This month’s articles are a little special. Usually, I pick out the articles that catch my eye, but it’s easy to imagine that my biases filter out a lot of interesting medical literature. As there were a number of experts descending on Berlin this month for SMACC, Casey Parker and I invited a few people to suggest a paper and discuss it with us over a beer for our podcast. The conversation was great, and can be found here. These are the articles that were picked:
Another month and another edition of the articles of the month. However, this time I have some very exciting news. I have teamed up with Casey Parker (the brilliant, smooth-talking Australian physician, not the adult film star) to produce an audio version of these summaries. You will be able to find this podcast on http://broomedocs.com/, a great FOAM website that everyone should probably be following anyway. This is the first edition, and we will likely tweak the format with time, so if you have any feedback (hopefully more constructive than, “Justin, you have the perfect voice for silent films”), we would love for you to get in touch. Continue reading “Articles of the month (July 2016)”
There are new sepsis definitions! Hurrah?
There are new sepsis guidelines. I guess that warrants headline news, and there has been a lot of excitement on the medical internet. However, they are really just the opinions of 19 experts, aren’t backed by any quality prospective data, and probably shouldn’t change your management. If you want to read more, I wrote a full post on the topic: Sepsis 3.0 – No thank you
Bottom line: Talk about qSOFA if you want to sound in the know, but clinically I would ignore this paper
Procedural sedation consent: “Don’t worry, it’s super safe… it’s the Michael Jackson drug.”
Bellolio MF, Gilani WI, Barrionuevo P. Incidence of Adverse Events in Adults Undergoing Procedural Sedation in the Emergency Department: A Systematic Review and Meta-analysis. Academic emergency medicine : official journal of the Society for Academic Emergency Medicine. 23(2):119-34. 2016. PMID: 26801209
What exactly are the risks of procedural sedation? I know them qualitatively, but when having an informed choice conversation, are you able to quote the actual incidence? I know I couldn’t. This is a systematic review and meta-analysis to determine the incidence of adverse events in ED procedural sedation (limited to after 2004). They found 55 articles that covered 9652 procedural sedations. The most common adverse events: hypoxia (40/1000 but only 23/1000 were <90%), vomiting (16/1000), hypotension (15/1000), and apnea (12/1000). The serious adverse events: laryngospasm (4/1000), intubation (1.6/1000), aspiration (1.2/1000). If you are interested, they do break some of these numbers down based on what agent was used. There was a fair amount of heterogeneity in the definitions used in the original studies. Also pediatrics was excluded.
Bottom line: Procedural sedation is safe, but we should have a sense of these numbers for adverse events.
Still not using topical anesthetics for corneal abrasions? Could topical NSAIDs be a better choice?
Calder LA, Balasubramanian S, Fergusson D. Topical nonsteroidal anti-inflammatory drugs for corneal abrasions: meta-analysis of randomized trials. Academic emergency medicine : official journal of the Society for Academic Emergency Medicine. 12(5):467-73. 2005. PMID: 15860701 [free full text]
Most people have heard me rant about the myth that topical anesthetics are harmful in corneal abrasions. (If you haven’t, watch for an upcoming episode of EMCases Journal Jam, or come to the North York General Emergency Medicine Update this year.) However, an essential part of informed choice is reviewing the alternatives. How do topical NSAIDs perform in managing the pain of corneal abrasions? (Hat tip to Nadia Awad @Nadia_EMPharmD for sending me this paper.) This is a systematic review and meta-analysis that identified 11 RCTs (they don’t report the total sample size, but they were all relatively small studies). I find this paper a little hard to follow, because they report 5 high quality studies to be included in the meta-analysis, but then include only 3 in the forrest plot. Looking at just these 3 trials (n=459), topical NSAIDs did decrease pain, with a weighted mean difference of -1.30 (95%CI -1.56 to -1.03) on a 10 point pain scale. There are a few issues with this data. First: it’s hard to interpret a weighted mean difference, but the minimum change on a 10 point pain score generally considered to be clinically important is 1.4. Second: there is a lot of data that could not be included because of the way the original trials were reported. Third: although a formal funnel plot couldn’t be done, the authors admit a possibility of publications bias. Fourth: There is not enough data on safety, but there was at least one recurrent corneal erosion in the NSAID group. Fifth: The funding source of the original trials was not discussed, but it might be important considering that not a single one of the trials had allocation concealment. Finally: the comparison groups were varied, but often just placebo. It might be better to compare to the less expensive oral NSAIDs (or topical anesthetics.)
