I took another month off, but the blog and accompanying podcast are back with what I think is an interesting collection of articles… Continue reading “Articles of the month (May 2017)”
Welcome to another edition of the First1oEM articles of the month – a collection of my favorite reads from the emergency medicine literature.
Location, location, location
Drennan IR, Strum RP, Byers A et al. Out-of-hospital cardiac arrest in high-rise buildings: delays to patient care and effect on survival. Canadian Medical Association Journal. 2016. [article]
This was a retrospective study looking at a cardiac arrest registry. They decided to look at the floor that you lived on to see if it impacted your survival from cardiac arrest (with the primary analysis looking above or below the 3rd floor). They found that living on higher floors was associated with an increased likelihood of death. In the raw numbers, 4.2% of patients living below the 3rd floor survived, compared to only 2.6% of those living on or above the 3rd floor (p=0.002). Survival above floor 16 was only 0.9%, and no one living above the 25th floor survived. The theory is that higher floors mean longer delays to EMS arrival, and therefore the ever important chest compression and defibrillation.
Bottom line: Choose your home wisely
What’s the best antibiotic to bring on your trip to Las Vegas?
Geisler WM, Uniyal A, Lee JY. Azithromycin versus Doxycycline for Urogenital Chlamydia trachomatis Infection. The New England journal of medicine. 373(26):2512-21. 2015. PMID: 26699167
This is a randomized, controlled non-inferiority trial comparing azithromycin (1 gram PO once) to doxycycline (100mg PO BID for 7 days) in 587 adolescents with chlamydia infections. For the primary outcome of treatment failure at 28 days, there were no treatment failures in the doxycycline group as compared to 5 (3.2% 95%CI 0.4-7.4%) in the azithromycin group. Based on their assumptions, they could not establish the noninferiority of azithromycin in this group, although I imagine the result will vary greatly depending on local resistance patterns.
Bottom line: I will continue using doxycycline as my first line agent
The Quixotic quest for the chest pain decision rule
Greenslade JH, Parsonage W, Than M. A Clinical Decision Rule to Identify Emergency Department Patients at Low Risk for Acute Coronary Syndrome Who Do Not Need Objective Coronary Artery Disease Testing: The No Objective Testing Rule. Annals of emergency medicine. 2015. PMID: 26363570
We would all love a good rule to use to send chest pain patients home. This is a secondary analysis of 2 prior prospective ED trials including a total of 2396 chest pain patients. They derive 3 different rules that are supposed to tell you which patients don’t need further testing after biomarkers and ECGs. (Of course, if you have listened to me in the past, you will know that stress testing is not helpful in our low risk chest pain patients.) I am not going to go into the rules themselves, because I think the study is too flawed to be helpful. Incorporation bias is the major downfall of this study. Classic cardiac risk factors are a large component of these rules, but previous research has consistently shown that having classic cardiac risk factors does not help predict whether a patient’s chest pain is ACS in the emergency department. So how could those risk factors possibly help in a decision rule? It’s because the definition of ACS included unstable angina and revascularization, both of which are subjective outcomes determined by the cardiologist, and the cardiologists had access to the risk factor information. A patient with 5 risk factors is more likely to be cathed, but that doesn’t mean the cath was necessary. Similarly, a patient with more risk factors is more likely to be given the diagnosis of unstable angina. The risk factors didn’t predict the diagnosis of ACS, they were the cause of it.
Bottom line: It is unlikely that we will find easy decision tools for chest pain patients, but for the time being we should be happy that most patients are so low risk that they should be sent home without stress testing.
How prepared are you to run a neonatal resuscitation?
Yamada NK, Yaeger KA, Halamek LP. Analysis and classification of errors made by teams during neonatal resuscitation. Resuscitation. 96:109-13. 2015. [pubmed]
I like the idea here: these authors videotaped a total of 250 real neonatal resuscitations and reviewed the tape to determine how well the neonatal resuscitation algorithm was followed. Continuous quality improvement in our most stressful resuscitations makes sense. These authors report that 23% of the actions observed were errors as compared to the published algorithm. However, I don’t think the errors were truly important errors. The most common error was failure to have a cap to place on the child’s head – is that really essential in the first minutes of resuscitation of an apneic neonate? There were some important errors reported, though, with half of the 12 intubation attempts lasting longer than 30 seconds. Although I don’t think this study really demonstrates it, neonatal resuscitations are stressful and rapid paced, making errors probable. Mental practice and simulation are great tools to help prevent these errors, in my very biased opinion.
Bottom line: Quality improvement in your most stressful resuscitations is a good idea.
Best treatment for pediatric gastro? Prevention
Soares-Weiser K, Maclehose H, Bergman H. Vaccines for preventing rotavirus diarrhoea: vaccines in use. The Cochrane database of systematic reviews. 11:CD008521. 2012. PMID: 23152260
This is a Cochrane systematic review of two different vaccines (monovalent versus pentavalent) for rotavirus. They identified 29 RCTs covering 101,671 infants for the monovalent vaccine and 12 RCTs covering 84,592 infants for the pentavalent vaccine. Unfortunately, most studies use the relatively non-sensical “rotavirus specific diarrhea” as an endpoint, but it definitely seems to be decreased (RR 0.33 95% CI 0.21-0.50 for the monovalent). All cause diarrhea was also decreased in the trials that looked at it, with an NNT of about 40 for any diarrhea and 100 to prevent a hospitalization. There was no change in mortality. They did not document an increase in adverse reactions, but efficacy studies often under report harms.
