Acute Chest Syndrome (Sickle Cell Disease)

The newest edition of the Skeptics’ Guide to Emergency Medicine “Hot Off The Press” covers this article on sickle cell acute chest syndrome: 

http://onlinelibrary.wiley.com/doi/10.1111/acem.13048/abstract

The Hot Off The Press series allows you to comment and ask questions of the authors of the paper. The best comments will be included in the summary that accompanies the paper in Academic Emergency Medicine. Before we get to the paper, let’s do a quick review. Continue reading “Acute Chest Syndrome (Sickle Cell Disease)”

Articles of the Month (September 2016)

It’s time for another edition of the articles of the month. I didn’t come across as many papers worth sharing as I usually do, but there are still a few gems in there. The good news is it is a quick read. Once again, I will be discussing these papers with Casey Parker on the BroomeDocs podcast, and we would love to hear feedback about the audio version of these posts. Until next time….

Continue reading “Articles of the Month (September 2016)”

Articles of the month (July 2016)

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)”

Articles of the month (April 2016)

My monthly summaries of the best medical literature that I have come across

Every month I select the best medical articles I have read and provide brief summaries and critical appraisals. Here are this month’s articles:

Headline of the month: No benefit from amiodarone in out of hospital cardiac arrest

Kudenchuk PJ et al. Amiodarone, Lidocaine, or Placebo in Out-of-Hospital Cardiac Arrest. NEJM 2016. PMID: 27043165

There is a lot that could be said about this paper. It was a large, randomized, double-blind placebo controlled trial that included 3026 patients in out of hospital cardiac arrest. It compared amiodarone to lidocaine to placebo. The simplistic answer: there was no difference. I am tempted to stop there, because I never thought amiodarone helped, but the data might be a little more granular than that. For the primary outcome of survival to hospital discharge, the numbers were: 24.4% with amiodarone, 23.7% with lidocaine, and 21.0% with placebo. There was no statistically significant difference, as the trial was powered to find a 6.3% difference, but the absolute difference of 3.4% in survival to discharge could be clinically important. Unfortunately, treatment with these antiarrhythmics is not without harm. More patients in both the amiodarone and lidocaine groups were admitted to hospital. That sounds great on the surface, but the last thing any patient wants is to spend their final days as a vegetable in the ICU. If they aren’t going home at the end of that ICU stay, I think this is an important harm to consider.

Bottom line: I will continue not using anti-arrythmics in cardiac arrest. However, I would not be surprised if future research found a subgroup in which they are actually helpful.

Note: Keep an eye open for a future episode of EMCases Journal Jam, as I will be speaking with a few of the authors to see how they interpret this data.


Where to go for that gush of air?

Laan DV et al. Chest Wall Thickness and Decompression Failure: A systematic Review and Meta-Analysis Comparing Anatomic Locations in Needle Thoracostomy. Injury 2015 [Epub Ahead of Print]. PMID: 26724173

This is a systematic review and meta-analysis that looked at a total of 28 studies that attempted to determine the best location for a needle decompression of pneumothorax. 15 studies were imaging based studies that looked at chest wall thickness, and found that the mean total chest wall thickness was 4.3cm in the traditional midclavicular 2nd intercostal space, 4.0 cm in the 5th intercostal space (anterior axillary line), and 3.4 cm in the 5th intercostal space (mid axillary line) (Not statistically different with p=0.08). 13 studies looked at at how frequently a 5cm angiocath failed to reach the pleural space, and the results were: 38% with the traditional mid clavicular 2nd intercostal space approach, 31% with the 5th intercostal space (anterior axillary line), and 13% with the 5th intercostal space (mid axillary line) (p=0.01).

Bottom line: It might be better to try to needle in the same position as you would insert a chest tube, but honestly I avoid this dilemma altogether by going straight to open (finger) thoracostamy if I am concerned about tension pneumothroax.


 Humans aren’t pigs (most of us at least)

White JM, Braude DA, Lorenzo G, Hart BL. Radiographic evaluation of carotid artery compression in patients with extraglottic airway devices in place. Academic emergency medicine : official journal of the Society for Academic Emergency Medicine. 22(5):636-8. 2015. PMID: 25903385

I love LMAs for cardiac arrest. No matter how slick the operator, intubation takes time, can interfere with compressions, and distracts from the real issue. LMAs are quick, easy, and provide everything we need for the initial resuscitation of cardiac arrest patients. However, a pig study in 2012 raised the concern that LMAs might compress the carotid arteries. Luckily, most humans don’t look like pigs. This is a cohort study of 17 trauma patients with supraglottic airway devices in place who were having CT imaging of their neck. None of the patients had any radiographic evidence of compression of their carotid arteries. This isn’t the strongest paper you will ever read, but nor was the study that raised these concerns in the first place.

Bottom line: Humans aren’t pigs. LMAs are great for the initial resuscitation of cardiac arrest


Experts love to change terminology, just to ensure they sounds smarter than us average Joes

Tieder JS, Bonkowsky JL, Etzel RA et al. Brief Resolved Unexplained Events (Formerly Apparent Life-Threatening Events) and Evaluation of Lower-Risk Infants. PEDIATRICS. 137(5):e20160590-e20160590. 2016. [free full text]

ALTE no longer exists. We now have BRUEs or brief resolved unexplained events. This is a clinical practice guideline from the American Academy of Pediatrics on the topic. Aside from the name change, here are some of my take-aways:

  • A BRUE is an brief event (<1 min) that occurs in infants (<1 year), now resolved, that involved 1 or more of cyanosis, pallor, absent, decreased, or irregular breathing, marked change in tone, or altered level of responsiveness
  • An event doesn’t count as a BRUE if there is a likely explanation (probably the biggest change from ALTE)
  • Choking and gagging are specifically not considered BRUEs because they usually have an explanation such as GERD or URI
  • A low risk BRUE is defined as all of: age >60 days, born ≥ 32 weeks and gestational age ≥ 45 weeks, no CPR by a trained medical provider, event < 1 min, and first event. For these children, they specifically say you should not get blood tests or xrays.

