Articles of the month (February 2015)

A monthly collection of the most interesting emergency medical literature I have encountered

Amoxicillin is the antibiotic of choice in pediatric pneumonia

Williams DJ et al. Narrow vs broad-spectrum antimicrobial therapy for children hospitalized with pneumonia. Pediatrics. 2013 Nov;132(5):e1141-8. PMID: 24167170

This was a retrospective record review of 15,564 admitted but not critically ill pediatric patients with community acquired pneumonia. They used propensity scoring, so the results could mean anything, but kids getting amoxicillin had the same outcomes as those with broad spectrum antibiotics such as cefotaxime or ceftriaxone. In fact, IDSA and peds infectious disease society both recommend narrow spectrum antibiotics, which is contrasted to the 90% of children in this study that were given broad spectrum.

Bottom line: Amoxicillin is probably best in pediatric pneumonia.


Hans and Franz want to pump you up (steroids for pediatric asthma)

Keeney GE et al. Dexamethasone for acute asthma exacerbations in children: a meta-analysis. Pediatrics. 2014;133(3)493-9. PMID: 24515516

A meta-analysis of 6 RCTs of prednisone versus dexamethasone in children with acute asthma exacerbations. There was no difference in relapse at 5 or 30 days. The dexamethasone group was less likely to vomit, both at home and in the ED. (Some studies used 2 doses of dex, some only used 1 versus generally 5 days of prednisone.)

Bottom line: Fewer doses and less vomiting, I am sold on dexamethasone. (My wife adds: “Well Duh! Pediapred tastes like s***. Dex is less volume and way easier to take.”)


The ugly stepchild of papers 1 and 2? Steroids for pneumonia

Blum, CA et al. 2015. Adjunct prednisone therapy for patients with community-acquired pneumonia: a multicentre, double-blind, randomised, placebo-controlled trial. Lancet (January 16). PMID: 25608756

I don’t buy what they are selling here, but I have already heard about this paper from at least 10 different sources, so you will likely hear about it as well. This is a large, multi-center, double blind RCT of 781 community acquired pneumonia patients, randomized to either get or not get prednisone 50mg PO daily for 1 week. It was a positive study, in that the primary outcome “time to clinical stability”, or ‘normal vital signs’, was 3 days in the prednisone group and 4.4 days with placebo. However, as important as vital signs are, are they really a patient oriented outcome? Has a patient ever said, I know I have this pneumonia, but what I really want is for my heart rate to be 95 instead of 105? Side effects: prednisone obviously caused hyperglycemia, but also (non statistically) doubled pneumonia associated complications. Previous studies showed higher recurrence rates with steroids.

Bottom line: Of course steroids make the numbers look better, but we are probably treating the doctor and not the patient here. Not for me.

Bottom line #2: If you are going to design a study, measure outcomes that matter.


Why do we use cervical collars?

Ala’a O et al. 2015. Should suspected cervical spinal cord injury be immobilised?: A systematic review. Injury Journal. (In press). PMID: 25624270

Like many of the things we do, this practice was started based on expert opinion in the pre-EBM era. There are a large number of cadaver and volunteer studies that show that C-collars really don’t prevent movement of the c-spine. What is the clinical evidence? There are a grand total of 8 observational studies ever done. In penetrating trauma, C-collar application was associated with an increase in mortality (OR 8.8), increase scene time, and concealment of neck injuries. In blunt trauma, one study showed that immobilization was associated with worse neurological outcomes. This is balanced by no evidence of benefit. They conclude “there is a clear need for large prospective studies to determine the clinical benefit of prehospital spinal immobilsation.”

Bottom line: I can’t imagine anyone changing their practice, but this does not speak very well to the benefits of cervical spine collars


Where are you drilling? Arm might be better than leg, or go straight towards the heart

Pasely J et al. 2015. Intraosseous infusion rates under high pressure: A cadaveric comparison of anatomic sites. Journal of Trauma and Acute Care Surgery 78(2)295-9. PMID: 25757113

Its a cadaver study, so take that as you will – but I am often drilling into dead people in code situations anyhow, so there might be some external validity here. They tried to infuse saline using a pressure bag, and the rates they could get were: 94ml/min in the sternum, 57ml/min in the humerus, and 30 ml/min in the tibia.