Bottom line: The rotavirus vaccine prevents serious diarrhea – maybe that’s an easier sell than the measles?
Overtreatment and anticoagulation for atrial fibrillation
Hsu JC, Chan PS, Tang F, Maddox TM, Marcus GM. Oral Anticoagulant Prescription in Patients With Atrial Fibrillation and a Low Risk of Thromboembolism: Insights From the NCDR PINNACLE Registry. JAMA internal medicine. 175(6):1062-5. 2015. PMID: 25867280
With the rise of the new, expensive anticoagulants, we are beginning to see a push to get these agents started for atrial fibrillation patients in the emergency department, ignoring the tiny daily risk of stroke and the importance for long term monitoring that we cannot provide. This is a registry based study. Out of a total of about 360,000 atrial fibrillation patients in the study, 11,000 had a score of 0 on two major stroke scales. However, 25% of this extremely low risk population was on blood thinner contrary to current guidelines.
Bottom line: We over treat patients. For everything. Remember that studies are generally the best possible scenario for medications, and that results in the real world will be worse as we expand treatment to patients who would not have been included in the studies. (If you want to watch this happen in real time, just watch interventional treatment for stroke over the next few years.)
This is a basic review of the Zika virus that is currently causing a significant pandemic through Central and South America, and has potentially been linked to a significant number of birth defects (microcephaly) in Brazil. Zika is another mosquito borne virus without a specific treatment (like Dengue or Chikungunya). The symptoms are described as a milder version of Dengue fever, with fever, myalgias, eye pain, and maculopapular rash. Treatment is supportive.
Bottom line: Another emerging illness to be aware of in the returned traveller.
Can you really multitask?
Skaugset LM, Farrell S, Carney M. Can You Multitask? Evidence and Limitations of Task Switching and Multitasking in Emergency Medicine. Annals of emergency medicine. 2015. PMID: 26585046
Emergency physicians are masters of multitasking – or so we think. This review explains that most of what we think of as multitasking is really rapidly switching between tasks, and even if you are good at it, this task switching slows you down and results in error. Unfortunately, the solution promoted in most other fields – limiting interruptions – just isn’t feasible in emergency medicine. Some suggestions this review makes to help: prioritize tasks according to acuity, recognize when interruptions can be delayed or redirected, practice skills so they become automatic (and don’t add to cognitive load), and use mental frameworks or external brains to limit cognitive work. Of course, optimizing your departmental workflow to limit interruptions, especially at critical times, is also important.
Bottom line: There is no such thing as multitasking, just rapid task-switching.
Should we add TXA to the water supply?
Fox H, Hunter F. BET 1: Intravenous tranexamic acid in the treatment of acute epistaxis. Emergency medicine journal : EMJ. 32(12):969-70. 2015. PMID: 26598634
This is another one of those situations that we have to make decisions in the absence of any real evidence. The authors of this review were unable to find any studies to answer their specific question about the use of IV TXA in acute epistaxis. However, they do note that there are a few studies that show benefit of oral TXA in epistaxis as well as the study of topical TXA that I have previously discussed in this newsletter. Furthermore, the use of intravenous TXA in elective sinus surgery seems to limit blood loss, and we all know about the evidence for IV TXA in trauma. So there is no direct evidence, but plenty of reasons we might guess it could help.
Bottom line: I have never used IV TXA for epistaxis, but use it topically all the time. You can bet if I have a patient with severe epistaxis, I will give it a shot.
Much like TXA, I love skin glue
Bugden S, Shean K, Scott M. Skin Glue Reduces the Failure Rate of Emergency Department-Inserted Peripheral Intravenous Catheters: A Randomized Controlled Trial. Annals of emergency medicine. 2015. PMID: 26747220
Tape and tegaderm has always seemed like a rather ineloquent method of securing IVs to me. In this non-blinded RCT of 380 peripheral IVs, they compared standard tegaderm and tape to skin glue (1 drop at the skin insertion site and one under the hub – this can be seen in this video.) For the primary outcome of IV failure (infection, phlebitis, occlusion, or dislodgement) at 48 hours, the skin glue was better (17% failure vs 27%, absolute difference 10% 95%CI 2-18%). The study was underpowered to assess the components of the composite outcome, but most of the failures were dislodgement. I don’t follow people for 48 hours – but a 27% failure rate with usual care seems high to me. Also, skin glue is likely more expensive. However, an NNT of 10 to avoid another IV stick would probably be attractive to many patients.
Bottom line: Skin glue is an option for securing PIVs – maybe difficult ones you really care about?
I love ultrasound for looking at things, but for breaking up clots?
Piazza G, Hohlfelder B, Jaff MR. A Prospective, Single-Arm, Multicenter Trial of Ultrasound-Facilitated, Catheter-Directed, Low-Dose Fibrinolysis for Acute Massive and Submassive Pulmonary Embolism: The SEATTLE II Study. JACC. Cardiovascular interventions. 8(10):1382-92. 2015. PMID: 26315743
This is a large prospective study, but I won’t get too much into the details because their primary outcomes were a bunch of surrogate markers rather than patient important outcomes. Why included it then? They used a novel device that uses ultrasound to try to break up the PE, and then gave tPA at the very slow rate of 1mg/hr. So far the lytics for submassive PE trials have shown some promise, but aren’t convincing. Alternate methods (non-bolus) of giving the medication might be the thing that tip the balance in favour of lytics. But mostly I wanted to include this article to bring up two excellent blog posts written by Josh Farkas about ultrasound guided thrombolysis and controlled thrombolysis of submassive PE.