Bottom line: There is a lot of stuff here, and not a lot of it has a high degree of evidence. It is worth a read, but I will still be asking a pediatrician to review all these babies for now


Practically predicting propofol pressure problems

Au AK, Steinberg D, Thom C. Ultrasound measurement of inferior vena cava collapse predicts propofol-induced hypotension. The American journal of emergency medicine. 2016. PMID: 27090394

This is a prospective observational study of a convenience sample of 40 patients getting propofol for induction of anesthesia for elective surgery. They used ultrasound to measure the collapse of the IVC pre-propofol, and calculated the percentage collapse as: (max IVC size – min IVC size)/max IVC size. Patients with IVC collapse >50% had more propofol-induced hypotension than those without (76% versus 39%, p=0.02). This would result in a sensitivity of 67%, a specificity of 77%, a positive predictive value of 71%, and a negative predictive value of 74%. None of those values is enough to rule-in or rule -out on their own, but they might be helpful as part of an overall assessment. Of course, isolated brief hypotension after propofol might not be all that relevant as an outcome. Also, the doses of propofol used here were pretty high (mean of 2.4mg/kg IV push) and these were healthy, elective surgery patients, so there are multiple reasons these numbers might not extrapolate the the ED.

Bottom line: IVC ultrasound has some correlation to propofol-induced hypotension, but its clinical utility in the ED is not clear.


The tomahawk

Silverton N, Youngquist S, Bledsoe J, Mallin M, Barton E. 71: Awake “Tomahawk” Video Laryngoscopy. Annals of Emergency Medicine. 56(3):S24-. 2010. [article]

This paper describes a technique I have found very useful in the past. Talking recently with my friend Dr. Joey Newbigging, I realized this might be new (and hopefully useful) for some people. Basically, while the patient is sitting upright, after providing some topical anesthetic, you insert the glidescope into their mouth using a “tomahawk” grip. Basically that means you hold the handle upside down, so the blade is coming out of the top of your hand. If that descriptions didn’t help, check out this blog post with pictures. I find it very useful for visualizing fish bones, especially when the fiberoptic scope is dirty, but also because it also allows for instrumentation of the airway. Using this approach, these authors were able to get grade 2 views of the cords in 94% of the awake, healthy volunteers.

Bottom line: A useful technique to keep in mind


Lump in your throat? Sorry – glucagon isn’t going to help

Weant KA, Weant MP. Safety and efficacy of glucagon for the relief of acute esophageal food impaction. American journal of health-system pharmacy : AJHP : official journal of the American Society of Health-System Pharmacists. 69(7):573-7. 2012. PMID: 22441787

In this review of IV glucagon for the treatment of esophageal food bolus, they identified only two studies that had a control group. Both were negative, with with dislodgement rate actually being lower (but not statistically so) with glucagon in one of the two trials.

Bodkin RP, Weant KA, Baker Justice S, Spencer MT, Acquisto NM. Effectiveness of glucagon in relieving esophageal foreign body impaction: a multicenter study. The American journal of emergency medicine. 2016. PMID: 27038694

This study is retrospective – but given how little evidence we have for glucagon, it might be worth looking at. They retrospectively identified 127 patients who were given 133 doses of glucagon (median dose 1mg IV) for esophageal food bolus, as well as a control group that was not given glucagon. Resolution occurred in 14% of patients given glucagon, which wasn’t statistically different from the 10% resolution seen with nothing. Vomiting occurred in 13% of patients given glucagon.

Bottom line: These patients need scopes, not medicines

You can read more here: A Closer Look at Glucagon for the Foreign Body


Could you ever really have too much ketamine?

Kannikeswaran N, Lieh-Lai M, Malian M, Wang B, Farooqi A, Roback MG. Optimal dosing of intravenous ketamine for procedural sedation in children in the ED—a randomized controlled trial. The American Journal of Emergency Medicine. 2016. [article]

This is a prospective, double-blind, RCT of 125 children aged 3-18 years comparing 3 different doses of ketamine (1, 1.5, and 2mg/kg). Not surprisingly, re-dosing was higher in the 1mg/kg group (16% vs 2.9% and 5%), but I’m not sure that is an important outcome. There weren’t any differences in sedation scores, sedation duration, or adverse events. Physician satisfaction was lower with 1mg/kg (80% vs 94% and 97%). Perhaps the most important numbers were from phone follow-up (although they did lose some patients). Vomiting: 10% with 1mg/kg, 12% with 15mg/kg, and 20% with 2mg/kg. Recall of the painful procedure: 19% with 1mg/kg, 7% with 15mg/kg, and 7% with 2mg/kg.

Bottom line: More vomiting, but less recall with higher doses. 1.5mg/kg seems like a sweet spot.


Game changer for head lice?