Bottom line: Topical NSAIDs may decrease pain from corneal abrasions, but I don’t think this data is enough to support using them over other agents (especially considering their cost.)
Xanthrochromia AKA hey Bob, does this look kinda yellow to you?
Chu K, Hann A, Greenslade J, Williams J, Brown A. Spectrophotometry or visual inspection to most reliably detect xanthochromia in subarachnoid hemorrhage: systematic review. Annals of emergency medicine. 64(3):256-264.e5. 2014. PMID: 24635988
This is a systematic review looking at studies (English only) that included patients presenting with a headache who had LPs where the CSF was sent for xanthrochromia. The gold standard for SAH was either angiography or follow up (not perfect). The studies were also highly heterogenous. Not surprisingly, visual inspection, AKA “hey Bob, does this look kinda yellow to you”, was not perfect, with a sensitivity of 84%, specificity of 96%, positive LR of 14.1 and negative LR of 0.35. However, the fancy spectrophotometry was not any better, with a sensitivity of 87%, specificity of 86%, positive LR of 6.6 and negative LR of 0.29. The included studies are not of high enough quality to be sure about any of those numbers. I just don’t understand how we don’t have something better yet – obviously some chemical is turning the fluid yellow – could the makers of super-ultra-sensitive troponins not just create a test that detects whatever this compound is?
Bottom line: Neither method of detecting xanthochromia is perfect, which adds another layer of complexity to the question of who we should be LPing after CT
Foley free pee?
Herreros Fernández ML, González Merino N, Tagarro García A. A new technique for fast and safe collection of urine in newborns. Archives of disease in childhood. 98(1):27-9. 2013. PMID: 23172785
Here is a contribution from Dr. Kate Bingham. You probably know how I feel about getting urines in pediatric patients. (If you don’t, you can read this.) However, for newborns, a urine culture is going to get done. This paper describes a technique to get the urine without a foley. Basically, feed kid, wait 25 min, clean genitals, hold baby under armpits (standing position), tap suprapubic area at 100/min for 30 seconds, then massage low back for 30 seconds. Repeat until pee is produced, and make sure you catch it in specimen bottle. Does it work? Of the 80 patients they tried this on (no comparison group), they were successful in 69 (86%). Median time to sample collection was 45 seconds. My only concern is if I miss the urine and I have to start all over again (maybe after antibiotics). This is interesting, but I so rarely get newborn urines, I will probably stick with a Foley for now.
Bottom line: You can make children pee using this technique. Not sure where to fit that into practice.
I never get tired of talking about nerve blocks
Dickman E, Pushkar I, Likourezos A. Ultrasound-guided nerve blocks for intracapsular and extracapsular hip fractures. The American journal of emergency medicine. 2015. PMID: 26809928
One rebuttal I have often encountered when talking about nerve blocks for hip fractures is that the block is less likely to work in certain fracture patterns. This is a secondary analysis of data from a previously conducted prospective RCT looking at 77 patients and comparing the effectiveness of ultrasound guided femoral nerve block in intracapsular versus extracapsular hip fractures. They were the same, and both were good (pain scores from 6.5/10 just under 4/10 at 2 hours).
Bottom line: I will keep using nerve blocks for all hip fractures. I’m not too worried about the location of the fracture.
Diverticulitis – antibiotics, seeds, or exercise
Stollman N, Smalley W, Hirano I, . American Gastroenterological Association Institute Guideline on the Management of Acute Diverticulitis. Gastroenterology. 149(7):1944-9. 2015. PMID: 26453777
This is the new acute diverticulitis guideline from the American Gastroenterological Association Institute (that was as hard to type as it was to read.) I found three of their recommendations interesting:
- “The AGA suggests that antibiotics should be used selectively, rather than routinely, in patients with acute uncomplicated diverticulitis. (Conditional recommendation, low quality of evidence).” (They note that so far the RCTs showing no benefit of antibiotics have been in inpatients with CT proven diverticulitis.)