Bottom line: My guess is that we will find that lytics are beneficial in submassive PE over the coming years, once we find the correct subset of patients and the best dose. (This is a big departure for me, because I am much more used to saying that things won’t work. That is almost always the safer bet.)
Ondansetron and the dreaded QT
Moffett PM, Cartwright L, Grossart EA, O’Keefe D, Kang CS. Intravenous Ondansetron and the QT Interval in Adult Emergency Department Patients: An Observational Study. Academic emergency medicine : official journal of the Society for Academic Emergency Medicine. 23(1):102-5. 2016. [pubmed]
Droperidol, possibly the most useful medication I have never had the opportunity to use, was taken away because of what it could do to the QT interval, right around the time when ondansetron was coming to market. Then, as ondansetron was coming off patent, we found out that it prolonged the QT just like droperidol did. OK, I will take off my tin foil hat to write the rest of this. This is a prospective observational trial of 22 adult patients receiving ondansetron at a single hospital. They did ECGs at baseline and every 2 minutes for 20 minutes. The QT did lengthen by 20 msec (95% CI 12-26 msec), but this is almost certainly clinically insignificant. There were no adverse events.
Bottom line: Yes, ondansetron will prolong the QT. No, it won’t be a problem. (Maybe avoid it if the patient overdosed on methadone, lithium, and haldol and tells you he has a family history of congenital long QT syndrome.)
But little Johnny just aint right
Nishijima DK, Holmes JF, Dayan PS, Kuppermann N. Association of a Guardian’s Report of a Child Acting Abnormally With Traumatic Brain Injury After Minor Blunt Head Trauma. JAMA pediatrics. 169(12):1141-7. 2015. PMID: 26502172
I’ve included papers on the low risk of significant head injuries in children with isolated vomiting and isolated loss of consciousness before. This time we will look at whether parental concern that their child is acting abnormally, in isolation, is indicative of blood in the brain. This is another secondary analysis of the PECARN database. Out of 43,399 children in the original study, only 1297 were reported as acting abnormally. Of those, 411 (32%) had abnormal behaviour as their only finding. Only 1 child of these 411 had a clinically significant injury (0.2% 95% CI 0-1.3%). Of the smaller subset who had CTs performed, 4 out of 185 (2.2%) had any sign of traumatic brain injury. So injuries were rare, even when the parents report the child is not behaving normally.
Bottom line: Once again, you have to evaluate the entire patient, not just single variables. Observation is probably a better test than CT.
How good is the ECG for hyperkalemia?
Montague BT, Ouellette JR, Buller GK. Retrospective review of the frequency of ECG changes in hyperkalemia. Clinical journal of the American Society of Nephrology : CJASN. 3(2):324-30. 2008. PMID: 18235147 [free full text]
Remember memorizing the classic progression of ECG changes in hyperkalemia: peaked Ts, prolonged PR, flatted Ps, wide QRS, then the deadly sine wave? Well, forget it. This is a chart review that looks at the ECGs of 90 hyperkalemic patients. (This is actually a reasonable topic for chart review, given that both the potassium level and the ECG are likely to be objective and easily identified on the chart.) Only half of the patients had any ECG signs of hyperkalemia, and only 18% met their strict criteria (which meant peaked Ts that were documented to resolve as the potassium decreased.) Although the ECG was insensitive for hyperkalemia, that might not be the important question. I don’t care as much about the number of the potassium, but whether it is affecting the heart – and the ECG might be a better marker of cardiac outcomes, but we don’t know from this study.
Bottom line: The ECG is not sensitive for hyperkalemia.
A guideline that say something sensical? I must be dreaming
Kearon C, Akl EA, Ornelas J et al. Antithrombotic Therapy for VTE Disease: CHEST Guideline. Chest. 2016. [free full text]
This is a new guideline from the American College of Chest Physicians covering antithrombotic therapy for VTE. The recommendation to know about: “For subsegmental PE and no proximal DVT, we suggest clinical surveillance over anticoagulation with a low risk of recurrent VTE (Grade 2C).” That’s right – they are suggesting NOT treating certain PEs! They also recognize the high false positive rate of CTPA, which I have discussed here before. When is a subsegmental PE likely to be a true positive? “We suggest that a diagnosis of subsegmental PE is more likely to be correct (i.e. a true-positive) if: (1) the CT pulmonary angiogram (CTPA) is of high quality with good opacification of the distal pulmonary arteries; (2) there are multiple intraluminal defects; (3) defects involve more proximal sub-segmental arteries (i.e. are larger); (4) defects are seen on more than one image; (5) defects are surrounded by contrast rather than appearing to be adherent to the pulmonary artery; (6) defects are seen on more than one projection; (7) patients are symptomatic, as opposed to PE being an incidental finding; (8) there is a high clinical pre-test probability for PE; and D-Dimer level is elevated, particularly if the increase is marked and otherwise unexplained.” The best way to avoid this dilemma all together is still to avoid ordering CTs in low risk patients.