Kolber MR, Pierse M, Nickonchuk T. The louse is (no longer) in the house. Canadian family physician Médecin de famille canadien. 62(4):322. 2016. PMID: 27076544 [free full text]

This review looked to answer the question: what is the best treatment for head lice? They found 2 RCTs comparing permethrin with dimeticone (a silicone-based product that suffocates lices). They conclude that dimeticone is superior to permethrin, with 1 extra cure for every 3 to 4 patients treated. Dimeticone also seems to be cheaper.

Bottom line: I am switching to dimeticone 4% applied once for 8 hours (can be repeated at 1 week)


Come on antibodies, leave the NMDA receptor for ketamine

Titulaer MJ et al. Treatment and prognostic factors for longterm outcome in patients with anti-NMDA receptor encephalitis: an observational cohort study. Lancet Neurol. 2013 Feb;12(2):157-65. PMID: 23290630 [free full text]

If you haven’t heard of or seen anti-NMDA receptor encephalitis, this prospective observational trial has some good take away points.

  • This is an autoimmune disease, primarily of young females. It is associated with teratomas
  • It is more common than HSV encephalitis in young patients – so if you are doing an encephalitis workup, it should probably be on your differential
  • There are generally 4 phases: 1.Viral prodrome 2.Psychosis phase with behavioral changes, hallucination, amnesia and seizures in up to 75% of patients 3.Unresponsive phase with catatonia, possible choreiform movements and orofacial dyskinesia and 4.A hyperkinetic phase with autonomic instability.
  • CSF should specifically be sent for anti-NMDA receptor antibodies
  • Treatment is high dose steroids and IVIG. There are usually good outcomes if treated, but the morality is as high as 10%, so you don’t want to miss it

Bottom line: Be sure to have anti-NMDA receptor encephalitis on the differential of young females with altered mental status.


Roids vs Uric acid

Rainer TH, Cheng CH, Janssens HJ. Oral Prednisolone in the Treatment of Acute Gout: A Pragmatic, Multicenter, Double-Blind, Randomized Trial. Annals of internal medicine. 164(7):464-71. 2016. PMID: 26903390

This is a multicenter, double blind RCT of 416 adult patients presenting to the ED with gout, comparing indomethacin to prednisolone. There really weren’t any differences, either in effectiveness or adverse events. Pain was decreased by 2.5/10 at rest and 4.5/10 with activity with both treatments. About 40% of each group had minor adverse events. Unfortunately, many of the side effects that make me want to avoid NSAIDs (primarily in older patients) are also present with steroids, so I am not sure when to choose one over the other. (I would love to see some single dose dexamethasone studies for gout, just for ease of dosing.)

Bottom line: Steroids are a reasonable alternative to NSAIDs for gout


Opioids cause nausea and vomiting – so we should try to prevent it right?

One of the most common requests I encounter from nursing is for prophylactic anti-emetics when I prescribe opioids. Understandable, considering that by the time the patient vomits, I am generally off somewhere else doing something more exciting. But do they work? Let’s look at a few papers:

Lambie B, Chambers J, Herbison P. The role of prophylactic anti-emetic therapy in emergency department patients receiving intravenous morphine for musculoskeletal trauma. Emerg Med Australas. 11(4):240-243. 1999. [article]

RCT of 214 emergency department patients getting intravenous morphine for analgesia, randomized to either metoclopramide 10mg IV or placebo prior to the morphine. 1.9% of the placebo group vomited as compared to 5.4% in the metoclopramide group (p=0.0009). Yeah – more vomiting in the metoclopramide group!

Bradshaw M, Sen A. Use of a prophylactic antiemetic with morphine in acute pain: randomised controlled trial. Emergency medicine journal : EMJ. 23(3):210-3. 2006. PMID: 16498159 [free open access]

Again, this is a RCT of 259 emergency department patients getting morphine for pain, comparing metoclopramide to placebo. There was no statistically significant difference in nausea and vomiting between the groups (1.6% with metoclopramide and 3.7% with placebo).

Simpson PM, Bendall JC, Middleton PM. Review article: Prophylactic metoclopramide for patients receiving intravenous morphine in the emergency setting: a systematic review and meta-analysis of randomized controlled trials. Emergency medicine Australasia : EMA. 23(4):452-7. 2011. PMID: 21824312

This is a systematic review and meta-analysis looking at whether prophylactic metoclopramide prevents vomiting from opioids. The conclusion is that there was no difference between metoclopramide and placebo.

As far as I am aware, there are no studies looking at prophylactic ondansetron.

Sussman G, Shurman J, Creed MR. Intravenous ondansetron for the control of opioid-induced nausea and vomiting. International S3AA3013 Study Group. Clinical therapeutics. 21(7):1216-27. 1999. PMID: 10463519

This study takes a different approach: it waits for nausea to develop first, before trying to treat it. It is a randomized, double blind, placebo controlled trial comparing placebo, ondansetron 8mg and ondansetron 16mg IV in patients who developed nausea after being given an opioid. Of 2574 patients given opioids, 520 developed nausea/vomiting and were therefore included in the study. Resolution of N/V with ondansetron was significantly better than with placebo (45.7% with placebo, 62.3% with 8mg, and 68.7% with 16mg.)

Overall bottom line: Vomiting after IV opioid administration is actually pretty rare in these studies. We don’t seem to be able to prevent it from happening. It makes sense to monitor for nausea, and give ondansetron only if it occurs.