Bottom line: Humerus seems twice as fast as the tibia, so maybe that should be our go to spot? I probably wouldn’t suggest drilling sharp things into the sternum, but some people seem to think it’s OK.


Speaking of IOs – they are fine for RSI

Barnard EBG et al. 2014. Rapid sequence induction of anaesthesia via the intraosseous route: a prospective observational study. Emerg Med J (electronic ahead of print). PMID: 24963149

OK, also not really definitive by any means. A prospective observational study, with no controls, in a military setting. 34 patients had their RSI drugs pushed through an IO, first pass success in all but 1 (97%) and that patient was intubated on the second attempt. Although no control, 97% compares well with historical controls.

Bottom line: Go ahead and give RSI drugs through an IO if that is what you have


First RCT of massive transfusion protocol

PROPPR Holcomb et al. Transfusion of Plasma, Platelets, and Red Blood Cells in a 1:1:1 vs a 1:1:2 Ratio and Mortality in Patients With Severe Trauma. The PROPPR Randomized Clinical Trial. JAMA. 2015; 313(5)471-82. PMID: 25647203

After a bunch of theoretical stuff and some observational trials, this was the first ever RCT comparing different ratios of PRBCs, FFP, and platelets in a massive transfusion protocol. They compared 1:1:1 PRBCs, FFP and platelets to 2 units of PRBCs for each 1 unit of FFP and platelet equivalent. This was a negative trial, in that there was no difference in mortality between the two groups. However, some people have argued that their goal of a 10% reduction in mortality was too high, that the non-significant trends (including a 4.3% absolutely mortality reduction) favoured the 1:1:1 group, and secondary bleeding end points also favoured the 1:1:1 group. (This study design makes the inherent assumption that some transfusion ratio is a good thing, in that they did not include a usual care arm. While this has been the trendy thing of late, it is entirely based on flawed observational studies.)

Bottom line: This study will be used to support whatever pre-existing beliefs you had on the subject.


The new AAP bronchiolitis guidelines are very nihilistic (maybe realistic?)

Ralston SL et al. 2014. Clinical practice guideline: the diagnosis, management, and prevention of bronchiolitis. Pediatrics 134(5)e1474-502. PMID 25349312

Quick summary:

Do NOT give ventolin

Do NOT give epinephrine

Do NOT give hypertonic saline (in the ED)

Do NOT give corticosteroids

Diagnosis on Hx/Px, no routine chest xrays

While these guidelines are very evidence based, my EBM self is fighting with my practical self. If there are no treatments, peds is going to have to see 30 kids a day in the ED. Should we just set aside a room for them?

Bottom line: The AAP says don’t do anything for bronchiolitic kids

Two for the price of one: pediatric head injuries aren’t cured by CT

Lee LK et al. (PECARN). Isolated loss of consciousness in children with minor blunt head trauma. JAMA Pediatrics 2014; 168(9)837-43. PMID: 25003654

This is a secondary analysis of the PECARN head injury algorithm. Although overall your chance of clinically important head injury was 2.5% with LOC and only 0.5% without, if you only had LOC and no other PECARN risk factors, your risk of a clinically important injury was the back to baseline at 0.5%.

Bottom line: Loss of consciousness, in the absence of other worrisome findings, has a low risk of clinically important injury and CT scan is unnecessary. (Look at the whole patient, not just one aspect of the history or physical.)

Dayan PS et al. (PECARN). Association of traumatic brain injuries with vomiting in children with blunt head trauma. Annals of Emergency Medicine 2014;63(6)657-65. PMID: 24559605

Another secondary analysis of the PECARN head injury algorithm. Vomiting, without any other PECARN risk factors, had an overall incidence of clinically important injury of 0.2%

Bottom line: Vomiting, in the absence of other worrisome findings, has a low risk of clinically important injury and CT scan is unnecessary. (Look at the whole patient, not just one aspect of the history or physical.)


Start sending those stroke patients to the cath lab?

After multiple negative trials in the past, we get 3 new trials on endovascular treatment of stroke. (Given that we aren’t a stroke center and this isn’t going to be a decision you will make in the ED, it is probably best to just skip to the next section. But they will be talked about at cocktail parties.)