- “The AGA suggests against routinely advising patients with a history of acute diverticulitis to avoid consumption of nuts and popcorn. (Conditional recommendation,very-low quality of evidence).” This is another one of those myths that we breeze over, but can really ruin patients’ quality of life
- “The AGA suggests advising patients with diverticular disease to consider vigorous physical activity. (Conditional recommendation, very low quality of evidence).” This makes sense, but it has not been part of my discharge script – until now.
People are going to start thinking I have a personal vendetta against antibiotics
Gágyor I, Bleidorn J, Kochen MM, Schmiemann G, Wegscheider K, Hummers-Pradier E. Ibuprofen versus fosfomycin for uncomplicated urinary tract infection in women: randomised controlled trial. BMJ (Clinical research ed.). 351:h6544. 2015. PMID: 26698878 [free full text]
Are antibiotics useful in UTI? I actually think so, but there have been previous studies that illustrate that a lot of UTIs will clear on their own. This was a randomized, double dummy, placebo controlled trial in which 484 women (18-65 years old) received either fosfomycin 3 grams PO or ibuprofen 400mg TID for three days. 69% of the women in the ibuprofen only group had complete resolution of their symptoms, and didn’t use any antibiotics in the next 28 days. That is impressive, but the antibiotics did provide some benefit. The ibuprofen group had more dysuria, based on their definition of ‘non-inferiority’, although the actual numbers for pain look pretty similar. Also there were 5 patients in the ibuprofen group who developed pyelonephritis as compared to only one in the fosfomycin group, although the difference was not statistically significant (p=0.12). I think antibiotics help, but this study reminds us that if you are on the fence, there is no reason to rush the antibiotics. Nearly 7/10 women will clear their UTI without your help. Also, if you call someone back with a positive culture, but they no longer have symptoms, they almost certainly don’t need treatment (assuming they aren’t pregnant).
Bottom line: Antibiotics probably help in UTIs, just not as much as you think
One more time: dex is as good as pred in asthma
Cronin JJ, McCoy S, Kennedy U. A Randomized Trial of Single-Dose Oral Dexamethasone Versus Multidose Prednisolone for Acute Exacerbations of Asthma in Children Who Attend the Emergency Department. Annals of emergency medicine. 2015. PMID: 26460983
I have covered this topic before, but repetition is key in both science and education. This was a randomized, open-label non-inferiority trial comparing a single dose of dexamethasone (0.3mg/kg orally) to prednisolone (1mg/kg PO for 3 days) in 245 children aged 2-16 with known asthma. There was no difference in the primary outcome of PRAM score at day 4 (0.91 versus 0.91; absolute difference 0.005; 95%CI 0.35 to 0.34), although I am not sure this is the most clinically important outcome. There weren’t any differences in the secondary outcomes, such as admission to hospital, length of stay, or return visits.
Bottom line: Once again, dex is great for asthma
Sticking with obvious pediatric topics: ondansetron works
Danewa AS, Shah D, Batra P, Bhattacharya SK, Gupta P. Oral Ondansetron in Management of Dehydrating Diarrhea with Vomiting in Children Aged 3 Months to 5 Years: A Randomized Controlled Trial. The Journal of pediatrics. 169:105-109.e3. 2016. PMID: 26654135
This is another paper I might have skipped because the results seem obvious, but I have recently seen it argued that we use ondansetron too liberally, so I guess it’s worth looking at. This is a well done, double blinded, placebo controlled RCT that enrolled 170 children between 3 months and 5 years of age with acute vomiting and diarrhea and clinical signs of dehydration. Although I worry that the primary outcome of failure of ORT, defined as features of some dehydration after 4 hours of ORT, is a little subjective, the trial was appropriately blinded and placebo controlled. Failure was 31% with ondansetron as compared to 61.5% with placebo, an absolute risk reduction of 30%, or a NNT of about 3. The 30% failure rate does seem high to me though, as I almost never have a kid fail ORT.
Bottom line: Surprise? Ondansetron does help vomiting kids orally hydrate.