Patient gone wild? Bring out the horse tranquilizer

Isbister GK, Calver LA, Downes MA, Page CB. Ketamine as Rescue Treatment for Difficult-to-Sedate Severe Acute Behavioral Disturbance in the Emergency Department. Annals of emergency medicine. 2016. PMID: 26899459

This is a subgroup analysis of a prospective RCT comparing droperidol to midazolam. It looks at 49 patients with acute agitation who had already not responded high dose sedatives (most commonly a total of 20mg of droperidol) and were given ketamine. 44 of the 49 were adequately sedated with ketamine, and 4 of the 5 not sedated were given less than 200mg ketamine IM. There were only 3 adverse events: 2 patients vomited, and 1 had his oxygen saturation drop to 90%. This obviously isn’t practice changing in itself, but ketamine is a very interesting option for sedating agitated patients because of its ability to keep respiratory drive and airway reflexes in tact.

Bottom line: Ketamine is an interesting option for managing severely agitated patients


#FOAMed of the month:

I’m going to have to cheat this month – there is just too much excellent stuff out there.

First, no matter what your level of expertise, some ECGs are so important that we need to continuously review examples to maintain our pattern recognition skills. Hyperacute T-waves are an example an essential finding that is easily overlooked without practice. Dr. Steve Smith had 2 great posts on this ECG finding this month: here and here.

Although I am sure that everyone is aware the moment Scott Weingart posts anything, if you haven’t heard his talk on OODA loops yet, it is a must listen to understand clinical reasoning in the resuscitation room.

I had to stop listing SMACC talks in this section, because they would have just dominated every month. Soon, Josh Farkas might be in the same category. For now, he had two amazing posts that immediately impacted my practice: first, he suggests an innovative way of documenting a difficult airway, using the allergy list; second, he provides some really great insight into vasopressor use in septic shock.

Last, but definitely not least, Choosing Wisely Canada has developed a number of useful implementation guides, such as “Bye-Bye, PPI”


Cheesy Joke of the month

I remember the last thing my grandpa said to me before he kicked the bucket.

He said “Hey, how far do you think I can kick this bucket?”

 

Articles of the month (November 2015)

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…

Bronchiolitis – it will take your breath away

Willwerth BM, Harper MB, Greenes DS. Identifying hospitalized infants who have bronchiolitis and are at high risk for apnea. Ann Emerg Med. 2006;48:(4)441-7. PMID: 16997681

Its that time of year. Some children are beginning to hold their breath in anticipation of Christmas. Or, maybe that was an apneic spell from bronchiolitis? Which children are at risk? This is a retrospective cohort of 691 children less than 6 months old who were admitted to the hospital for bronchiolitis looking at risk factors associated with apnea. The authors found that full term babies less than 1 month old, preterm babies less than 48 weeks post-conception, and babies whose caregivers had already witnessed an apnea spell were at higher risk for further apnea spells. Overall 19 (2.5% 95%CI 1.7-4.3) children had apnea spells while admitted, and all 19 met one of the criteria above.

Bottom line: 2.5% is relatively low risk, but breathing is relatively important. I would have the pediatricians review the kids that fall into these categories.


More bronchiolitis and the need for oxygen

Cunningham S, Rodriguez A, Adams T. Oxygen saturation targets in infants with bronchiolitis (BIDS): a double-blind, randomised, equivalence trial. Lancet (London, England). 386(9998):1041-8. 2015. PMID: 26382998

This is a multi-center, randomized, controlled trial of children aged 6 weeks to 12 months admitted to hospital with bronchiolitis. This children were either placed on a standard sat probe or one that was altered so that a sat of 90% would display as 94%. Staff were instructed to provide oxygen to any child with a sat less than 94%. (94% seems like a pretty high target. I am more interested in whether we should be starting oxygen at say 92% or 88% or even lower.) I think they chose a pretty poor primary outcome: time to resolution of cough. For what it’s worth, it was equivalent, but did we really think oxygen could cure cough? Some secondary outcomes were also not affected, but none capture why I give oxygen. Oxygen is given when children are approaching the steep portion of the oxygen-hemoglobin dissociation curve to prevent precipitous drops, desaturations, and bad outcomes. The authors do report no change in ‘adverse events’, but if you look at the supplement, respiratory adverse events were things like cough and otitis media. Although I believe we probably over-treat bronchiolitis, this is another in a slew of papers that fails to actually prove that it is safe to withhold oxygen or discharge patients with low oxygen saturations.

Bottom line: Oxygen saturation is still an important parameter to monitor in bronchiolitis. We don’t know the ideal saturation to target.  


Children inhaling salt water – no, not drowning, but bronchiolitis treatment

Silver AH, Esteban-Cruciani N, Azzarone G. 3% Hypertonic Saline Versus Normal Saline in Inpatient Bronchiolitis: A Randomized Controlled Trial. Pediatrics. 2015. PMID: 26553190

This is a randomized, double-blind, controlled trial from a single pediatric hospital comparing 4 ml of either 3% saline or 0.9% saline nebulized every 4 hours in 227 children under 12 months old with bronchiolitis. There was no difference in any of the many outcomes they measured, including length of stay, ICU admission, readmission, and objective respiratory findings. Of course, it’s possible that normal saline is more therapeutic than no treatment – but, come on, you know that nothing works in bronchiolitis.

Bottom line: No treatments work in bronchiolitis. Do you think we will ever come to terms with that?


It might just be the season, but it seems like I am obsessed with wheezing kids

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 dexamethasone versus prednisone for asthma before, but here is another RCT. In 245 pediatric patients (aged 2-16) with asthma, they compared a single dose of dexamethasone (0.3mg/kg) to prednisolone (1mg/kg) for 3 days. Their primary outcome was a PRAM score on day 4 and there was no difference between the two.