Bottom line: Not all PEs are really PEs. Not all PEs require treatment.
Speaking of which
Nielsen HK, Husted SE, Krusell LR. Anticoagulant therapy in deep venous thrombosis. A randomized controlled study. Thrombosis research. 73(3-4):215-26. 1994. PMID: pubmed
I may have included this one before. Its really the only RCT of anticoagulation for VTE that exists as far as I know. This is a prospective, randomized trial of 90 patients with proven, symptomatic DVTs comparing anticoagulation (heparin followed by warfarin) with an NSAID (phenylbutazone). All the patients had VQ studies performed, both initially and for follow up. About half of the patients had PEs (asymptomatically). There was no difference between the groups with regards to regression of DVT, recurrent DVT, or PE up to 60 days. In terms of mortality, there was one death in the anticoagulation group and none in the NSAID group. The only difference was that the anticoagulation group had an 8% rate of bleeding complications while they report no adverse events from the NSAID. Now this is a small and imperfect study – but quite amazingly, it’s the only real study of anticoagulation for VTE, and it’s negative!
Bottom line: In the only RCT of anticoagulation in DVTs (half of whom had PEs), there was no difference between using an anticoagulant or an NSAID. I know which I would prefer.
You thought diagnostics was difficult? How about pain caused by analgesics?
Tabner A, Johnson G. Codeine: An Under-Recognized and Easily Treated Cause of Acute Abdominal Pain. The American journal of emergency medicine. 33(12):1847.e1-2. 2015. PMID: 25983269
I have no idea what to do with this one. They present 2 case reports of patients with abdominal pain in whom the ultimate diagnosis was sphincter of Oddi spasm secondary to codeine use. Both patients’ pain resolved rapidly with naloxone (400mcg), which is not one of my usual analgesics. But how should we use this information? I imagine that you could do a lot of harm trying to treat abdominal pain with naloxone. This is definitely an interesting diagnosis – and one that I have never seen, or at least recognized.
Bottom line: Maybe one more reason that codeine should not be used
Back pain? Do we really have to talk about back pain? Ugh
Friedman BW, Dym AA, Davitt M. Naproxen With Cyclobenzaprine, Oxycodone/Acetaminophen, or Placebo for Treating Acute Low Back Pain: A Randomized Clinical Trial. JAMA. 314(15):1572-80. 2015. PMID: 26501533
It’s sort of frustrating that trial after trial comes out telling us nothing really works for low back pain. Obviously we need to do something for our patients. This is a randomized, double-blind, placebo controlled trial comparing naproxen plus placebo to naproxen plus cyclobenzaprine and to naproxen plus oxycodone and acetaminophen in adults with acute non-traumatic lumbar back pain. For the primary outcome of a scale measuring pain and function, there was no difference between the groups. There were more adverse effects in the cyclobenzaprine and oxydodone/acetaminophen groups. The biggest weakness of this study was that there was relatively poor compliance with all treatment regimens, but that makes it more like real life.
Bottom line: Naproxen monotherapy is probably better. Adding cyclobenzaprine or oxycodone/acetaminophen just increases adverse effects.
Sir, you have a severe antibiotipenia – we need to start an infusion, STAT
The BLISS trial: Abdul-Aziz MH, Sulaiman H, Mat-Nor MB. Beta-Lactam Infusion in Severe Sepsis (BLISS): a prospective, two-centre, open-labelled randomised controlled trial of continuous versus intermittent beta-lactam infusion in critically ill patients with severe sepsis. Intensive care medicine. 2016. PMID: 26754759
This wasn’t even on my radar: should we be giving antibiotics (specifically beta-lactams) as a continuous infusion? I know, we all heard about time dependent versus dose dependent antibiotics in medical school, but I honestly thought that was useless pharmacological drivel, because the studies I have seen so far have indicated that dosing regimen doesn’t matter much when we are giving antibiotics. (Maybe because we are giving so many antibiotics to people who really don’t need them?) Anyhow, on to the study: this was a prospective, randomized, open-label study of 140 adult ICU patients with severe sepsis being treated with cefepime, meropenem, or piperacillin/tazobactam. They were randomized to either receive their antibiotics as a continuous infusion, or by the usual intermittent dosing. The primary outcome was clinical cure, and was lower in the continuous group (56% vs 34%; absolute difference 22% 95%CI 10-40%, p=0.011). Unfortunately, I’m not sure that is the most important outcome, and the study wasn’t powered for mortality, so there was no significant mortality difference despite the numbers being better in the continuous group.
Bottom line: Continuous administration of beta-lactam antibiotics is interesting, and definitely warrants further study focusing on mortality differences
Want to see how quickly I can contradict myself?
Dulhunty JM, Roberts JA, Davis JS. A Multicenter Randomized Trial of Continuous versus Intermittent β-Lactam Infusion in Severe Sepsis. American journal of respiratory and critical care medicine. 192(11):1298-305. 2015. PMID: 26200166
Hold your horses. The previous study was open-label, but there is another, larger study that was double-blinded. This is a double-blind, double-dummy multi-center randomized controlled trial of 432 ICU patients with severe sepsis being treated with meropenem, ticarcillin-clavulanate, or piperacillin-tazobactam, again comparing continuous versus intermittent dosing. For the primary outcome, ICU free days alive at day 28, there was no significant difference between the groups (18 vs 20 day, p=0.38). 90 day mortality was also the same, 26% in the continuous group vs 28% with intermittent antibiotics (p=0.67). So was the previous study just an example of the bias that can occur with open-label studies, or might there be a small but real difference that these studies were just under-powered to detect?
