg ibuprofen seemed slightly more effective, while 800 mg seemed slightly more effective in the other.  However, there are no data to support any statistically significant difference between ibuprofen groups in the article.

The second article, by Laska et al. in 1986 was a double blind parallel group study with 200 patients post oral surgery compared doses of 400 mg , 600 mg and 800 mg of ibuprofen.  There was no evidence of a dose response efficacy difference between 400, 600 and 800 mg.

Considering that dental pain hurts like hell, I’m inclined to believe these studies are sufficiently representative of ED patients with most injuries.  *As an aside, learn to do dental blocks, they are invaluable to patients.

With regards to ketorolac, this double blind RCT from Staquet in 1989 compared 10 mg, 30 mg and 90 mg IM ketorolac with placebo in 128 patients with cancer pain.  Again, no difference was found between the 3 ketorolac dosing regimens, with all being much superior to placebo.

Other similar studies have been done and show 10 mg is probably the ceiling dose of ketorolac both orally and parenterally.  

In the next parts of the NSAID saga, we’ll discuss side effects profiles of various NSAIDs, and NSAID hodgepodge such as effect on fracture healing, use in renal colic and more.

Cheers,

SOCMOBEM

References:

The post NSAIDs part 2: The Ceiling Effect appeared first on SOCMOB Blog.

Battle Preparation 2: The Buddy Shift

This is the 2nd part in the Battle Preparation series by SOCMOB guest blogger Damon Tedford.

In part 1, we looked at a checklist of items that new learners and staff should identify and examine prior to their first shift in a new ED.  Today we will be looking at the critical questions to ask on your buddy shifts before venturing off alone in your new ED.  These posts are most oriented to the level of senior residents who will become new staff physicians in the near future.  However, the checklists will also be very beneficial to anyone entering a new department, including nurses, junior residents, respiratory therapists, etc.  The ability to find proper equipment is more important than the proper strategy in dealing with a problem.  Amateurs discuss strategy, experts discuss logistics.  

Important questions in this document include:
- What radiology tests do I have access to, and at what times of day?
- How do I set a patient up for outpatient antibiotic therapy?
- Is there a crisis worker for psychiatric patients or do I see them first?
- What are the expectations in our group for shift handover?
and many more...


Let me use a story to emphasize the importance of logistics versus strategy.  A few months ago on a CCU rotation, I was managing a chest pain patient in the ED.  He had hyperacute T-waves on his ECG.  It was about 2 AM, the ED was packed, and it would be about 45 minutes until he could get to the cath lab.  In the meantime, he required management of his chest pain and a nitroglycerin infusion had been started at 10 mcg/min.  His nurse was only intermittently in the room, so frequent titration of his nitro would have been impossible unless I knew how to do it myself.  Fortunately, I had made sure to learn to use our IV pumps; thus I could quickly increase his nitro infusion independent of nursing staff requirements.
This same concept applies to everything you do in the ER; from inserting a urinary catheter to preparing a patient for inter-department transport.  Self-reliance and total logistic knowledge of your environment is a must.  Pretend you're an anesthetistHave you ever seen an anesthetist who didn't set up his/her own pumps or draw up his/her own meds?

Here is a link to part 2 of the Battle Preparation: Buddy Shift Questions


Cheers,

Damon Tedford (@DamonTedford), Chris Krause and Chris Bond (@SocmobEM)


Battle Preparation 2: The Buddy Shift

This is the 2nd part in the Battle Preparation series by SOCMOB guest blogger Damon Tedford.

In part 1, we looked at a checklist of items that new learners and staff should identify and examine prior to their first shift in a new ED.  Today we will be looking at the critical questions to ask on your buddy shifts before venturing off alone in your new ED.  These posts are most oriented to the level of senior residents who will become new staff physicians in the near future.  However, the checklists will also be very beneficial to anyone entering a new department, including nurses, junior residents, respiratory therapists, etc.  The ability to find proper equipment is more important than the proper strategy in dealing with a problem.  Amateurs discuss strategy, experts discuss logistics.  