Bottom line: I will continue using the easier single dose dexamethasone over prednisone.


More shots fired in the continuing Roc versus Sux RSI battle

Tran DT, Newton EK, Mount VA, Lee JS, Wells GA, Perry JJ. Rocuronium versus succinylcholine for rapid sequence induction intubation. The Cochrane database of systematic reviews. 10:CD002788. 2015. PMID: 26512948

This one is going to ruffle a few feathers. Let’s start with the author’s conclusions: “Succinylcholine created superior intubation conditions to rocuronium in achieving excellent and clinically acceptable intubating conditions.” This is a cochrane review that includes 50 trials covering 4151 patients. For “excellent intubating conditions” succinylcholine was superior to rocuronium (RR 0.86 95%CI 0.81-0.92). The problem with this conclusion is the significant heterogeneity in the included studies. For me, the biggest concern is varying doses. In fact, the authors even conclude that if you use 1.2mg/kg of rocuronium (the appropriate dose for RSI) there was no difference between roc and sux. Unfortunately, they make the erroneous conclusion that sux is still better because it has a shorter duration of paralysis. In emergent airways, short paralysis is not a good thing.

Bottom line: Ignore the conclusions, rocuronium at a proper dose (1.2mg/kg) is a great paralytic for RSI.


One of my favorite myths to rant about – and apparently some very smart people out there agree with me

Swaminathan A, Otterness K, Milne K, Rezaie S. The Safety of Topical Anesthetics in the Treatment of Corneal Abrasions: A Review. The Journal of emergency medicine. 49(5):810-5. 2015. 26281814

I spoke about topical anesthetics for corneal abrasions at rounds earlier this year. (My handout from that talk can be found here.) This is a systematic review looking at the same topic. They identify 2 emergency department studies and 4 ophthalmology studies (after a procedure called photorefractive keratectomy – essentially a iatrogenic corneal abrasion) that prospectively evaluated the use of topical anesthetics for corneal abrasions.  All the studies were small. Topical anesthetics resulted in no complications. Overall, topical anesthetics appear to be effective, with clinically and statistically significant pain score reduction in 5 of 6 studies.

Bottom line: Treat your patient’s pain. A short course of topical anesthetic is probably safe and almost certainly effective for corneal abrasions.


Acute HIV – a diagnosis I am probably missing

Rosenberg ES, Caliendo AM, Walker BD. Acute HIV infection among patients tested for mononucleosis. The New England journal of medicine. 340(12):969. 1999. PMID: 10094651 [free full text]

Early HIV infection presents as a mononucleosis-like infection, making it very difficult to diagnose. Although I generally dislike using the emergency department for public health screening, if HIV is not diagnosed during this initial stage, many years may pass before it is diagnosed, not only hurting the patient, but also putting their many contacts at risk. This is a letter to the editor describing a study where they retrospectively took all blood samples that were sent for epstein barr virus at Massachusetts General Hospital and tested them for HIV RNA. They found that 1.2% (7/563) has an acute HIV infection and another 0.8% (4/563) had chronic HIV.

Bottom line: This is well above the threshold for screening for HIV. Perhaps monospot and HIV testing should be paired?


1 more: Non specific viral illness or acute HIV?

Pincus JM, Crosby SS, Losina E, King ER, LaBelle C, Freedberg KA. Acute human immunodeficiency virus infection in patients presenting to an urban urgent care center. Clinical infectious diseases : an official publication of the Infectious Diseases Society of America. 37(12):1699-704. 2003. PMID: 14689354 [free full text]

Sticking with the same topic, these authors tested all patients presenting with viral symptoms and 1 or more HIV risk factors at their urban urgent care centre for HIV. (They were very broad with their HIV risk factors: any sexual contact, any injection drug use, any crack use, or any alcohol use in the last 2 months.) Of the 499 patients included, 5 (1.0%) were diagnosed with an acute HIV infection and another 6 (1.2%) were diagnosed with chronic HIV. They did not have any false positives.

Bottom line: Depending on your work environment, it may be worth screening for HIV in patients with viral illnesses.


It’s all about that aVL

Bischof JE, Worrall C, Thompson P, Marti D, Smith SW. ST depression in lead aVL differentiates inferior ST-elevation myocardial infarction from pericarditis. The American journal of emergency medicine. 2015. PMID: 26542793

Is that Inferior ST elevation indicative of STEMI? Or is it pericarditis? aVL might hold the key. This is a retrospective look at 3 different groups. Of 154 patients with a final diagnosis of inferior STEMI, all 154 had some degree of ST depression in aVL. Of the 49 patients with pericarditis, 49 had some degree of inferior ST elevation, but none had any ST depression in aVL. There was a third cohort with subtle inferior ST elevation (less than 1mm) but confirmed vessel occlusion on cath. Of these 54 patients, 49 had ST depression in aVL. The authors conclude that ST depression is highly sensitive for inferior STEMI and specific for pericarditis.