Bottom line: This will require a massive trial to answer definitively. For now, intermittent dosing is just so much easier that it should probably remain the preferred method of antibiotic administration.
Cheesy Joke of the Month
Why did the scarecrow get an an award?
He was outstanding in his field
#FOAMed of the month
We vastly overestimate the benefits of many of the medications that we tell our patients are essential. As a result, you can hear many of the elderly coming well before you see them from the rattle of all the pills. A large percentage of emergency department visits are from medication side-effects, but most of these are misdiagnosed. So although this tool was designed more for family physicians, I think it probably has a role in emergency medicine as well
This is a tool developed by some very intelligent Canadian doctors (including the team behind another amazing FOAMed resource: The Best Science Medicine podcast) to help clinicians and patients make decisions about reducing or stopping medications. The thing I miss most about family medicine was the ‘drugectomy’: it was astounding how many patients would feel so much better just because we stopped a few of their less necessary or unnecessary medications.
A monthly collection of the most interesting emergency medical literature I have encountered
Here is this month’s summary of my favorite reads from the medical literature.
Simple and brilliant: A pediatric rainbow
Moreira ME, Hernandez C, Stevens AD, et al. Color-Coded Prefilled Medication Syringes Decrease Time to Delivery and Dosing Error in Simulated Emergency Department Pediatric Resuscitations. Ann Emerg Med. 2015;66:(2)97-106.e3. PMID: 25701295
Pediatric resuscitations are stressful at the best of times and pediatric medication doses can be complicated, increasing the risk of medication errors. This group came up with an ingenious solution: single pre-filled syringes that are color-coded in a rainbow pattern that corresponds to the Broselow tape we all know and love. All you have to do is discard down to the color that corresponds to the size of the child and you are sure to be giving the right dose (best explained by looking at a picture).This study assessed the speed and accuracy of medication administration in simulated pediatric resuscitations. 10 teams consisting of physicians and nurses participated in a cross over study, so that they did one simulation with the new syringes and one without. Time to delivery of medications was quicker with the new syringes (47 versus 19 seconds, a difference of 27 seconds; 95%CI 21-33 seconds). Teams were also more accurate using the new color-coded syringes, with dosing errors occurring 17% of the time with the conventional approach and 0% of the time with the new syringes (absolute difference 17%; 95% CI 4-30%). Obviously a simulation based study is not real life – but I would actually expect more stress and therefore more errors during a real resuscitation.
Bottom line: Simple. Brilliant. Worth looking into.
The same group replicated basically the same study with similar results, but this time running the simulations with paramedics:
Stevens AD, Hernandez C, Jones S, et al. Color-coded prefilled medication syringes decrease time to delivery and dosing errors in simulated prehospital pediatric resuscitations: A randomized crossover trial. Resuscitation. 2015. PMID: 26247145
Fingers, toes, nose and hose. The epinephrine myth
Ilicki J. Safety of Epinephrine in Digital Nerve Blocks: A Literature Review. J Emerg Med. 2015. PMID: 26254284
I’ve talked about this before, but possibly not in the articles of the month. This is a systematic review looking at the safety of using epinephrine in digital nerve blocks. They found a total of 39 relevant articles, although only 12 of them were RCTs. They report no cases of necrosis attributable to epinephrine. In total, they found 2797 reported cases of digital nerve blocks using epinephrine without any important complications.
Bottom line: This was a myth. Epinephrine is almost certainly safe in fingers and toes if you think it might help you.
Physicians might not be so great around genitals
Stewart CM, Schoeman SA, Booth RA, Smith SD, Wilcox MH, Wilson JD. Assessment of self taken swabs versus clinician taken swab cultures for diagnosing gonorrhoea in women: single centre, diagnostic accuracy study. BMJ. 2012;345:e8107. PMID: 23236033 [free full text]
This is a prospective cohort of 3859 women aged 16 and over who presented to a single sexual health clinical in the UK. Before undergoing their consultation, they were asked to perform a vulvovaginal swab on themselves which was sent for nucleic acid amplification (NAAT). They then had the normal examination by the physician, with urethral and endocervical swabs sent, both for NAAT and culture. Overall, 2.5% of women tested positive for gonorrhoea (using a gold standard of either positive culture or two different NAAT markers being positive.) The self swabs were the most sensitive (99%), followed by physician swab for NAAT (96%), with the endocervical culture being the least sensitive (81%). In patients with symptoms suggestive of STI, both physician and self swab NAAT were 100% sensitive, but the endocervical culture was only 84% sensitive.