Important questions in this document include:
- What radiology tests do I have access to, and at what times of day?
- How do I set a patient up for outpatient antibiotic therapy?
- Is there a crisis worker for psychiatric patients or do I see them first?
- What are the expectations in our group for shift handover?
and many more…


Let me use a story to emphasize the importance of logistics versus strategy.  A few months ago on a CCU rotation, I was managing a chest pain patient in the ED.  He had hyperacute T-waves on his ECG.  It was about 2 AM, the ED was packed, and it would be about 45 minutes until he could get to the cath lab.  In the meantime, he required management of his chest pain and a nitroglycerin infusion had been started at 10 mcg/min.  His nurse was only intermittently in the room, so frequent titration of his nitro would have been impossible unless I knew how to do it myself.  Fortunately, I had made sure to learn to use our IV pumps; thus I could quickly increase his nitro infusion independent of nursing staff requirements.
This same concept applies to everything you do in the ER; from inserting a urinary catheter to preparing a patient for inter-department transport.  Self-reliance and total logistic knowledge of your environment is a must.  Pretend you’re an anesthetistHave you ever seen an anesthetist who didn’t set up his/her own pumps or draw up his/her own meds?

Here is a link to part 2 of the Battle Preparation: Buddy Shift Questions



Cheers,

Damon Tedford (@DamonTedford), Chris Krause and Chris Bond (@SocmobEM)


The post Battle Preparation 2: The Buddy Shift appeared first on SOCMOB Blog.

NSAIDs Part 1: Which one is best?



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

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:RAPactually 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 DIFFERENCEin 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. 


NSAIDs Part 1: Which one is best?

–>

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:RAPactually 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 DIFFERENCEin 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. 

The post NSAIDs Part 1: Which one is best? appeared first on SOCMOB Blog.

Battle Preparation: Getting Ready for Your First Shift in the ER

Today is a first for the SOCMOB blog, as we have our first guest blogger.  Damon Tedford is one of my fellow EM residents, and is also in his final year of training.  Combining his military background with the works of Cliff Reid and Scott Weingart, Damon had the fantastic idea of creating a checklistto familiarize oneself with the ED prior to their first shift.  This will be released in two parts, a walk-about checklist today, followed by a list of key questions later in the week.

Battle Preparation: Getting Ready for Your First Shift in the ER


As the end of residency approaches, I often hear of the tumultuous emotional trajectory that awaits the recently certified ER doc.  "Plan for three months of fear.  It slowly gets easier after that."  I expect some growing pains after shedding the training wheels, but have we not figured out a better way of assisting physicians with this transition? After all, it is a yearly event.

In the few places I have interviewed, it would seem that buddy shifts are the norm for newcomers.  Physicians are eased into their working environment over a number of shifts with a local, experienced physician.  It is a great, but imperfect idea, as the value of the orientation depends on the cases of the day and what your mentor thinks you need to know. In addition to these shifts, I plan on adding a more active and ordered approach, leaving less to chance.

Before my medical days, I trained as an army officer in the Canadian Forces, and if anyone can do order, it's the army.  During those days, we were taught a regimented approach to mission planning.  We called the process "Battle Procedure."  Reconnaissance, or a "Recce," is a key component of Battle Procedure, so much so that all army leaders know the axiom, “Time on recce is seldom wasted”.  

During the planning stage, a commander will draft a recce plan to identify factors that will waylay the mission (What equipment do I have at my disposal? What aspects of the ground will impact my team? Where am I vulnerable and how can I mitigate that risk?) These are some examples of questions the leader seeks to answer during his recce. During the recce, the leader walks the ground with a plan in mind.  If this is impractical, he/she reviews maps, satellite photography, or accounts from first-hand witnesses to get a sense of the environment he/she will be operating.  The commander then completes a plan and shares it with the team.  Together they may "war-game" it, playing out each phase of the operation, identifying oversights or unique aspects of the operational environment that necessitate changes to how they have done business in the past.

Battle Procedure is a deliberate process, and one I have used to work through some complex problems.  If the military analogy does not work for you, have a listen to Scott Weingart's Podcast #49 - Mind ofthe Resus Doc: Logistics over Strategy.  It's one of my favorites and a major inspiration for the checklists you will find below. 