Bottom line: I will certainly look at aVL, but would love to see this repeated prospectively

If you want to read more about this and see some example ECGs, check out the blog post by senior author Dr Steve Smith: http://hqmeded-ecg.blogspot.ca/2015/11/new-paper-published-on-significance-of.html


 

Cold – the pure green coffee (ask Dr. Oz) of the brain

Andrews PJ, Sinclair HL, Rodriguez A. Hypothermia for Intracranial Hypertension after Traumatic Brain Injury. The New England journal of medicine. 2015. PMID: 26444221 [free full text]

Another in the cold brain is not healthy brain category. This is a multicentre, randomized controlled trial of 387 adult patients (out of 2498 screened patients) with traumatic brain injury and persistently elevated ICP after sedation, elevation of the head of the bed, and mechanical ventilation. They were randomized to either get or not get hypothermia (target between 32 and 35 degrees Celsius for 48 hours.) The trial was stopped early for harm. Their primary outcome (neuro status based on the extended Glasgow outcome scale) was worse in the hypothermia group (OR 1.53 95%CI 1.02-2.30). Mortality was also worse (OR 1.45 95%CI 1.01-2.10). The biggest problem with the study was that they included patients up to 10 days after injury, which could just be too late for the magical power of cold to work.

However, I don’t think we should find this too surprising. Hypothermia has been tried for many conditions, including TBI, in the past with limited success. The general failure of hypothermia is one of the reasons to remain highly skeptical of those two small, biased trials that indicated that it worked in cardiac arrest. It may be reasonable to continue using hypothermia for the time being, but if anyone gets around to actually repeating the hypothermia versus placebo trial in cardiac arrest, we shouldn’t be surprised if it turns out to have no effect.

Bottom line: No hypothermia for trauma


Dual antiplatelets for stroke/TIA?

Wang Y, Pan Y, Zhao X. Clopidogrel With Aspirin in Acute Minor Stroke or Transient Ischemic Attack (CHANCE) Trial: One-Year Outcomes. Circulation. 132(1):40-6. 2015. PMID: 25957224

This is one of those trials that will get talked about, but I worry we will over apply the results. This is a large multicenter randomized trial in which 5170 Chinese patients with high risk TIA or minor CVA were randomized to either clopidogrel 75mg daily for 3 months plus aspirin 75 mg daily for 21 days or aspirin 75 mg daily for 3 months. The primary outcome of stroke at 1 year occurred in 10.6% of the combo group as compared to 14.0% of the aspirin alone group (hazard ratio, 0.78; 95% confidence interval, 0.65-0.93; P=0.006). Bleeding was the same in both groups. I think there are a few important caveats. First, you should question the generalizability of these results to your patients unless you work in China, because the rates of smoking in China are unlike those anywhere else in the world. Second, it is unlikely that the combination of ASA and clopidogrel has the same bleeding rates as ASA alone. That doesn’t fit well with previous studies or general experience. This should remind us that RCTs are usually not well designed to identify harms and will often over estimate the benefit to harm ratio.

Bottom line: I would not be changing my practice to include dual antiplatelet therapy based on this study alone.


Great ultrasound tip – try using both probes for IUP

Tabbut M, Harper D, Gramer D, Jones R. High-frequency linear transducer improves detection of an intrauterine pregnancy in first trimester ultrasound. The American Journal of Emergency Medicine. Article in Press. PMID:

Traditionally, we are taught to use a curvilinear abdominal probe when performing transabdominal ultrasound to detect first trimester pregnancy. This study looked at adding the high frequency linear transducer after failure to identify IUP with the standard transducer. Of 81 initial scans, 27 patients did not have an IUP visualised with the curvilinear probe. Of those, 9 (33%) were found to have an IUP by using the linear probe.

Bottom line: It’s probably worth trying the linear probe if you can’t see an IUP with the curvilinear.


Cricoid pressure: the evidence?

Algie CM, Mahar RK, Tan HB, Wilson G, Mahar PD, Wasiak J. Effectiveness and risks of cricoid pressure during rapid sequence induction for endotracheal intubation. The Cochrane database of systematic reviews. 11:CD011656. 2015. PMID: 26578526

This is a Cochrane review designed to look for any RCT evidence of the value of cricoid pressure in either emergent or elective airways. The review really says nothing of value, because there is no evidence to review. So why include it? Because sometimes it’s important to know that there is no evidence to review. If anyone ever gets too dogmatic on either side of the cricoid pressure debate, they should probably be ignored.

Bottom line: There is no evidence supporting the use of cricoid pressure. I abandoned it a long time ago, but I would be happy to see an RCT done to confirm or contradict my current practice.  


Sex is better than flomax!

Doluoglu OG, Demirbas A, Kilinc MF. Can Sexual Intercourse Be an Alternative Therapy for Distal Ureteral Stones? A Prospective, Randomized, Controlled Study. Urology. 86(1):19-24. 2015. PMID: 26142575

By now, everyone should know that tamsulosin does not help patients with kidney stones, but that doesn’t mean we should give up on our patients. Is there anything else we can do to help? In this randomized, controlled study 75 adult patients with nephrolithiasis were randomized to either 1) being asked to have sex at least 3-4 times a week, 2) tamsulosin 0.4mg a day, or 3) usual care. There were no placebos (although if you can come up with a placebo version of sex I want to hear about it.) The mean time to stone expulsion was only 10 days (95%CI 4.2-15.8 days) in the sex group, versus 16.6 (95%CI 8.1-25.1 days) with tamsulosin and 18 (95%CI 15.5-23.5 days) with usual care (p=0.0001). I foresee a large number of men looking for medical notes explaining this therapy to their wives. Perhaps there may even be a few malingerers without stones looking to get this prescription?

Bottom line: Sex is good


When is dementia not dementia?