When your heart leaves you speechless
Wasserman JK, Perry JJ, Dowlatshahi D. Isolated transient aphasia at emergency presentation is associated with a high rate of cardioembolic embolism. CJEM. 17(6):624-30. 2015. PMID: 25782453
This is a prospective cohort of 2360 TIA patients, 41 of whom had isolated aphasia at the time of presentation. Patients with isolated aphasia were twice as likely to have a cardiac source of embolism (22.0% vs 10.6%, p=0.037). This is strong, believable data, but I disagree with the authors’ conclusion that “emergency patients with isolated aphasia with a TIA warrant a rapid and thorough assessment for a cardioembolic source”. Non-aphasic patients still had an 11% chance of a cardiac source as compared to 22% with aphasia. Those two numbers clearly necessitate the exact same work up.
Bottom line: This is interesting trivia, but the association of aphasia with cardioembolism is clinically irrelevant.
A Salter Harris Myth Update
Boutis K, Plint A, Stimec J. Radiograph-Negative Lateral Ankle Injuries in Children: Occult Growth Plate Fracture or Sprain? JAMA pediatrics. 170(1):e154114. 2016. PMID: 26747077
Almost everyone has heard my Salter 1 Rant. Here is some more evidence. This is a prospective cohort of 140 children between 5 and 12 years of age with clinically suspected Salter Harris 1 fractures of the ankle. They were all treated with a removable splint (yes – the pediatric tertiary centers are doing this, so you can too). Then all of the children had an MRI at one week. Of the 140 children, 108 had ligamentous injuries on MRI. So take home #1: Despite the old dogma about ligaments being stronger than pediatric bone, children do get ligamentous injuries. Another 27 had isolated bone contusions. Only 4 children (3.0%, 95% CI 0.1-5.9%) actually has Salter Harris 1 fractures, and only 2 of those had any evidence of growth plate injury. And even more important, at 1 month follow up, there was no difference in function between those with MRI confirmed fracture and those without.
Bottom line: Salter Harris 1 fractures are rare and of questionable clinical relevance. Stop casting all these kids.
How important are c-spine precautions in submersion victims?
Watson RS, Cummings P, Quan L, Bratton S, Weiss NS. Cervical spine injuries among submersion victims. The Journal of trauma. 51(4):658-62. 2001. PMID: 11586155
This is a chart review of all submersion victims in the Seattle area between 1974 and 1996. There were a total of 2244 submersion victims, 34% of whom survived until hospital discharge. The prevalence of c-spine injury was 0.49% overall and 0.38% of those who received any medical care (not pronounced dead on scene). All people with c-spine injuries had obvious trauma. (One, for example, was a victim from a plane crash.) The biggest pitfall of this chart review is that someone with a spine injury from submersion might only be coded as a spine injury at discharge, because that was the important injury. These patients would not have been found by the review. However, this isn’t the only reason to be skeptical of cervical collars, so I have no problem removing it if I need better access to a submerged patient’s airway.
Bottom line: A submerged patient is very unlikely to have a c-spine injury if there isn’t obvious signs of trauma
Modified Sgarbossa criteria – now for more than just ECG geeks?
Meyers HP, Limkakeng AT, Jaffa EJ. Validation of the modified Sgarbossa criteria for acute coronary occlusion in the setting of left bundle branch block: A retrospective case-control study. American heart journal. 170(6):1255-64. 2015. PMID: 26678648
This paper is worth a look, if just to review some ECGs. It is a retrospective case-control study looking to validate a modified Sgarbossa rule for diagnosing STEMI in LBBB. This rule uses the ratio of ST elevation to S wave, rather than a set 5mm cut off for the anterior leads. Based on their 258 patients (only 9 with true STEMI), they report a better sensitivity than the original criteria (80% vs 49%, p<0.001) and equal specificity (99% vs 100% p=0.5). I already use these criteria, but I think we should be cautious about the current evidence base. This is retrospective and based on only 9 patients with acute coronary occlusion. More importantly, I wonder about the inter-rater reliability when we are taking multiple measurement in millimetres and dividing them. I already know from reading Dr Smith’s (excellent) blog that he frequently sees small amounts of ST depression that I would have missed or measured differently.
Bottom line: Like many things on the ECG, proportion probably matters, but it isn’t well studied.
How many diseases can you diagnose at 20 feet?
