Articles of the Month (March 2017)

A monthly collection of interesting emergency medicine articles appraised to keep your practice informed.

I decided to take a break last month, for the first time in a few years. I imagine some people were hoping I would take I much more extended vacation, but I am sorry to say, you are stuck with me. I might be a little rusty, though, after a month off, so cut me some slack…

As always, the audio version is available on the BroomeDocs podcast (if you can tolerate very poor quality banter that Casey and I produce).
Continue reading “Articles of the Month (March 2017)”

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 (July 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.

Sick kids look sick

Vaillancourt S, Guttmann A, Li Q, Chan IY, Vermeulen MJ, Schull MJ. Repeated emergency department visits among children admitted with meningitis or septicemia: a population-based study. Ann Emerg Med. 2015;65:(6)625-632.e3. PMID: 25458981

This is a retrospective cohort of children 30 days to 5 years old who were hospitalized with the final diagnosis of either meningitis or septicemia. They were looking specifically at the children that had bounce backs. In total, 521 children were diagnosed with meningitis or septicemia, 114 (21.9%) of whom had been seen at a hospital in the 5 days prior to that diagnosis. The children all had similar mortality, lengths of stay, and critical care use whether you diagnosed them on the first visit or on the bounce back. Furthermore, meningitis and septicemia is very rare in pediatrics. There were a total of 511 cases in all of Ontario over the entire 5 years of this study. That is 511 out of 2,397,427 ED visits in this age group, or 0.02%, and you are only missing 20% of those on the first visit.

Bottom line: Emergency doctors are doing fine at diagnosing sick children. We don’t need fancy tests like CRPs or procalcitonins. Even if you miss the rare child, as long as you ensure good follow up, outcomes will be identical.


Green SM, Nigrovic LE, Krauss BS. Sick kids look sick. Ann Emerg Med. 2015;65:(6)633-5. PMID: 25536869

This is the excellent editorial that goes with the above paper. I just wanted to include a few quotes:

“A second explanation, simpler and more plausible, is that sepsis or meningitis was not present at the initial visit. The first diagnoses of nonserious viral or bacterial infections were not in error; however, after discharge these children had the rare misfortune of an unanticipated progression of illness.” Ie, don’t kick yourself too hard if you have a bounceback

“The study data of Vaillancourt et al suggest that, outside of the neonatal period, sepsis and meningitis are not occult conditions and that, accordingly, “sick kids look sick.” ”

“The status quo is working.”

“These results encourage emergency physicians to trust the power and value of their clinical gestalt.”


Dead? Kick him in the chest

Trenkamp RH and Perez FJ. Heel compressions quadruple the number of Bystanders who can perform chest compressions for ten minutes. Am J Emerg Med. 2015. In Print. PMID: not yet available

This is an observational study in which a convenience sample of 49 individuals, who acted as their own controls, were asked to perform 10 minutes of chest compressions, first in the standard fashion, then using their heel. They describe this process as: the shoeless rescuer straddles the patient’s head facing the patient’s feet, with one foot next to the patient’s ear and the heel of the other foot placed on the chest at the standard CPR point. (A video of this maneuver is provided.) Defining adequate compressions as 100-120 two inch compressions per minute, overall 16% were able to maintain manual compression at 10 minutes and 65% were able to do 10 minutes of heel compressions. Performance of both got worse with age.

Bottom line: If you are a lone bystander who will have to perform prolonged CPR, you might want to consider using your foot.


But might a machine be better than a kick in the chest?

Perkins GD, Lall R, Quinn T, et al. Mechanical versus manual chest compression for out-of-hospital cardiac arrest (PARAMEDIC): a pragmatic, cluster randomised controlled trial. Lancet. 2015;385:(9972)947-55. PMID: 25467566

This is a prospective, randomized control trial of 4471 adult patients with out of hospital cardiac arrest, comparing mechanical CPR (the LUACS-2 device) to conventional CPR. There was no difference in return of circulation, or survival to hospital, at 30 days, at 90 days, or at 1 year. Personally, I find these results confusing. Although I am always biased to assume that new technologies are not going to be better than current practice (because they so rarely are), in this case we know that the one thing that matters for survival in cardiac arrest is consistent, good chest compressions. We also know that people tire and generally don’t provide great compressions, whereas the machine never tires. Based on that theory, the machine should clearly be better. Obviously we are missing something. Maybe it takes too long to get the machine on in the first place? Maybe no technology is capable of raising people from the dead?

Bottom line: There is no benefit to mechanical CPR, so don’t go blowing your budgets yet, but they are probably as good as manual CPR, so might be useful in certain specific scenarios (ongoing chest compressions during cardiac cath?)


Did everyone invest in CT scanners when I wasn’t looking?

Zonfrillo MR, Kim KH, Arbogast KB. Emergency Department Visits and Head Computed Tomography Utilization for Concussion Patients From 2006 to 2011. Acad Emerg Med. 2015. PMID: 26111921

This is a large database study looking at CT usage in concussion from 2006 to 2011 in the US. Overall, 0.5% of ED visits ended in a diagnosis of concussion. Although you might think we all know the CT head decision rules by now, the rate of CT in concussion increased by an absolute value of 11%. Conversely, the injury severity score decreased.