Djukic M, Wedekind D, Franz A, Gremke M, Nau R. Frequency of dementia syndromes with a potentially treatable cause in geriatric in-patients: analysis of a 1-year interval. European archives of psychiatry and clinical neuroscience. 265(5):429-38. 2015. PMID: 25716929

Dementia is a horrible diagnosis that we can’t do anything about. But is it always? In this retrospective review of patients admitted to hospital with dementia, the authors searched for reversible causes. Of the patients previously diagnosed with dementia, the authors were able identify a potentially reversible cause in 23%. Of the newly diagnosed dementia, 31% had potentially reversible causes. The common reversible causes included low B12, depression, alcoholism, and normal pressure hydrocephalus. I wouldn’t hang my hat on any of the numbers, given the retrospective nature of the trial, but this should serve as a reminder that we might be able to help some of these patients. If you can reverse dementia, that is a true save.

Bottom line: Some dementia is reversible. These causes should be searched for.


Dikembe Mutombo is wagging his finger – Block!

Riddell M, Ospina M, Holroyd-Leduc JM. Use of Femoral Nerve Blocks to Manage Hip Fracture Pain among Older Adults in the Emergency Department: A Systematic Review. CJEM. 2015. PMID: 26354332

My appraisal may be biased because I love nerve blocks, especially when I can do them with an ultrasound. This is a systematic review of randomized control trials asking the question: does the use of a femoral nerve block reduce pain, opioid use, delirium, or improve function in adults over 65 with an acute hip fracture. They found 7 RCTs covering a total of 224 patients – so the studies were small. Also, only one trial was placebo controlled. The remainder compared the nerve block to opioids. The authors appropriately did not perform a meta-analysis, as the studies were heterogenous, so a single numerical summary is not possible. The best summary is that the nerve block group consistently had both statistically and clinically significant reduction in their pain scores as compared to placebo, used less opioid, and had fewer complications.

Bottom line: Nerve blocks work great for hip fractures. We should be using these.


From Dikembe Mutombo to Mark Spitz

Browne KM, Murphy O, Clover AJ. Should we advise patients with sutures not to swim? BMJ (Clinical research ed.). 348:g3171. 2014. PMID: 24859900

I always find it a little frustrating when my non-medical friends ask me questions about medicine that seem really simple, but that I honestly can’t answer. What exactly did I learn in all those years of school? The most recent question was: “when can I started swimming again after getting stitches?” This is a review, if you can call a search that unearthed only a single case report a review, trying to answer that question. Yes, apparently in the entire medical literature there is a single reported case of a wound infection that occurred after swimming – and that was in a hospital rehab pool which is probably more likely to be colonized with strange bugs than your average swimming pool. The authors try to shape this into a practical answer, but I think the best answer we can give is “we don’t know”. Early showering after surgery has been shown to be safe, so maybe you could extrapolate from that.

Bottom line: There is much in medicine that we simply don’t know


Which is more important: rinsing your dishes before they go in the dishwasher, or rinsing out the inside of an abscess?

Chinnock B, Hendey GW. Irrigation of Cutaneous Abscesses Does Not Improve Treatment Success. Annals of emergency medicine. 2015. PMID: 26416494

I was never taught to irrigate abscesses in residency. It was only this year that I discovered that this has been suggested by numerous guidelines. But not so fast. This is a non-blinded RCT of 209 patients with cutaneous abscesses randomized to irrigation or no irrigation. There was no difference in the need for further treatment (I&D, antibiotic change, or admission) at 30 days between the 2 groups (15% vs 13%). Unfortunately a huge number of these patients were put on antibiotics (91% in the irrigation and 73% in the no irrigation group), which we know are unnecessary in most abscesses, but contaminate the results here.

Bottom line: This wasn’t common practice where I trained and we never saw many bouncebacks. I won’t start irrigating abscesses based on this.


Should the Bee Gees pause for a breath (at 30:2)?

Nichol G, Leroux B, Wang H. Trial of Continuous or Interrupted Chest Compressions during CPR. The New England journal of medicine. 2015. PMID: 26550795 [free full text]

“Well, you can tell by the way I use my walk, I’m a woman’s man. No time to talk… Ah,ha,ha,ha, stayin’ alive”. This is a large randomized controlled trial of 23,711 adult patients with out of hospital cardiac arrest comparing the standard 30:2 ratio of chest compressions to rescue breaths, to continuous chest compressions at 100/min with 10 asynchronous breaths a minute. The primary outcome of survival to hospital discharge was identical, 9.0% in the continuous chest compression group and 9.7% in the 30:2 group. Neurologically intact survival was 7.0% and 7.7% respectively. The biggest issue with the data is that everyone got extremely high quality CPR, and the compression fraction was almost identical in both groups, so it would have been difficult to demonstrate any difference.

Bottom line: Personally, I like continuous compressions with asynchronous breaths more, but this trial supports whatever you are comfortable with as long as you are doing high quality CPR.


A quick and easy rule out blood test for aortic dissection? Get real

Asha SE, Miers JW. A Systematic Review and Meta-analysis of D-dimer as a Rule-out Test for Suspected Acute Aortic Dissection. Annals of emergency medicine. 66(4):368-78. 2015. PMID: pubmed

This is a systematic review and meta-analysis looking to determine the diagnostic accuracy of D-dimer as a rule out test of aortic dissection. In total they found 5 studies including a total of 1600 patients. My first point of concern is that 1035 of those patients came from a single study, which could potentially dominate a meta-analysis, and that study was not designed to test the accuracy of D-dimer. In fact, the study enrolled 1455 patients, but only 1035 were counted in this meta-analysis, because the other patients never even had a D-dimer drawn. The results they present are pretty impressive, with a pooled sensitivity of 98% (95%CI 96-100%), specificity of 42% (95%CI 39-45%), negative likelihood ratio of 0.05 and positive likelihood ratio of 2.11. However, I would be very careful interpreting those results. Not only are the majority of the patients from a registry where D-dimer didn’t have to be drawn, but these were almost all patients admitted to CCUs, so very different from our ED population. Finally, although you would be using this test to try to avoid CTs, the poor specificity in a lower risk population could actually paradoxically lead to increased CT usage, much like D-dimer for PE.