Narayana S, McGee S. Bedside Diagnosis of the ‘Red Eye’: A Systematic Review. The American journal of medicine. 128(11):1220-1224.e1. 2015. PMID: 26169885
I’ll just do a very quick note on this systematic review. because I found two numbers interesting. For ruling in “serious eye disease”, photophobia is good (LR+ = 8.3; 95%CI 2.7 – 25.9), but photophobia by indirect illumination (shining the light in the opposite eye) is amazing (LR+ = 28.8; 95%CI 1.8 – 459). The other number I found interesting is that bacterial conjunctivitis can almost be ruled out by “failure to observe a red eye at 20 feet”, although I am not sure there is huge clinical value of differentiating bacterial from viral conjunctivitis.
Bottom line: Worth a read through if you want to better understand your eye exam.
Hoegberg LC, Bania TC, Lavergne V. Systematic review of the effect of intravenous lipid emulsion therapy for local anesthetic toxicity. Clinical toxicology (Philadelphia, Pa.). 2016. PMID: 26853119
Another quick one: A systematic review of intralipid therapy in local anesthetic toxicity. It might be worth a deep dive, but the quality of the evidence is just so poor that it’s hard to trust any conclusions. For what it is worth, they conclude that intralipid appears effective, but there is no evidence that it is more effective than vasopressors.
My real reason for bringing this up is to lament the quality of toxicology literature in general. I have heard people argue that it would be unethical to randomize these dying patients in order to get good data, but we have to remember that in the absence of good data, the care they are getting is entirely random anyway. The random factor is just the belief of the physician who happens to be on that day. Although these are rare cases, we have the technology to gather data from around the world. We need to do better.
Bottom line: I will probably use intralipid if this comes up, but we really need better science in toxicology.
Osteoarthritis is not an xray diagnosis
This study looks at data from 2 large cohort studies: The Framingham study (in which every patient over 50 got a pelvic x-ray, regardless of symptoms) and the osteoarthritis initiative study (which included 4366 patients thought to be at risk for knee arthritis, and again everyone was imaged.) Xray is not predictive of osteoarthritis. In Framingham, only 15.6% of patients with frequent pain (clinical OA) had radiographic evidence of OA and only 20.7% of those patients whose xray indicated OA actually had clinical symptoms. Likewise, In the osteoarthritis initiative study, only 9.1% of patients with symptoms had xray changes, and only 23.8% of patients with xray changes had symptoms.
Bottom line: Xray cannot provide any valuable information about osteoarthritis of the hip
Should we let residents use Google on shift?
Kim S, Noveck H, Galt J, Hogshire L, Willett L, O’Rourke K. Searching for answers to clinical questions using google versus evidence-based summary resources: a randomized controlled crossover study. Academic medicine : journal of the Association of American Medical Colleges. 89(6):940-3. 2014. PMID: 24871247 [free full text]
Rushing around the emergency department, it is obviously tempting to just google something rather than find a specific medical resource, but how good is google? This is a prospective, randomized, controlled, crossover study in which they took 48 internal medicine residents and asked them to answer a series of medical questions. They were randomized to answer 5 questions, either using Google or using their choice of DynaMed, First Consult, or Essential Evidence Plus. They then ‘crossed over’ and answered another 5 questions using the opposite tool. This was repeated for 48 weeks. There was no difference in time to correct answer, response rate, or accuracy. They found answers for 80% of the questions, but the correct answer in only 60%.
Bottom line: Google doesn’t look worse than these specific medical tools, but I really want my residents to be right more than 60% of the time in an open book test.
Cheesy Joke of the Month
What did the pirate say on his 80th birthday?
#FOAMed of the Month
I often lament the current state of medical science. Data is unreported. Secondary outcomes are reported as primary. Harm outcomes aren’t even mentioned.
COMPare (CEBM Outcome Monitoring Project) is a group of people trying to fix this. You can read a short blog post about it here. In short, they compare publications with the original trial protocol, report discrepancies, write letters to the editors, and report on their progress. It’s an interesting project that is worth checking out.
However, I guess that’s not really education, so I will add a second #FOAMed selection:
Have ever heard of BRASH syndrome? You’ve probably seen it, but if you are like me, you had probably never heard of it before this month:
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.