Here at SOCMOBEM, we have completed a recce plan for the new ER physician, but this could easily be used by anyone new to the department.  Our goal is to ease the transition of new ER team members and get them ready for peak performance on day one.

Identifying the key tasks we could be called upon to complete during our first shift, we have created a list of equipment for time sensitive resuscitation tasks as well as those that are more regular but routine.  Finding the equipment before your first shift prevents loss of valuable time and also improves department flow.  However, the document is more than a medical scavenger-hunt.  
While checking off items, ask yourself:

What is the state of repair of the equipment?
Are there shortages of essential items within the procedure bundles that I will need to complete the task?
Would I be able to set up this ventilator alone?
How do I see a resuscitation playing out here?
Does equipment location make sense?
Where could things potentially go wrong for my team and what could I do about it?  

You get the idea.

With a fresh set of eyes, we may identify opportunities to improve patient care and efficiency.  A word of caution: no one likes a know-it-all.  Unless patient safety is an issue, save the recommendations for an appropriate time and venue and deliver those suggestions tactfully.  

The second document will contain a list of questions that will guide the conversation between mentor and new ER physician.  Perhaps it could be done over a coffee.  Some examples of these questions include:

What services are available after hours?
How do we handle mass casualties?
Do we have a massive transfusion protocol?
Where can I find this and other protocols?  


Look for a second post and question list here within the week.  

We hope these posts help those who find themselves in a new emergency department.  If you have suggestions, let us know.  Peer review is key to improvement.  

Cheers,

Damon

Battle Preparation: Getting Ready for Your First Shift in the ER

Today is a first for the SOCMOB blog, as we have our first guest blogger.  Damon Tedford is one of my fellow EM residents, and is also in his final year of training.  Combining his military background with the works of Cliff Reid and Scott Weingart, Damon had the fantastic idea of creating a checklistto familiarize oneself with the ED prior to their first shift.  This will be released in two parts, a walk-about checklist today, followed by a list of key questions later in the week. 

*For part 2, click here.


Battle Preparation: Getting Ready for Your First Shift in the ER


As the end of residency approaches, I often hear of the tumultuous emotional trajectory that awaits the recently certified ER doc.  ”Plan for three months of fear.  It slowly gets easier after that.”  I expect some growing pains after shedding the training wheels, but have we not figured out a better way of assisting physicians with this transition? After all, it is a yearly event.

In the few places I have interviewed, it would seem that buddy shifts are the norm for newcomers.  Physicians are eased into their working environment over a number of shifts with a local, experienced physician.  It is a great, but imperfect idea, as the value of the orientation depends on the cases of the day and what your mentor thinks you need to know. In addition to these shifts, I plan on adding a more active and ordered approach, leaving less to chance.

Before my medical days, I trained as an army officer in the Canadian Forces, and if anyone can do order, it’s the army.  During those days, we were taught a regimented approach to mission planning.  We called the process “Battle Procedure.”  Reconnaissance, or a “Recce,” is a key component of Battle Procedure, so much so that all army leaders know the axiom, “Time on recce is seldom wasted”.  

During the planning stage, a commander will draft a recce plan to identify factors that will waylay the mission (What equipment do I have at my disposal? What aspects of the ground will impact my team? Where am I vulnerable and how can I mitigate that risk?) These are some examples of questions the leader seeks to answer during his recce. During the recce, the leader walks the ground with a plan in mind.  If this is impractical, he/she reviews maps, satellite photography, or accounts from first-hand witnesses to get a sense of the environment he/she will be operating.  The commander then completes a plan and shares it with the team.  Together they may “war-game” it, playing out each phase of the operation, identifying oversights or unique aspects of the operational environment that necessitate changes to how they have done business in the past.

Battle Procedure is a deliberate process, and one I have used to work through some complex problems.  If the military analogy does not work for you, have a listen to Scott Weingart’s Podcast #49 – Mind ofthe Resus Doc: Logistics over Strategy.  It’s one of my favorites and a major inspiration for the checklists you will find below. 


Here at SOCMOBEM, we have completed a recce plan for the new ER physician, but this could easily be used by anyone new to the department.  Our goal is to ease the transition of new ER team members and get them ready for peak performance on day one.

