October 2016 Journal Club with First10EM

Welcome back to the podcast for October’s Articles of the Month

Another month of interesting reading with Dr Justin Morgenstern.  Check out the First10EM blog for full written version.

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Below are the written summaries and the links to the original papers:

Coming soon: Daily home D-Dimer testing
Prandoni P, Lensing AW, Prins MH et al. Prevalence of Pulmonary Embolism among Patients Hospitalized for Syncope. N Engl J Med. 375(16):1524-1531. 2016.
This paper will definitely be the most talked about of the month. It has the potential to be the most misunderstood paper of the month as well, and cause problems between emergency physicians and our specialist colleagues, but hopefully we can get ahead of it and understand the data for what it really shows. The paper’s misleading conclusion is “pulmonary embolism was identified in nearly one of every six patients hospitalized for a first episode of syncope.” Pulmonary embolism can definitely cause syncope, and there may even be a few patients with no other symptoms, but this data does not support working up PE in otherwise asymptomatic syncope patients.
Bottom line: You will hear about this. You will be asked to order CTs. Don’t. Use your clinical judgement and continue to assess patients for PE like you have been. Your patients will be better off for it.
Read more: R.E.B.E.L.EM, EM Nerd, St. Emlyn’s, EM Lit of Note

That’s not a knife… that’s a knife (I’m always alright when I’m with you, Dundee)
Pracy JP, Brennan L, Cook TM. Surgical intervention during a Can’t intubate Can’t Oxygenate (CICO) Event: Emergency Front-of-neck Airway (FONA)? British journal of anaesthesia. 2016. PMID: 27646054
This statement from the UK Difficult Airway Society gives a clear recommendation, based on the evidence, on how to deal with a can’t intubate can’t oxygenate scenario: you should immediately proceed to a surgical cricothyroidotomy. Specifically, they recommend the scalpel-bougie technique. They have removed all needle or catheter based approaches from their algorithms, because in real life settings, these techniques fail at a very high rate.
Bottom line: Anyone who manages airway should be prepared to cut the front of the neck. I don’t work a shift without a scalpel in my pocket.

I’ve included the NAP4 trial in these reviews before, but just as a review:
Cook TM, Woodall N, Harper J, Benger J, . Major complications of airway management in the UK: results of the Fourth National Audit Project of the Royal College of Anaesthetists and the Difficult Airway Society. Part 2: intensive care and emergency departments. British journal of anaesthesia. 106(5):632-42. 2011. PMID: 21447489
This was a massive undertaking. Based on a network of reporters from local institutions, all major airway complications in the United Kingdom over the course of a year were recorded. With regards to surgical airways, there were 75 incidents in that year. Needle cricothyroidotomy failed about 60% of the time, whereas surgical cricothyroidotomy was 100% successful.
Bottom line: It’s not an RCT but it’s as good as we have: you don’t use a needle for an emergency cricothyroidotomy, you use a scalpel.

Jet ventilation: complications
Duggan LV, Ballantyne Scott B, Law JA, Morris IR, Murphy MF, Griesdale DE. Transtracheal jet ventilation in the ‘can’t intubate can’t oxygenate’ emergency: a systematic review. British journal of anaesthesia. 117 Suppl 1:i28-i38. 2016. PMID: 27566790
My concern about relying on needle based anterior neck airway approaches in can’t intubate can’t oxygenate situations is that, especially when under pressure and your hands are shaking, I think they will be slower and less reliable. This study describes another major problem with relying on transtracheal jet ventilation: barotrauma. This is a systematic review, looking at both published and unpublished literature, that found 44 papers describing transtracheal jet ventilation. There is a very high failure rate in the literature. In the papers describing transtracheal jet ventilation for the can’t intubate, can’t oxygenate situation, device failure occurred 42% of the time, barotrauma 32% of the time, and the total number of procedures with one or more complications was 51%. When a patient is dying in front of me and every second counts, I definitely want something more reliable than a coin flip. Scalpel, finger, bougie cricothyrotomy is the way to go. (Unfortunately none of these papers give us much insight on what to do for young children.)
Bottom line: Jet ventilation is a procedure with a high failure and high complication rate
Read (or listen) more: Scott Weingart had the lead author (Laura Duggan) on EMCrit to discuss this paper.