MR CLEAN Berkhemer OA et al. A randomized trial of intraarterial treatment for acute ischemic stroke. N Engl J Med. 2015;372:(1)11-20. PMID: 25517348

RCT comparing intra-arterial treatment versus usual care in stroke patients. Good neurological outcome (MRS 0-2 at 90 days) in intra-arterial group was 32% versus only 19% in the usual care group. (These are both way worse outcomes than other stroke trials, like NINDS)

EXTEND-IA Campbell BC et al. Endovascular Therapy for Ischemic Stroke with Perfusion-Imaging Selection. N Engl J Med. 2015. (Ahead of print) PMID: 25671797

RCT (phase II trial) of patients getting TPA within 4.5 hours with a middle cerebral or internal carotid clot AND evidence of salvageable brain tissue plus or minus endovascular therapy. Was stopped early after only 70 patients (they had to screen over 7,000 patients at 10 hospitals over 2 years to find these 70 patients – so they are highly selected to say the least). There were multiple primary outcomes (bad) but importantly if you got treated 80% had good neurological improvement at 3 days, versus only 37% of those without the endovascular treatment.

ESCAPE Goyal M et al. Randomized Assessment of Rapid Endovascular Treatment of Ischemic Stroke. N Engl J Med. 2015. (Ahead of print) PMID: 25671798

RCT of patients up to 12 hours with proximal anterior circulation occlusions and evidence of good collateral flow plus or minus endovascular therapy. Also stopped early, with a total of 316 patients (wanted 500 originally). They also only managed to recruit about 1 patient a month at each of the 22 hospitals involved – so also very highly selected patients. Functional independence (MRS 0-2) at 90 days was 53% in the endovascular arm and 29% in the usual care arm.

Overall bottom line: The benefit described in these trials is impressive. They are small and all have some flaws (stopping them early probably exaggerates the benefit), but I think it is likely they represent a true benefit. However, the number of eligible patients was tiny. Maybe they have finally found the subset of stroke patients that will benefit from revascularization – like the STEMI patient in a sea of chest pains.


Dr. Oz Sucks

Korownyk C et al. Televised medical talk shows–what they recommend and the evidence to support their recommendations: a prospective observational study. BMJ 2014;349:g7346. PMID: 25520234

OK, this isn’t really all that valuable or surprising, because anyone that has ever turned on a TV realizes that Dr. Oz rarely has anything credible to say, and seems to be a lot more interested in selling snake oil than actually helping patients. But in case any one was wondering, these authors prospectively evaluated the claims made on Dr. Oz and The Doctors, and even if a single case report was counted as “evidence” only 50% of the claims made on the shows had any evidence based backing, and a full 15% were completely contradictory to available evidence.

Bottom line: Don’t get your medical advice from a TV shill


Let’s review an older one: TTM, putting dead people on ice

Nielsen N et al. Targeted temperature management at 33°C versus 36°C after cardiac arrest. N Engl J Med. 2013 369(23):2197-206. PMID: 24237006

An ‘older’ paper that I am sure everyone has heard about, but it is good to include at least one practice changing quality study every month. After 2 small, low quality studies were published in 2002 (well before I started medical school in case you were wondering), the medical world went nuts for therapeutic hypothermia. But when I started in medicine, there were still some intelligent people (like Jerry Hoffman) who tried to remind us these were small studies, with inherent biases, and that a corner stone of science is replication. (There is a lesson here for so many other topics – but I don’t think I have the balls to mention NINDS and tPA.)

So this was a large, randomized control trial (not blinded) where 950 patients with ROSC after out of hospital cardiac arrest were either brought to 33 or 36 degrees Celsius. There was no difference in outcome.

The comments about this paper have been all over the map. The favorite statement by a lot of very smart people seems to be “this confirms that we desperately need to avoid fever, but 36 degrees is probably good enough.” I would point out, this study says nothing about avoiding fever. In fact, I don’t know of any study that compared fever or no fever post cardiac arrest. So people are either expressing their left over love of hypothermia, or is basing it on animal models, which are – well animal models.

Another approach would be to ask if we have any reason to believe this would work (the beginning of Bayesian reasoning). There were some animal models that support hypothermia, but probably more important is that hypothermia has been tested in humans for a number of conditions other than cardiac arrest – and it doesn’t seem to work.