Identifying the key tasks we could be called upon to complete during our first shift, we have created a list of equipment for time sensitive resuscitation tasks as well as those that are more regular but routine.  Finding the equipment before your first shift prevents loss of valuable time and also improves department flow.  However, the document is more than a medical scavenger-hunt.  

While checking off items, ask yourself:

What is the state of repair of the equipment?
Are there shortages of essential items within the procedure bundles that I will need to complete the task?
Would I be able to set up this ventilator alone?
How do I see a resuscitation playing out here?
Does equipment location make sense?
Where could things potentially go wrong for my team and what could I do about it?  

You get the idea.

With a fresh set of eyes, we may identify opportunities to improve patient care and efficiency.  A word of caution: no one likes a know-it-all.  Unless patient safety is an issue, save the recommendations for an appropriate time and venue and deliver those suggestions tactfully.  

The second document will contain a list of questions that will guide the conversation between mentor and new ER physician.  Perhaps it could be done over a coffee.  Some examples of these questions include:

What services are available after hours?
How do we handle mass casualties?
Do we have a massive transfusion protocol?
Where can I find this and other protocols?  


We hope these posts help those who find themselves in a new emergency department.  If you have suggestions, let us know.  Peer review is key to improvement.  

Cheers,

Damon

The post Battle Preparation: Getting Ready for Your First Shift in the ER appeared first on SOCMOB Blog.

New Surviving Sepsis Guidelines 2012: WTF?

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

The post New Surviving Sepsis Guidelines 2012: WTF? appeared first on SOCMOB Blog.

New Surviving Sepsis Guidelines 2012: WTF?

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

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.


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.


The post Thiamine Before Glucose will not cause Wernicke’s Encephalopathy appeared first on SOCMOB Blog.

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.  However, 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.  YouTube has a huge number of videos for performing the procedure itself, so I'll direct you there if you are unfamiliar with it.

I have to give Scott Weingart from EMCrit credit for suggesting this 2004 Anesthesiology article.  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.

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.

The post How to make your own Cricothyrotomy Trainer appeared first on SOCMOB Blog.

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.

The post Drinking the PPI Hate-O-Rade appeared first on SOCMOB Blog.

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.

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

The post Choosing your Battles: My Christmas Pearl of 2012 appeared first on SOCMOB Blog.

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

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.

 

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.

 

The post Evidence Based Laceration Repair appeared first on SOCMOB Blog.

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. 

All about chest tubes


Of all the interventions we perform, chest tube insertion is one of the most dangerous, complicated and misunderstood.  Today I'll discuss not only the myths, but also some unfortunate realities that we must understand when we undertake this procedure.

Myth # 1

Bigger is better

I'm pretty sure we've all been told, partially thanks to ATLS, that we better put a 36 or 40 French chest tube in during trauma, otherwise the blood will clog up the tube and drainage will cease.  Wrong, wrong, wrong!

This prospective, non randomized trial of trauma patients over a 3 year period from 2007-2010 compared small (28-32 French) with large (36-40 French) chest tubes.  The operator chose tube size, and sicker patients got bigger tubes (More ISS >25, GCS <8, sBP <90, (all p<0.01) for large chest tube group)  However, there was no difference in thoracic trauma pathology between the two groups (eg. flail chest, pulmonary contusions, PTX, pneumomediastinum, etc.)

Overall, there was no difference in the rate of complications between the two groups.  This includes pneumonia, empyema and retained hemothorax.  Further, there was no difference in interventions required for retained hemothorax (Additional chest tube insertion, intrapleural throombolysis, IR guided catheter insertion, VATS and thoracotomy)
When adjusted for ISS, GCS and sBP, there was still no difference between the two groups, with respect to complication rates or interventions for retained hemothorax. 

When pneumothoraces were analyzed separately, there was no difference in rate of complications or requirement for further intervention in this group either.

The second hypothesis of this study was that bigger tubes are more painful, and a visual analogue scale was used to rate patient pain.  There was no difference in VAS scores between the small and large chest tube groups.

Bottom Line: Any tube that is at least 28 French is suitable for draining a chest.  