Good suction – a key to preventing cricothyroidotomies
Kei J, Mebust DP. Comparing the Effectiveness of a Novel Suction Set-up Using an Adult Endotracheal Tube Connected to a Meconium Aspirator vs. a Traditional Yankauer Suction Instrument. The Journal of emergency medicine. 2016. PMID: 27751699
OK, one last airway paper. Blood and vomit don’t mix well with airway management. There is nothing that can ruin a shift faster than a routine intubation disappearing behind a curtain of blood and vomit. And of course, the standard Yankauer suction immediately clogs on the chunks. Scott Weingart has suggested attaching a meconium aspirator to the back of your endotracheal tube to turn it into a large bore suction device that can also be used to secure the airway. These authors decided to test that set-up. This isn’t a clinical trial. They were just testing how well a Yankauer suction worked as compared to an 8.0 endotracheal tube with a meconium aspirator when sucking fluids out of a pitcher. However, they did use real blood (pig’s), as well as blended hamburger, french fries, and soda for realism. The meconium setup was faster when suctioning water and blood (although the differences weren’t huge). Both devices clogged when trying to suction hamburger, but the meconium device managed to remove 90 mL whereas the Yankauer removed 0 mL.
Bottom line: Clearly this isn’t the kind of research that should lead to wholesale clinical practice changes, but it is a good technique that I would like to have in my arsenal when managing a difficult airway.

The pediatric assessment triangle
Horeczko T, Enriquez B, McGrath NE, Gausche-Hill M, Lewis RJ. The Pediatric Assessment Triangle: accuracy of its application by nurses in the triage of children. Journal of emergency nursing: JEN : official publication of the Emergency Department Nurses Association. 39(2):182-9. 2013. PMID: 22831826
This prospective observational trial looked at the outcomes of 528 children for whom the triage nurse had performed an assessment using the pediatric assessment triangle (PAT) at a large academic pediatric emergency department. Two pediatricians, blinded to that triage assessment, retrospectively reviewed the chart to determine the final diagnosis (of stable versus unstable). The biggest weakness of this data is that although 1002 charts were selected for review, only 528 contained adequate data for inclusion. The PAT did a good job screening for instability (97.3% sensitive 95%CI 64.6-98.8%), although like most screening tools it does overcall (specificity of 22.9% with 95%CI 17.0-30.0%). The triangle was reasonable for identifying respiratory distress (LR+ 4, 95% CI 3.1-4.8), respiratory failure (LR+ 12, 95% CI 4.0-37), shock (LR+ 4.2, 95% CI 3.1-5.6), central nervous system/metabolic disorder (LR+ 7, 95% CI 4.3-11), and cardiopulmonary failure (LR+ 49, 95% CI 20-120). Perfect identification of the final assessment is not the role of a triage tool, like the PAT. The PAT tool performed well here, but perhaps a more appropriate measure would have been something like the number of children who become unstable within the first hour who were missed by the PAT?
Bottom line: The pediatric assessment triangle is an excellent triage tool, but you still have to follow it with a complete medical assessment.
The pediatric assessment tool was also featured in the most recent First10EM post: the crashing infant.