Bottom line: There is no benefit from hypothermia post cardiac arrest. No one knows much about fever, but many people will talk about it a lot.

Bonus section: This Penn and Teller vaccination video should play continusouly in the waiting room

Cheesy Joke of the Month

It was a cold February so:

What is the difference between snowmen and snowwomen?


Articles of the month (January 2015)

A monthly collection of the most interesting emergency medical literature I have encountered

Each month my inner nerd comes out, and I bore my group with an e-mail containing the most interesting EM papers I have read in those 30 days. I figured I would start sharing those summaries here as well, starting at the beginning of 2015. These are obviously very brief, informal summaries. I always suggest reading the paper for yourself. Now to catch up, starting with January 2015…

Beta-blockers might be useful in refractory V.Fib.

Driver BE et al. 2014. Use of esmolol after failure of standardcardiopulmonary resuscitation to treat patients with refractory ventricular fibrillation. Resus 85(10):1337-41. PMID: 25033747

Not a definitive paper (it was retrospective) but raises a treatment that I have never used, or seen used, but have heard talked about a lot recently. In patients with refractory V.fib/ electrical storm, we don’t usually reach for anti-hypertensives, but beta blockers might be a good idea. Use of esmolol in these patients was associated with more ROSC and more neurologically in-tact survival.

Bottom line: Esmolol 500mcg/kg bolus over 1 min then start at 50mcg/kg/min.


Patients with a listed penicillin allergy get more C.Diff, MRSA, VRE

Macy E, Contreras R. 2014. Health care use and serious infection prevalence associated with penicillin “allergy” in hospitalized patients: A cohort study. J Allergy Clin Immunol. 133(3):790-6. PMID: 24188976

This was a large retrospective cohort study of 51,000 patients in California. Patients with a listed penicillin allergy received more clinda, vanco, and quinolones. They also had 23% more C.Diff, 14% more MRSA, and 30% more VRE (relative numbers) as compared to their matched, non penicillin allergic patients.

Bottom line: It might be worth digging more into those penicillin allergies.


Tranexamic acid topically stops epistaxis

Zahed R et al. 2013. A new and rapid method for epistaxis treatment using injectable form of tranexamic acid topically: a randomized controlled trial. Am J Emerg Med. 31(9):1389-92. PMID: 23911102

A good sized RCT (216 patients) compared usual packing to 500mg (5ml) of TXA on a cotton ball in the anterior nose. This worked quickly (bleeding was stopped at 10 min in 70% of the TXA group compared to only 30% of ant pack group) and lasted (no significant difference in 24 hour rebleed rate between groups, but only 5% in TXA versus 10% in ant pack group had rebleeds). Patients preferred the TXA to packing (what a surprise). Biggest problem with the paper: unable to blind (and I am pretty sure that less than 70% of my anterior packings are still bleeding at 10 minutes.)

Bottom line: Worth trying, as I wouldn’t want to go home with an anterior pack (but my personal experience with this isn’t nearly as positive)


Let’s stay on topic: CRASH 2: TXA reduces mortality in trauma

Effects of tranexamic acid on death, vascular occlusive events, and blood transfusion in trauma patients with significant haemorrhage (CRASH-2): a randomised placebo-controlled trial. Lancet 2010; 376: 23-32. PMID: 20554319

I didn’t actually read this this month, but it is a landmark paper, so why not review. I was originally skeptical, but we probably should be doing this until we know better. Summary: Huge RCT (over 20,000 patients) of adult trauma patients the doc thought was at risk of significant bleeding, got 1 gram of TXA over 10min and then another over 8 hours. They showed an absolute decrease in mortality of 1.5% or an NNT of 68. Why was I skeptical – the majority of these patients were in a very rural setting, without access to trauma surgeons (some sites did not even have a fax machine for the randomization procedure) so this may not apply in Canada, and TXA was supposed to work by decreasing bleeding, but it didn’t. However – I am starting this think this might apply to us. We don’t have a trauma surgeon and a lot of time might pass during transfer, so maybe we are more like rural Africa than I originally thought. I would caution however – they conclude that there were no side effects from TXA. However, when looking for side effects the setting might really matter. If a patient in rural Africa gets a DVT or a PE, how easy do you think it is to get the test to prove it? Therefore, this study could easily have missed blood clots in patients sent back to their villages.

