Articles of the month (May 2017)

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I took another month off, but the blog and accompanying podcast are back with what I think is an interesting collection of emergency medicine articles…

It’s confirmed: I don’t understand WOMAN

WOMAN trial collaborators . Effect of early tranexamic acid administration on mortality, hysterectomy, and other morbidities in women with post-partum haemorrhage (WOMAN): an international, randomised, double-blind, placebo-controlled trial. Lancet (London, England). 2017; PMID: 28456509 [free full text]

This is a big and long awaited trial looking at the use of tranexamic acid in postpartum hemorrhage. It is a double-blind RCT that included 20,060 women aged 16 and older with postpartum hemorrhage (diagnosed clinically by the treating physician). They were randomized to 1 gram of TXA IV or placebo. A second gram could be given if bleeding continued after 30 minutes or restarted within 24 hours. To be eligible, the physician had to be uncertain about whether to use TXA, which could result in significant selection bias, with an unclear impact on the results. The primary outcome was mortality or the need for hysterectomy, but they realized that physicians were making the decision about performing a hysterectomy at the same time as the patients were being randomized, so it was impossible to change that outcome. They therefore had to increase the sample size from the originally planned 15,000 to 20,000.

There was no change in the primary outcome (5.3% with TXA vs 5.6%, p=0.65). There was no change in all-cause mortality (2.3% vs 2.6%, p=0.16). The simple answer, therefore, is that this is a negative trial. Despite demonstrating no change in the primary outcome, the authors report the study as positive, and the editors for some reason let them get away with it, based on a secondary outcome: bleeding death. I have lamented disease specific mortality many times before, but once again it rears its ugly head. The cause of death in this study was determined by what the treating physician wrote on the death certificate, so there is a reasonable chance that the reported difference isn’t real at all. Even if it is real, all cause mortality is unchanged, so it just means that for every life saved from bleeding one was lost due to an unnamed harm. TXA, in that scenario, does nothing except change what is written on the death certificate. Similar to CRASH-2, the amount of blood transfused was not different between the groups, which doesn’t really support the biologic hypothesis that this drug limits bleeding. On the other hand, there was no harm reported in the treatment group, so it seems that TXA is safe, although a trial like this could easily miss harms.

So what does this mean? After CRASH-2, we all started using TXA fairly liberally, and with good reason. It was an excellent trial and demonstrated a benefit in all cause mortality, but there were reasons to be skeptical of the outcomes. Although this is a very different patient population, I think this gives us some insight into the benefit of TXA in bleeding patients, and the results don’t look great. There could be a tiny benefit here (0.2% absolute benefit in all cause mortality with a p value of 0.16), but the honest truth is that this is a huge trial with a clearly negative primary outcome. It does seem like TXA is safe, although the more I read about TXA, the more I think we don’t really understand the underlying physiologic mechanisms at play. The women in this trial mostly had moderate bleeds, and medications are more likely to work in patients with severe pathology, but unfortunately that subgroup is not presented in the data here. For me, this trial raises more questions than it answers. Based on this data and CRASH 2, my guess is that TXA is ineffective in postpartum hemorrhage (and probably for most trauma patients as well), but this is pretty close to 50/50 for me. TXA seems safe and cheap, so for now, I will probably keep using it, but it would not take a lot to change my practice at this point.

Bottom line: This is the best trial we have on tranexamic acid for postpartum hemorrhage, and it was clearly negative. What that means for our practice is far less clear.

Read more: Casey has some great thoughts about this trial on and the trial has also been reviewed on REBEL EM and The Bottom Line

I’m not dead. ‘Ere, he says he not dead. Yes he is. I’m not.

Olaussen A, Nehme Z, Shepherd M. Consciousness induced during cardiopulmonary resuscitation: An observational study. Resuscitation. 2017; 113:44-50. PMID: 28161214

I have had this happen to me. Start chest compressions, the patient is awake; stop, and he is dead. I have struggled with this throughout a 2 hour code, and have discussed it with the patient months later. Thankfully he is alive. Unfortunately, he still suffers from nightmares and flashbacks to that resuscitation. This is a retrospective registry-based study from Australia looking at more than 16,000 EMS based resuscitations. There were 112 (0.7%) cases of CPR induced consciousness identified. The outcomes in these patients were excellent (43% survival to hospital discharge), despite the fact that CPR was presumably stopped repeatedly in the face of consciousness. There are a ton of problems with this data, as identifying these cases retrospectively is fraught with error, but the point is that this happens and you need to have a plan. In the future, I would use ketamine as my sedative of choice.