Bottom line: Self taken swabs were the most sensitive at detecting gonorrheal infection in these women
Schoeman SA, Stewart CM, Booth RA, Smith SD, Wilcox MH, Wilson JD. Assessment of best single sample for finding chlamydia in women with and without symptoms: a diagnostic test study. BMJ. 2012;345:e8013. PMID: 23236032 [free full text]
This is another study by the same group, using essentially the same methods, but this time focusing on Chlamydia. They included a total of 3973 women. Again, the self swab outperformed the physician performed swab with a sensitivity of 97% (95%CI 95-98%) as compared to 88% (95%CI 85-91%). The reported specificity of 100% is essentially meaningless because they were using the test itself as the gold standard. Similarly, the sensitivity of both tests might be lower than reported as they were not compared to any other gold standard.
Bottom line: Women do a better job collecting swabs for Chlamydia than physicians do
Overall Bottom line: If there is not another reason for a speculum exam, it does not have to be performed solely to obtain cervical swabs. Unfortunately urine testing was not included in these studies, so we do not know how it compares to self swabs.
Using tamsulosin for kidney stones? You must not be reading these e-mails.
This is a prospective, randomized, double-blind trial of 403 adults with CT confirmed ureteric stones comparing tamsulosin 0.4mg daily to placebo. There was no benefit for the primary outcome of stone expulsion at 28 days, with 87% passed in the tamsulosin group and 81.9% in the placebo group (5.1% difference; 95%CI -3 to 13%). There was a difference in a secondary outcome, distal stones sized 5-10mm, with 83.3% passing as compared to 61%. Of course this is a secondary outcome, so should not affect your practice. More importantly, the vast majority of these people should not being getting imaged, so you will never know the size of the stone, making this information clinically useless. There was no difference in urologic interventions, pain, or analgesia requirements.
Bottom line: Tamsulosin doesn’t help patients with ureteric stones.
Just in case that wasn’t enough to convince you
Berger D, Ross M, et al. Tamsulosin does not increase one-week passage rate of ureteral stones in Emergency Department patients. Am J Emerg Med. 2015. In Print. PMID:
This is yet another paper indicating tamsulosin has no role in ureterolithiasis. (Its too bad we can’t just start with the high quality studies, rather than following the predictable pattern of a handful of garbage studies showing questionable benefit followed by a lot of time and money spent on multiple good trials that prove that there was never any benefit.) This was a prospective, double-blind RCT with 127 adult patients with CT confirmed ureterolithiasis, randomized to either tamsulosin 0.4mg daily or placebo. There was no difference in the number of patients in whom the stone did not pass (tamsulosin 62.1% 95CI 49-75%; placebo 54.4% 95%CI 40-67%.) There was also no difference in pain scores or analgesic use.
Bottom line: There is no reason to be using tamsulosin in renal colic patients.
Sticking with urology: systematic reviews are pointless if there isn’t any original literature
Hulme P and Wylie K. Towards evidence based emergency medicine: best BETs from the Manchester Royal Infirmary. BET 1: tranexamic acid in life-threatening haematuria. Emerg Med J. 2015;32:(2)168-9. PMID: 25605262
They decided to do a review of tranexamic acid use in life-threatening hematuria. They managed to find 3 case reports and 1 prospective observational trial of 8 patients. There were no controls, so its hard to know what to make of the outcomes. It is good to know that none of the patients broke the emergency medicine rule that all bleeding stops… eventually.
Bottom line: For patients peeing blood, you are free to make it up as you go.
It just might be safe to pee in the Amazon
Bauer IL. Candiru–a little fish with bad habits: need travel health professionals worry? A review. J Travel Med. 2013;20:(2)119-24. PMID: 23464720
This is one of those really weird medical myths that I heard when I was younger and just stuck with me as a true. Apparently if you urinate in the Amazon river, there are little fish, called Candiru, that are attracted to the urine and will swim up your urethra. Once there, they have small barbs that lock them into place. These authors did an extensive review of both the scientific and non-scientific literature and report that there has never actually been a confirmed case of this occurring. For some reason, that is an amazing relief to me (and I have never even been to South America). Was I the only one raised on this particular myth?
Bottom line: Feel free to pee in the Amazon, if that’s your thing.
Don’t write off those vital signs just yet
Rodrigo GJ, Neffen H. Assessment of acute asthma severity in the ED: are heart and respiratory rates relevant? The American journal of emergency medicine. 2015. PMID: 26233619
This is a retrospective look at data that was collected prospectively as part of 7 other asthma trials done at a single emergency department. In total, 1192 adult patients were included. They compared heart rate and respiratory rate between two predefined groups: severe asthma (defined as an FEV1 31-50% of expected) and life threatening asthma (defined as an FEV1 <= 30% expected). The HR and RR were not different between the groups (mean of 102 and 22 respectively). They then use logistic regression to show that only FEV1 and O2 saturation were related to the outcome of admission to hospital. Based on this, they conclude that HR and RR are not determinants of acute asthma severity. I think this is probably the wrong interpretation. They use FEV1 as their definition of illness severity rather than hard outcomes. The lack of correlation between FEV1 and vital signs in this study might equally indicate that FEV1 is not a good indicator of disease severity. (It is a disease oriented, not a patient oriented outcome.) Although FEV1 was correlated with admission rates at this hospital, I imagine this just represents the local practices of the hospital: they believe in FEV1 and therefore admit you to hospital if your FEV1 is low, even if you had no other indications for admission.
Bottom line: I would still strongly suggest assessing patients clinically, including vital signs. Don’t let surrogate outcomes like the FEV1 or peak flow rates confuse you in asthma.