Bottom line: Probably all trauma patients sick enough to transfer should get TXA 1 gram IV.


Anti-emetics don’t work in adults?

Egerton-Warburton et al. 2014. Antiemetic Use for Nausea and Vomiting in Adult Emergency Department Patients: Randomized Controlled Trial Comparing Ondansetron, Metoclopramide, and Placebo. Annals of Emergency Medicine 64(5): 526-32. PMID: 24818542

This was a prospective, double blind, RCT of 270 patients from Australia comparing zofran versus maxeran versus placebo. And you guessed it, much like everything we do: our treatments don’t work. Or, more accurately, placebo and both the drugs decreased nausea scores by about 2.5 out of 10. More side effects with maxeran. Two problems: 1) Dose – zofran only 4mg, but we often given more; maxeran – they gave 20mg – which might explain the side effects. 2) They only measured outcomes at 30 minutes – maybe anti-emetics help at 2 or 3 hours? However, it was a good RCT and treatment was no better than placebo.

Bottom line: Maybe we slightly overuse these medications?


AEDs may have some major problems

Calle PA et al. 2015. Inaccurate treatment decisions of automated external defibrillators used by emergency medical services personnel: Incidence, cause and impact on outcome.Resuscitation (Ahead of print) PMID: 25556589

This one worries me, but I am not sure what to do about it. For 135 consecutive patients (837 total cardiac rhythms) these authors retrospectively looked at the rhythm strip and compared it to what the AED actually did. Out of 148 rhythms that should have been shocked, the AED missed 23 (16%) mostly due to artifact or fine v.fib. It also shocked when it should not have, although with no obvious harm, 4% of the time. (I can’t remember the model of the AED – maybe some are better or worse?)

Bottom line: AEDs might miss shock-able rhythms 16% of the time!!!


Apneic oxygenation decreases desaturations during intubation

Wimalasena Y et al. 2014. Desaturation rates during rapid sequence intubation by an Australian helicopter emergency service. Annals of Emergency Medicine. (Online ahead of print) PMID: 25536868

This was one of the papers I spoke about at grand rounds. Not high quality, being a retrospective before and after study. Essentially, this pre-hospital/ retrieval helicopter EMS service in Australia added the use of a nasal canula to their protocol for all intubations. Historically, 22.6% of patients had some desat. With nasal oxygen 16.5% had some desat.

Bottom Line: Essentially no cost, and a NNT of 16 to prevent a desat. Blow some Os up their nose.


Mortality decreases when all the best cardiologists are out of the country

Jena AB et al. 2014. Mortality and Treatment Patterns Among Patients Hospitalized With Acute Cardiovascular Conditions During Dates of National Cardiology Meetings. JAMA Intern Med. PMID: 25531231

This article is relatively useless from a science standpoint – but I love the relatively absurd conclusions. It is a retrospective chart review where they looked at the cardiac outcomes for patients admitted during national cardiology meetings (and therefore when all the “top” cardiologists and cardiac surgeons were away). Many fewer procedures were done and MORTALITY WENT DOWN.

Bottom line: Have your heart attack when the leading cardiologists are all out of town.


A better aproach to PEA

Littmann L et al. 2014. A simplified and structured teaching tool for the evaluation and management of pulseless electrical activity. Medical Principles and Practice. 23:1-6. PMID: 23949188 Free full text:

The standard epinephrine and push treatment is actually associated with worse outcomes in PEA. To that end, most guidelines say that in PEA the essential action is to determine the underlying cause.  But the Hs and Ts are hard to remember during a code, and also don’t tell you which cause is the most likely. This new algorithm does through 3 simple steps: 1) QRS wide or narrow? 2) Ultrasound to find cause (Or use clinical judgement) 3) Empiric treatment based on the first 2. This is not one where my summary will suffice – its a 4 page paper and its free. I strongly suggest taking 20 minutes and reading it through. (Or, you can read the First10EM blog post: The simplified approach to PEA)

Bottom line: There is a better way to approach PEA

Cheesy Joke of the Month

A man awoke in the recovery room after a bad car accident. He screamed for his doctor: “Doctor, doctor, I can’t feel my legs!!”

The doctor replied: “I know you can’t – I’ve cut off your arms.”