Bottom line: Good quality CPR can result in consciousness. The outcomes are good, but have a plan to manage this awareness.

Wellen’s syndrome

Morris N, Howard L. BET 1: In patients with suspected acute coronary syndrome, does Wellens’ sign on the electrocardiograph identify critical left anterior descending artery stenosis? Emergency medicine journal 34(4):264-266. 2017. PMID: 28341793

This review looks at 6 papers trying to answer the question: in adult patients with suspected acute coronary syndrome, does Wellen’s sign on the ECG identify critical stenosis of the left anterior descending artery. Their bottom line is yes (biphasic t wave inversion in V2-V3 should alert the clinician to a possible LAD stenosis). The studies are a mix of retrospective and prospective observational studies. The big problem is the variety of outcomes. We care mostly about clinically important outcomes, such as MI or death, whereas these studies are mostly looking at the surrogate outcome of stenosis. However, finding a 70% LAD stenosis in a patient with anginal symptoms is probably a reasonable surrogate. The heterogeneity here doesn’t allow for a single estimate, but if you identify Wellen’s syndrome, there is a high likelihood (somewhere between 50-90% in these studies) that the patient has a >70% LAD lesion. The thing to remember is that Wellen’s is not an ECG finding alone, but rather an ECG finding in combination with history. Part of the definitions of Wellen’s syndrome is a recent history of angina.

Bottom line: We should know what Wellen’s syndrome is and watch for it

ACEP policy on carbon monoxide

ACEP, Wolf SJ, Maloney GE, Shih RD, Shy BD, Brown MD. Clinical Policy: Critical Issues in the Evaluation and Management of Adult Patients Presenting to the Emergency Department With Acute Carbon Monoxide Poisoning. Annals of emergency medicine. 2017; 69(1):98-107.e6. PMID: 27993310 [free full text]

This is an ACEP clinical policy that covers carbon monoxide poisoning. They cover 3 questions:

  1. In ED patients with suspected acute CO poisoning, can noninvasive COHb measurement be used to accurately diagnose CO toxicity? Level B recommendation: “Do not use noninvasive COHb measurement (pulse CO oximetry) to diagnose CO toxicity in patients with suspected acute CO poisoning.” The reason that they make this recommendation is that, based on the available literature, non-invasive testing is not sensitive enough to diagnose this severe but treatable condition. The specificity looks great, however, so don’t discount a positive reading if your EMS crews have these devices.
  2. In ED patients diagnosed with acute CO poisoning, does hyperbaric (HBO2) therapy as compared with normobaric oxygen therapy improve long-term neurocognitive outcomes? Level B recommendation: “Emergency physicians should use HBO2 therapy or high-flow normobaric therapy for acute CO-poisoned patients. It remains unclear whether HBO2 therapy is superior to normobaric oxygen therapy for improving long-term neurocognitive outcomes.” In other words, do whatever you want. The evidence is mixed, and controversial, but probably trends towards hyperbaric treatment not showing benefit.
  3. In ED patients diagnosed with acute CO poisoning, can cardiac testing be used to predict morbidity or mortality? Level B recommendation: “In ED patients with moderate to severe CO poisoning, obtain an ECG and cardiac biomarker levels to identify acute myocardial injury, which can predict poor outcome.” Like always, an elevated troponin is associated with worse outcomes. However, it’s not clear that we can actually do anything about this, and most of the bad outcomes reported were in outpatients in the months to years after the exposure, so I imagine this is just a marker of underlying coronary disease, rather than anything specific to CO.

Bottom line: Nothing much changes here. Keep managing CO as you are used to. The guideline hedges enough that you can do whatever you want about hyperbaric therapy.