Another quick note on measuring asthma severity
Huff JS and Diercks DB. Use of Peak Expiratory Flow Rate Monitoring for the Management of Asthma in Adults in the Emergency Department. Revision of: American College of Emergency Physicians. Use of Peak Expiratory Flow Rate Monitoring for the Management of Asthma in Adults in the Emergency Department. Ann Emerg Med. 2001;38:198.
Without going into all the problems with the base literature on the use of peak flow rates in emergency medicine, I thought I would include the ACEP policy statement for reference. This is an update of their previous policy statement from 2001, with 27 new studies identified and reviewed. Their summary: “The use of PEFR monitoring has not been shown to improve outcomes, reliably predict need for admissions, or limit morbidity or mortality when used during the ED management of adult patients with acute exacerbations of asthma.”
Bottom line: Peak flow is a disease oriented outcome. Focus on patient oriented outcomes.
Sepsis and the rush to early antibiotics
de Groot B, Ansems A, Gerling DH. The association between time to antibiotics and relevant clinical outcomes in emergency department patients with various stages of sepsis: a prospective multi-center study. Critical care. 2015;19:194. PMID: 25925412
This is a prospective, multicentre observational cohort study including a total of 1,168 adult patients with sepsis (although their definition was anyone admitted to hospital with an infection who received IV antibiotics.) The overall mortality of their cohort was 10%, so significantly lower than the trials of severe sepsis we are used to. In this cohort, the length of time it took to give antibiotics was not associated with mortality. Much like the prior studies that showed a higher mortality in patients with delays to antibiotics, we must be aware of the mantra: association is not causation. In the current study, the delay to antibiotics might have been because patients had less severe infections. On the other hand, in prior studies in which antibiotic delays were associated with increased mortality, we might guess that patients were misdiagnosed or inappropriately dispositioned, which could be the true cause of increased mortality. Why did this study come to a different conclusion? One possibility is simply the timing of the studies. It is impossible to practice emergency medicine these days without a keen awareness of sepsis. This heightened awareness may lead to over-treatment in general, such that the few patients that don’t get early antibiotics really don’t require them.
Bottom line: Once you know there is a bacterial infection, obviously give antibiotics. However, there are many factors that will affect the timing of antibiotic administration and it should not be used as a quality of care metric.
We should probably just install CT scanners at triage
Claessens YE, Debray MP, Tubach F, et al. Early Chest CT-Scan to Assist Diagnosis and Guide Treatment Decision for Suspected Community-Acquired Pneumonia. Am J Respir Crit Care Med. 2015. PMID: 26168322
Bottom line: Just say no to CT scans for pneumonia
Glue works for abrasions too
Singer AJ, Chale S, Taylor M. Evaluation of a liquid dressing for minor nonbleeding abrasions and class I and II skin tears in the emergency department. The Journal of emergency medicine. 48(2):178-85. 2015. PMID: 25456777
This is an open label observational trial with no comparison group,using a convenience sample of 40 patients and 50 total wounds. The wounds were either abrasions or skin tears. They used a cheaper skin adhesive that has not been tested for tensile strength (unlike dermabond). If tensile strength was required, a steristrip was applied before the glue. In follow up, there were no infections and only one patient needed anything else: his glue peeled off on day 3 and he had bandage applied. Of course, with no comparison group, all we can say is “Mikey likes it”.
Bottom line: Glue works in skin. Perhaps there is a role for stocking the cheaper liquid bandaid products sold at drug stores?
A simple, life-saving therapy I didn’t know about
Jamtgaard L, Manning SL, Cohn B. Does Albumin Infusion Reduce Renal Impairment and Mortality in Patients With Spontaneous Bacterial Peritonitis? Ann Emerg Med. 2015. PMID: 26234193
I always find it funny that I finished residency with a head full of practices, like PPIs for GI bleeds, that are demonstrably unhelpful, but at the same time there are potentially life saving treatments that I have never heard about. Albumin for spontaneous bacterial peritonitis is one of those treatments. These authors report a systematic review and meta-analysis of RCTs studying albumin for SBP. In total they found 4 studies that include 288 patients with limited heterogeneity and no evidence of publication bias. Only 1 trial was blinded, but with a hard outcome of mortality that might be less important. The administration of albumin (the 2 largest trials made sure to give it within 6 hours, so this might be an ED therapy) was associated with less renal impairment (OR 0.21 95%CI 0.11-0.42) and lower mortality (OR 0.34 95%CI 0.19-0.60). Dosing varied among studies, but the largest trial used 1.5grams/kg IV at the time of diagnosis and 1gram/kg on day 3.
Bottom line: These are small numbers, but I will be giving albumin to SBP patients until we see more.
Diverticulitis is not necessarily a reason to promote antibiotic resistance
Chabok A, Påhlman L, Hjern F, Haapaniemi S, Smedh K; AVOD Study Group. Randomized clinical trial of antibiotics in acute uncomplicated diverticulitis. Br J Surg. 2012 Apr;99(4):532-9. PMID: 22290281
I included the meta-analysis a few months back, but here is a multicentre RCT of 623 adult patients with CT confirmed uncomplicated diverticulitis (defined as lower abdo pain plus fever, an elevated WBC, and CT consistent with diverticulitis but no abscess or free air) randomized to either antibiotics or not. They used pretty big gun antibiotics: either a 2nd/3rd gen cephalosporin plus metronidazole or a carbapenem or piperacillin-tazobactam. There were no statistical differences between the groups. There were 3 perforations in each group. There were 3 abscesses in the no antibiotics group compared to none in the antibiotics group. 10 patients (3.2%) that started with no antibiotics were given antibiotics eventually. There were no differences in length of hospital stays or recurrent diverticulitis.