Hey doc, this patient has a wide complex tachycardia. OK, give me a minute to find my callipers
Pava LF, Perafán P, Badiel M. R-wave peak time at DII: a new criterion for differentiating between wide complex QRS tachycardias. Heart rhythm. 7(7):922-6. 2010. PMID: 20215043
This is an interesting study looking at a way to distinguish between SVT and ventricular tachycardia in patients with wide complex tachycardias. Looking at 218 ECGs of VTach (obtained during electrophysiologic studies done for a variety of reasons) 2 cardiologists measured something called the “R-wave peak time” in lead II. Using a cutoff of 50 msec, it was 93% sensitive and 99% specific, with a positive likelihood ratio of 51 and a negative likelihood ratio of 0.06. Those are excellent numbers (although we might want more than 93% sensitivity for VTach. I am not sure how accurate most of us are when measuring 50 msec on an ECG. The biggest problem is that this is a derivation study, and I am not aware of any validation studies. An R-wave peak time of 50 msec in lead II is incredibly specific, and you could imagine that the authors might have measured other variables as well, resulting in p-hacking that would undermine the validity of this study. If validated, this looks far more promising, both in terms of accuracy and ease of use, than any other V tach tool. However, I am still not sure where the value of these tools is for emergency physicians. If the patient has a wide complex tachycardia, I still think the safest and best approach is propofol followed by electricity. These algorithms are more important for cardiologists deciding on long term management.
Bottom line: R-wave peak time is interesting, but I wouldn’t use it in the emergency department based only on this study.

You just can’t beat good old ASA
Johnston SC, Amarenco P, Albers GW. Ticagrelor versus Aspirin in Acute Stroke or Transient Ischemic Attack. The New England journal of medicine. 375(1):35-43. 2016. PMID: 27160892
Although not strictly emergency medicine, we are often asked to start long term treatment on patients. Also, we have already seen a huge rise in ticagrelor use for MI despite a lack of convincing evidence of superiority, so staying on top of the literature seems like a good idea. This is a large, international, double-blind, randomized, controlled trial comparing ticagrelor (180mg loading dose then 90mg BID) to aspirin (300mg loading dose then 100mg daily) in 13,199 patients with low risk stroke (NIHSS score <6) or high risk TIA (ABCD2 score >3) for 90 days. The primary outcome was a composite of stroke (ischemic or hemorrhagic), myocardial infarction, or death. It was the same in both the groups (6.7% vs 7.5%, p=0.07).
Bottom line: Stick with aspirin in your CVA and TIA patients.

Another old, but excellent medication: nitroglycerin
Wilson SS, Kwiatkowski GM, Millis SR, Purakal JD, Mahajan AP, Levy PD. Use of Nitroglycerin by Bolus Prevents ICU Admission in Patients with Acute Hypertensive Heart Failure. The American Journal of Emergency Medicine. 2016.
One of the most satisfying emergencies to manage is flash pulmonary edema, because the patients dramatically improve when put on CPAP and given nitroglycerin. This is a chart review of all adult patients who were given IV nitroglycerin for acute heart failure (according to the diagnostic coding) at a single large academic emergency department. They compared the outcomes of patients given a bolus of nitroglycerin to those who received an infusion and those who received both. The boluses they used here are much larger than most of us are using. They push 2 mg of nitroglycerin at at time. On the other hand, the infusion rate is lower than I would use, with a starting dose of 20 mcg/min and a maximum rate of 35 mcg/min. They report that patients receiving bolus therapy alone were less likely to need ICU admission than either the infusion alone or a bolus plus infusion (48% versus 69% vs 83%.) I wouldn’t get too hung up on the differences, though, as the groups were not randomized, and there is evidence that the infusion groups were sicker than the bolus alone group (higher resp rate and more total nitro given). Really, I include this to point out the value and safety of nitro boluses. One patient received 10 boluses (20mg of nitro total) without harm. Even with 2 mg IV boluses, the incidence of hypotension (whether clinically significant or not) was only 2%.
Bottom line: Acute hypertensive pulmonary edema needs nitro. Early boluses are a good idea.