A PESIT update that I wish we didn’t need

Verma AA et al. Pulmonary Embolism and Deep Venous Thrombosis in Patients Hospitalized With Syncope: A Multicenter Cross-sectional Study in Toronto, Ontario, Canada. JAMA Intern Med. Published online May 08, 2017. Doi: 10.1001/jamainternmed.2017.1246

This paper already had its own blog post. (I might start posting more frequently about individual papers, rather than waiting for the end of the month. Let me know what you think). The quick summary is that in this somewhat flawed database, the prevalence of PE among admitted syncope patients was only 1.4%. In all comers to the emergency department, the number will be less than that.

Bottom line: Syncope should prompt a PE workup only if there are signs, symptoms, or risk factors for PE.

Cus knowing is half the battle

Cram N, McLeod S, Lewell M, Davis M. A prospective evaluation of the availability and utility of the Ambulance Call Record in the emergency department. CJEM. 2017; 19(2):81-87. PMID: 27620168

This is an interesting study that gets at one of my major pet peeves. Emergency medicine is a team sport, but all too often, the prehospital and in-hospital personnel seem to be divided into separate teams. We already know about the many difficulties that occur when paramedics hand over critically ill patients. It is an area that we should all work on improving, but at least in the resuscitation room, we see the paramedics face to face. We hear their story. What about lower acuity patients who are dropped off and have to wait to be seen? This is a neat study that looked at how often the EMS record was available to the treating emergency physician. It is a prospective cohort looking at the adult patients transported by ambulance to either of the 2 academic emergency departments in London, Ontario (Canada). They did an education campaign about the study before it started in order to ensure maximal recruitment to the study, but this might have also resulted in the Hawthorne effect, in that if paramedics know they are being watched, they might try to get their charting done quicker. Even with the education campaign, enrollment wasn’t great: 869 study forms were completed out of 4466 total EMS patients. The numbers aren’t surprising. The EMS record was available at the time of the first physician assessment 19% of the time. (However, another 20% of the records had been completed and faxed at this time, but just hadn’t made it out of the mysterious fax universe and onto the patients’ charts.) Records were available at some point during the patient’s ED stay for 31% of patients. (There were some verbal handovers, but still almost half of patients had no information available from EMS.) When the report was available, the physicians said it changed their management about 30% of the time. When a report wasn’t available, physicians though it would be help about 60% of the time. Where I currently work, I see an EMS report on less than 5% of my patients, so this certainly rings true to me. It’s not clear how to fix this problem. The reports that were just sitting on a fax machine somewhere represent a simple but important systems fix, but that isn’t the case for most of these patients. I would prefer verbal handover, but when the department is busy, it is never clear which doctor will be responsible for the patient. Would love to hear some solutions from readers.

Bottom line: Paramedics are an extremely important part of our team, and it is important that we hear their stories. Unfortunately, it would seem that much of the time we are not.

In a surprise twist, plastic in the trachea doesn’t restart hearts

Andersen LW, Granfeldt A, Callaway CW. Association Between Tracheal Intubation During Adult In-Hospital Cardiac Arrest and Survival. JAMA. 2017; 317(5):494-506. PMID: 28118660

This is a retrospective cohort study based on data collected prospectively for the get with the guidelines resuscitation registry. There were 143,810 adult patients from 668 US hospitals, but 35,731 had missing data, so 108,079 were included in the final analysis. Among patients with in-hospital cardiac arrest, they compared patients successfully intubated in the first 15 minutes to those who were not. They matched patients 1 to 1 based on propensity matching. Of course, we can’t know the physicians’ thinking during the arrest, and the many reasons that patients may or may not be intubated are the confounders that make this data unreliable. For the primary outcome of survival to hospital discharge, the intubation group did worse in both the unadjusted (33.2% vs. 17%, RR 0.58; 95% CI 0.57-0.59) and adjusted analyses (19.4% vs. 16.3%, RR 0.84 95% CI 0.81-0.87). Return of spontaneous circulation and neurologic function were also worse in the intubated group. Although the observational nature of this data means it shouldn’t immediately change practice, I think it fits with what we know about airway management in cardiac arrest. We have over-emphasized the importance of airway management for a long time. Without a beating heart, and endotracheal tube doesn’t do you much good. I am a big fan of LMAs or other supraglottic airways during cardiac arrest. Intubation is a procedure best done in a relaxed, controlled environment after the patient has been resuscitated. That being said, there will still be arrests with a primary airway or hypoxic component that need immediate airway management. Clinician judgement is essential. Ideally, based on this data, we will see a proper RCT comparing airways strategies in this group of patients.