Bottom line: It may well be that we don’t need antibiotics for diverticulitis, but these patients were all treated as inpatients, so its probably not up to us to make that call.
Read enough and I might sound like an antibiotic nihilist
Matthys J, De Meyere M, van Driel ML, De Sutter A. Differences among international pharyngitis guidelines: not just academic. Annals of family medicine. 5(5):436-43. 2007. PMID: 17893386 [free full text]
I love this article, probably because it hits on two of my favorite soapbox topics: guidelines and antibiotics for sore throats. They searched for any major pharyngitis guidelines and found 10 from different countries and organizations. Two people individually coded each guidelines for all the major recommendations. The key finding of this paper is that despite all of these guidelines being “evidence based”, they arrive at wildly different recommendations. Several guidelines recommend prescribing antibiotics only if the patient is very sick or high-risk, but others suggest treating almost everyone. (If you want to find a guideline that tells you not to give antibiotics, look to Belgium, the Netherlands, England, or Scotland. Interestingly, these were the guidelines that were written by family doctors, as compared to specialists – I knew we had brains.) Not a single publication, including the Cochrane review, was cited by all the guidelines.
Bottom line: Unfortunately, guidelines are rarely an adequate source of evidence based clinical information. (Also, for most parts of the world, pharyngitis probably doesn’t need antibiotics.)
When is a clot a clot?
Morgan C, Choi H. BET 1: Do patients with a clinically suspected subsegmental pulmonary embolism need anticoagulation therapy? Emergency medicine journal : EMJ. 32(9):744-7. 2015. PMID: 26293150
What is the evidence for treating subsegmental pulmonary emboli? This review identified 2 observational trials that included patients with subsegmental PEs who were not anticoagulated. Of the total of 47 patients with untreated subsegmental PEs, none had recurrent venous thromboembolism at 3 months. It would not be surprising if the harms of anticoagulation outweighed the benefits, but 47 patients can’t give enough information to decide either way.
Bottom line: We still really don’t know what to do, but any treatment benefit is likely to be small.
Positive troponins are negative for patients
Hakemi EU, Alyousef T, Dang G, Hakmei J, Doukky R. The prognostic value of undetectable highly sensitive cardiac troponin I in patients with acute pulmonary embolism. Chest. 2015;147:(3)685-94. PMID: 25079900
This is a retrospective chart review of 298 patients with confirmed PEs looking at the prognostic value of a positive high sensitivity troponin. 45% of the group had a negative troponin and therefore 55% had a positive trop. If the troponin was negative, no patients died, needed CPR, or received lytics. Among those with a positive trop, 6% died and 9% had either CPR or lytics given. For a retrospective study, this one is more likely than usual to give us a correct answer as death, lytics, troponin, and to a lesser extent CPR are objective values that are likely to be accurately recorded on a chart.
Bottom line: It’s not surprising, but a positive troponin is likely a bad prognostic factor for PE patients.
Less relevant than the pee fish article?
Morgenstern J, Hegele RA, Nisker J. Simple genetics language as source of miscommunication between genetics researchers and potential research participants in informed consent documents. Public Underst Sci. 2015;24:(6)751-66. PMID: 24751688
This isn’t directly related to emergency medicine, but I was excited that after a few years of being “in press” the article based on my master’s thesis actually got published in print. This was a study that used qualitative methods to analyze the language of informed consent documents in genetics research. The main finding was that apparently simple, easy to understand language can be a source of miscommunication. This can occur because different people or groups of people will understand words differently. An example would be geneticists conceptualizing “disease” as an entity that may or may not cause actual symptoms in the future based on genetic predispositions, while their research participants may think of a “disease” as something they definitely have and will notice the effects of. Might this be applicable to emergency medicine? I think so, but without any good evidence. However, we know that when patients hear the words “congestive heart failure” they envision something that will kill within days – after all, their heart is failing – but this is not necessarily what we are trying to convey with those words. Similarly, we might talk about “low risk chest pain”, but different people might understand those words to indicate a 2% risk, or a 1 in a thousand risk, or a 1 in a million risk.
Bottom line: Communication is essential in emergency medicine. It is an area that probably deserves more attention.
Cheesy Joke of the Month
What is the difference between surgeons and God?
God doesn’t think he is a surgeon
FOAM resource of the month
A new site and podcast that I think will benefit all emergency physicians is:
Rather than being focused on clinical aspects of care, this site is run by Jason Brooks, a performance enhancement coach, with the goal of improving performance (both in the ED and in life in general) and making it sustainable. High level athletes have coaches, why shouldn’t we? I really enjoyed the first few podcasts.
Enjoy the free open access medical education? Think you know someone else who might? It would help me a lot if you spread the word and shared this resource with just one of your friends or colleagues. Even easier, you could also help by just clicking the like button on Facebook. Thank you so much!
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: http://www.karger.com/Article/Pdf/354195
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.”