Although it might not hurt less than a larger tube, it may still pass through the intercostal space a little more easily, so go ahead with those smaller tubes.  The logical next question is: Are tubes smaller than 28 French adequate?  That remains to be studied.

Myth #2

Directing the chest tube.  ie: Up for air, down for blood.


Every medical student/resident is asked this question repeatedly throughout their training.  "Where would you put the tube for a hemothorax?  What about a pneumothorax?"  The answers is always posterobasal for fluid and apical for air, right? 

2 things about this myth.  First, once the tube gets inside the chest, our ability to direct it is poor.  Second, as long as you are in the pleural space, you'll be fine.  It is a closed system and you have suction.  The fluid will drain regardless.  You may still have complications, but it's not because you put the tube in the apex of a hemothorax.

More important than directing the chest tube is ensuring it's in the pleural space, not advancing when you meet resistance and not causing any other complications.

There is a BestBets on this topic which can be found here.  There really isn't great data on this, so it is more of a physics myth than anything else.

Truth #1

Complications of chest tubes - This is not a myth, this is for real.

This is one critical point for all of us, but especially for residents inserting chest tubes.

The morbidity associated with chest tube insertions is astronomical!  About 25-30% of chest tube insertions have a complication, regardless of who inserts them.  A 2012 AAST study looking at post-traumatic empyema rates in major trauma centers is 27%.  That is crazy.
However, as an EM resident, I was disappointed to read this article that suggests EM residents may be the worst of all.  Really it's only a trend toward significance, and a retrospective study, but I'm still a bit sad to read it.  

We have to do something to get these rates of complications down.  

Use of antibiotic prophylaxis when inserting chest tubes is a topic of controversy.  EAST (The Eastern Association for the Surgery of Trauma) published a guideline in 2000 suggesting antibiotic prophylaxis for chest tube insertion.  More recently, this meta-analysis reviewing antibiotic prophylaxis was published in 2012.

For penetrating trauma, I would say that at least a single dose of antibiotic (1st gen cephalosporin) should be given at the time of insertion, if time and resources allow. This results in reduced rates of empyema and pneumonia, which in turn affects hospital and ICU LOS. 

For blunt trauma, which is the majority of what we see in Canada, no statistically significant reduction in infectious complications was found, and you may choose to withhold antibiotics in this group.

In all cases, duration of therapy is controversial.  It appears that short term (single dose or 24 hours) is equally effective as prolonged antibiotics (until time of chest tube removal).

Bottom line: Our rates of post-chest tube complications (empyema and pneumonia) are ridiculously high, even in major trauma centers.  A single dose of cefazolin at the time of chest tube insertion is a pretty benign intervention, and in my opinion warranted, particularly in penetrating trauma.

I'm curious who is giving antibiotics and if so, is it single dose, 24 hours, or longer?

Summary:


1)Any chest tube at least 28 French is suitable for traumatic hemo/pneumothorax.

2)Get the tube in the pleural space but direction doesn't matter.

3)Complications of chest tubes are exceedingly high.  Give a single dose of peri-procedure antibiotics (particularly in penetrating trauma) and use sterile technique.

Until next time, I'll be standing on the corner, mindin' my own business. 

Cheers,

@SOCMOBEM

References and some chest tube links from people much more intelligent than me:

Own the chest tube with Chris Nickson at Life in the Fast Lane

Michael McGonigal's Trauma Professionals Blog has some great videos and posts about chest tubes as well.

Eastern Association of Surgeons for Trauma (EAST) Guidelines for Hemothorax and Occult PTX can be found here.

EAST Guideline on antibiotic prophylaxis for tube thoracostomy can be found for free here.
This is the reference. J Trauma. 48(4): 758-759, April 2000.

2012 Meta-analysis for antibiotic prophylaxis
Bosman A, de Jong MB, Debeij J, van den Broek PJ, Schipper IB.  Br J Surg. 2012 Apr;99(4):506-13

Chest tubes: Does Size Matter
Inaba, K et al. J Trauma 72(2):422-427, 2012.





Post-traumatic chest tube empyema rates
J Trauma 73(3):752-757, 2012.