Bottom line: Cardiac arrest shouldn’t reflexively result in an endotracheal tube. Use your clinical judgement.

Are you prepared?

Okumura T, Suzuki K, Fukuda A. The Tokyo subway sarin attack: disaster management, Part 1: Community emergency response. Academic emergency medicine. 1998; 5(6):613-7. PMID: 9660289 [free full text]

Okumura T, Suzuki K, Fukuda A. The Tokyo subway sarin attack: disaster management, Part 2: Hospital response. Academic emergency medicine. 1998; 5(6):618-24. PMID: 9660290 [free full text]

I think this pair of articles should be essential reading for anyone working in emergency medicine. I was initially prompted to pick up these papers after reading about the assassination of Kim Jong-nam. Then, as I was reading these papers, there was another major event that occurred at my alma mater. The 30 vehicle collision on a major highway would have already made for a busy day in the ED, but one of the trucks was carrying chemicals, and a massive amount of what was later identified as fluorosilicic acid was dumped on the road, exposing many of the people on scene. From all reports, the staff at Kingston General Hospital did an outstanding job setting up an external decontamination area and managing the influx of patients, but I was left wondering how my department would respond. Unlike terrorist attacks, which seem rare enough (especially in Canada) that we can ignore the possibility, accidents and natural disasters will happen and emergency departments need to be prepared. So on to the articles. This is a pair of articles that looks at the trials and tribulations faced by emergency services in response to the sarin attacks on the Tokyo subway system in 1995.

The first article focuses on the pre-hospital environment. Some take-aways for me:

  • Because of the massive number of calls, communication and radio systems went down. EMTs in Japan at the time required verbal orders from an MD for almost all medical interventions, and because the medics could not reach the base physician, not a single patient was intubated or had an LMA or combitube placed, and only 1 had an IV placed. Clearly, there needs to be room for flexibility in these kinds of emergencies.
  • 10% of EMTs developed acute symptoms of sarin exposure!
  • EMTs transferred 452 patients, but more than 4,000 were transported by private vehicles. 2 of the 3 cardiac arrest patients were transported by private vehicle. This means any plans to distribute patients evenly among hospitals will be impossible. It also means that if you expect not to see these patients because you are not a major trauma center and so would normally be bypassed – you are wrong.
  • 25% of the patents were transferred by taxi. They make the interesting point that taxis have a great communication network and often have eyes and ears all over the city. This is a great resource, and after this disaster, they now have a taxi emergency system, which I think is interesting. (Although, with Uber, it won’t be around for long. These days, Twitter will probably serve as the first source of information in an emergency.)
  • The police identified the unknown substance as sarin. However, the emergency department only learned of that development via the news. Would we have better communication?
  • None of the patients were decontaminated in the field.
  • They note that disaster drills were common in Tokyo, because of earthquake risk, but the drills only take place within single organizations. Things fell apart here because fire, police, EMS, and the many hospitals train separately, but have to act together.
  • We rely heavily on the poison center, which I think is great for day to day practice. However, we have to be cognizant of the fact that they likely will not be available in a timely manner in any mass casualty situation. I don’t know: does the poison center have a disaster plan?

The second paper focuses on the hospital response:

  • Almost 25% of hospital staff reported symptoms of acute poisoning. They blame this high rate on poor ventilation and the lack of a decontamination area.
  • They went through 2800 ampoules of atropine – the hospital only stocks 1020, requiring emergency deliveries. Same is true of 2-PAM.
  • Charting is nightmare in an emergency. Usual registration procedures will fail. You need to have an emergency charting system.

Bottom line: Disasters happen. Emergency departments need to be prepared for them, but I wonder how many of us are?

Cheesy Joke of the Month

I recently had a patient who swallowed all the scrabble tiles… his next crap could spell disaster.

Cite this article as:
Morgenstern, J. Articles of the month (May 2017), First10EM, May 29, 2017. Available at:

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