Bottom line: This study isn’t enough to support D-dimer to rule out aortic dissection in the ED.


“Unreasonable haste is the direct road to error” – Moliere

Fanari Z, Abraham N, Kolm P. Aggressive Measures to Decrease “Door to Balloon” Time and Incidence of Unnecessary Cardiac Catheterization: Potential Risks and Role of Quality Improvement. Mayo Clinic proceedings. 2015. PMID: 26549506

An important lesson in unintended consequences. We know that short door to balloon times are important for STEMI patients. This is a study from a single hospital where they instituted a number of measures to decrease the door to balloon time. And it worked! Well – they managed to get the door to balloon time decreased by 15 minutes, which is excellent. However, it’s important to measure patient oriented outcomes and in this cohort the false positive STEMI rate rose from 7.7% to 16% and there was an increased mortality in this false positive group.

Bottom line: Inappropriate benchmarks can result in physicians rushing, more errors, and patient harms.


Don’t let an endotracheal tube make your patient worse

Kim WY, Kwak MK, Ko BS. Factors associated with the occurrence of cardiac arrest after emergency tracheal intubation in the emergency department. PloS one. 9(11):e112779. 2014. PMID: 25402500 [free full text]

Emergency physicians love procedures and intubation is one of our favorite. Sometimes this leads to us being a little overzealous about intubating very early, when an immediate airway is not necessary. This is a case control study of 41 critically ill adult patients that had a cardiac arrest after intubation (out of a total of 2404 critically ill patients who were intubated – or 1.7%.) Pre-Intubation hypotension (a systolic blood pressues ≤ 90) was independently associated with post-intubation arrest (OR 3.67 95%CI 1.58-8.55.) The case control design may not provide precise numbers, but I think this is a good reminder that some patients need good resuscitation before we attempt intubation.

Bottom line: Resuscitation before intubation in hypotensive patients


Cheesy Joke of the Month

There are two cows in a field. The first cow turns to the second and asks, “did you hear about the outbreak of mad cow disease?” The second cow responds: “Good thing I am a helicopter.”


 

#FOAMed of the month

Every month this section could probably just be filled with my favorite talks from SMACC. I will try to include some different FOAM in coming months, but these talks were so go that even though I listened to them live, I have listened to them all again at home. This is why I have been telling everyone who will listen they should join me in Dublin in June. The first tickets sold out very fast, but some more will go on sale December 1st at 5pm EST (if my math is right.)

For now, these talks were amazing:

Lessons from the Princess Bride (Amal Mattu)

When to stop resuscitation (Roger Harris)

What is a good death (Ashley Shreves)

Crack the chest. Get crucified. (John Hinds) – I know I have recommended this one before, but it is worth more than one watch.

Dogmalysis and pseudoaxioms (David Newman)

Bouncing back after tragedy (Rob Rogers)

Educational theory for the clinician (Jonathon Sherbino)

 

Neonatal (Newborn) Resuscitation 2015 update

A summary of the resuscitation of the newborn infant, updates with the 2015 ILCOR guidelines

Case

Code pink in labour and delivery, and you are the only doctor in the hospital tonight…

(This is an update of a prior version of this post based on the newest 2015 ILCOR/AHA/ERC guidelines)

The biggest changes are:

  • We no longer intubate and suction for meconium. The resuscitation proceeds identically whether or not meconium is present
  • Heart rate is monitored using ECG leads, rather than the classic palpation of the umbilicus
  • CPAP is added as an option for laboured breathing or persistent cyanosis
  • The first 30 second assessment has been removed because it was unrealistic. The goal is to just get an initial assessment and initial maneuvers done in the first minute.

Continue reading “Neonatal (Newborn) Resuscitation 2015 update”

Articles of the month (August 2015)

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.

Furyk JS, Chu K, Banks C, et al. Distal Ureteric Stones and Tamsulosin: A Double-Blind, Placebo-Controlled, Randomized, Multicenter Trial. Ann Emerg Med. 2015. PMID: 26194935 [free full text]

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

I think this paper is a little ridiculous and I include it only so you can ignore anyone who talks about it (including me, if you would like.) These authors enrolled 319 adult patients with clinically suspected community acquired pneumonia and subjected them to both a chest xray and a CT scan. Not surprisingly, the CT scan found what were interpreted as infiltrates in 33% of patients who had normal chest xrays. The CT findings were used to change management, both in terms of use of antibiotics as well as decision to admit, in a reasonable number of patients. However, it is not clear if any of those management changes were actually warranted. The authors want to use this data to conclude that patients suspected of community acquired pneumonia should all get CT scans. That is absolutely nutty. If we were missing 33% of clinically important pneumonias with current practice, our morgues would be full. Either these are tiny infiltrates that we fight off ourselves (after all, the human species has survived millennia without antibiotics), they are false positives, or we catch the pneumonia on a follow up xray 2 days later with a substantially lower radiation burden. (As a side note, be prepared for a similar problem of overdiagnosis in the many studies I assume will soon be published about using ultrasound for pneumonia, even if it has the advantage of no radiation.)

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:

https://www.phenomenaldocs.com/

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.


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