McDonald RJ, McDonald JS, Carter RE. Intravenous contrast material exposure is not an independent risk factor for dialysis or mortality. Radiology. 273(3):714-25. 2014. PMID: 25203000
I can’t resist a good myth. I have been holding off of including papers on this topic for a while, however, because this is a decision we can’t make on our own, and I don’t like provoking fights with our colleagues. This is a large chart review looking at patients undergoing CT, and comparing those who received contrast material to those who didn’t. This is a relatively good topic for a chart review, as creatinine, dialysis, death, and CT scans are all objective events that are likely to be clearly recorded in the chart. They only included patients who had a Cr measured in the 25 hours before a CT and also in the period of 24-72 hours after the scan. They also excluded patients already on dialysis and those who were given multiple contrast doses. Ultimately they ended up with 21,346 patients who they matched 1:1 based on a propensity score so they had 2 groups: contrast and no contrast. Overall, the rate of acute kidney injury was 5%. The rate was the same whether you received contrast or not (4.8% versus 5.1%, p=0.38). The incidence of emergent dialysis was the same in both groups, and extremely low (0.2% vs 0.3%). The 30 day mortality rates were also similar, at 8.0% and 8.2%. Although the propensity matching done here means the results could be flawed, it highlights the important issue that led us to think contrast is dangerous: older and sicker patients tend to need contrast CTs, and they are at a high risk of developing acute renal failure in the first few days of their illness, whether or not they get the contrast. The contrast is just an easy scapegoat. This trial is not enough to demand changes in policy from radiology, but I think it fits with the bulk of the literature. I will attempt to do a deeper dive on the topic in the future.
Bottom line: Contrast may not be the kidney killer we have all been taught.

Wichmann JL, Katzberg RW, Litwin SE. Contrast-Induced Nephropathy. Circulation. 132(20):1931-6. 2015. PMID: 26572669
A review on the same topic that concludes: “The risk of AKI from CM, especially when administered intravenously for the purpose of noninvasive imaging, has been exaggerated by previous, noncontrolled studies. More recent evidence from controlled studies suggests that the risk is likely nonexistent in patients with normal renal function. There may be a risk in patients with renal insufficiency; however, even in this patient population, the risk of contrast-induced AKI is probably much lower than is widely accepted.”

I seem to have a thing for Roller Coaster Studies
Mitchell MA, Wartinger DD. Validation of a Functional Pyelocalyceal Renal Model for the Evaluation of Renal Calculi Passage While Riding a Roller Coaster. The Journal of the American Osteopathic Association. 116(10):647-52. 2016.
I had to throw this one in, because it contained some excellent quotes, such as “we thank Walt Disney World Resort’s Magic Kingdom theme park for allowing us to conduct this research on the park’s premises” and “seat assignment on the roller coaster was random and determined as a function of place in the waiting line.” Aside from the great quotes, I’m not sure the paper means much. They made a silicone model of a urinary collecting system containing 3 real kidney stones, and report that the stones had moved in location after the roller coaster was finished. This is clearly not ready for time prime, and I can’t imagine that people with back pain from renal colic are going to be excited to be getting on rickety old roller coasters. I will stick to suggesting sex for now.
Bottom line: Sometimes I just include papers for fun

Commins SP, Jerath MR, Cox K, Erickson LD, Platts-Mills T. Delayed anaphylaxis to alpha-gal, an oligosaccharide in mammalian meat. Allergology international. 65(1):16-20. 2016. PMID: 26666477 [free full text]
This story is fascinating, and I actually found it through an excellent Radiolab podcast rather than through the thousands of abstracts sent to me each week. If you asked me if adults could suddenly develop a new anaphylactic reaction to red meat (you know, the same stuff that makes up our muscles), I would have said you were crazy. In fact, until a few years ago, almost all allergists would have too. But there were a slew of patients reporting exactly that. Their doctors though they were wrong. But then a new cancer drug also started causing a lot of allergic reactions, and the allergist looking into it discovered that the cause was galactose-alpha-1,3-galactose – which also happens to occur in red meat. But why were people suddenly developing an allergy to this almost universal antigen later in life? In turns out that these meat allergies were only being reported in certain communities, and by searching through maps, the allergist was ultimately able to find one that overlapped: the distribution of the lone-star tick (the same tick that carries Rocky Mountain Spotted Fever). It turned out that the tick bites were sensitizing patients to this sugar found in all red meat, and that was resulting in seemingly impossible allergies.
Bottom line: First, if you love red meat as much as I do, don’t go hiking anywhere you might find this tick. I mean really, this is scary stuff. And second, it is never a good idea to call patients with unexplained symptoms crazy. Unexplained symptoms will sometimes be explained in the future.
The Radiolab podcast is excellent and worth a listen. You can also read about this in the New Yorker.

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