Bottom line: Although I though the CAEP choosing wisely choices were incredibly weak, because they should all already be part of basic good clinical practice, I will quote their first recommendation: Don’t order CT head scans in adults and children who have suffered minor head injuries (unless positive for a head injury clinical decision rule).


Should patients on warfarin should just have a daily head CT?

Nishijima DK, Offerman SR, Ballard DW, et al. Immediate and delayed traumatic intracranial hemorrhage in patients with head trauma and preinjury warfarin or clopidogrel use. Ann Emerg Med. 2012;59:(6)460-8.e1-7. PMID: 22626015

This is a prospective observational trial of 1064 adult patients with blunt head trauma on either warfarin (768 patients) or clopidogrel (296 patients) designed to look for delayed intracranial hemorrhage. These were patients with relatively minor trauma, mostly ground level falls, and 88% having a GCS of 15 at the time of examination. 7% had a bleed on the first scan (12% if on clopidogrel and 5% on warfarin). No patients on clopidogrel and 4/687 (0.6% 95%CI 0.2-1.5%) of patients on warfarin had a delayed intracranial hemorrhage. The major limitation of this study is that not everyone had CT scans.

Bottom line: The rate of delayed intracranial hemorrhage after a normal CT is low. It almost certainly doesn’t warrant routine repeat scans or admissions, but good patient instructions and follow up are reasonable.


Diltiazem over metoprolol for atrial fibrillation. Surprised?

Fromm C, Suau SJ, Cohen V, et al. Diltiazem vs. Metoprolol in the Management of Atrial Fibrillation or Flutter with Rapid Ventricular Rate in the Emergency Department. J Emerg Med. 2015. PMID: 25913166

This is a randomized, double-blind study comparing metoprolol (0.15mg/kg) and diltiazem (0.25mg/kg) in 106 adult patients with atrial fibrillation. The primary outcome of HR<100 at 30 minutes was achieved in 95.8% of the diltiazem group and 46.4% of the metoprolol group (p<0.0001). Diltiazem was better at all time points measured. There was no difference between in groups in term of adverse outcomes (hypotension or bradycardia).

Bottom line: Another small trial illustrating that calcium channel blockers are probably more effective than beta-blockers at controlling atrial fibrillation in the ED.


This doesn’t change anything: Asymptomatic hypertension still shouldn’t be treated in the ED

Levy PD, Mahn JJ, Miller J, et al. Blood pressure treatment and outcomes in hypertensive patients without acute target organ damage: a retrospective cohort. Am J Emerg Med. 2015. PMID: 26087706

A retrospective cohort of 1016 adult patients with a blood pressure greater than 180/110 and no signs or symptoms of acute organ damage. About 43% were given some kind of treatment, and there was no difference in ED revisits or mortality whether you were treated or not. Of course, this type of association doesn’t prove anything – maybe there was a reason some people were treated and others weren’t.

Bottom line: We still shouldn’t be treating (or working up) asymptomatic hypertension in the ED.


On that note, I might as well include the ACEP clinical policy:

Wolf SJ, Lo B, Shih RD, et al. American College of Emergency Physicians Clinical Policies Committee. Clinical policy: critical issues in the evaluation and management of adult patients in the emergency department with asymptomatic elevated blood pressure. Ann Emerg Med. 2013 Jul;62(1):59-68. PMID: 23842053

A few points from this policy (the policy contains only level C recommendations):

1) In ED patients with asymptomatic markedly elevated blood pressure, routine screening for acute target organ injury (eg, serum creatinine, urinalysis, ECG) is not required.

2) In patients with asymptomatic markedly elevated blood pressure, routine ED medical intervention is not required

Bottom line: (Cut and paste from above). We still shouldn’t be treating (or working up) asymptomatic hypertension in the ED.


We no communicate so good

Newman DH, Ackerman B, Kraushar ML, et al. Quantifying Patient-Physician Communication and Perceptions of Risk During Admissions for Possible Acute Coronary Syndromes. Ann Emerg Med. 2015;66:(1)13-18.e1. PMID: 25748480

This is a great paper by David Newman. They did paired surveys of patients being admitted to rule out ACS and their treating physicians to determine if patients and their physicians were on the same page with regards to the risk of MI (the reason the patient was being admitted). After having a conversation about admission, the patient and physician estimates of risk were only within 10% of each other 36% of the time. When asked about the chance of dying if an MI occurred at home, patients estimated the mortality at 80% compared to physicians estimates at 10%.

Bottom line: We do a poor job communicating to patients why we want to admit them to hospital. Without an understanding of their risk, patients cannot possibly make informed decisions that account for their own values and personal risk tolerance.


If you aren’t using bedside ultrasound, you probably also won’t be able to find this post on the internet, but congratulations on your upcoming retirement…

Stein JC, Wang R, Adler N, et al. Emergency physician ultrasonography for evaluating patients at risk for ectopic pregnancy: a meta-analysis. Ann Emerg Med. 2010;56:(6)674-83. PMID: 20828874

This is a systematic review and meta-analysis that includes 10 studies of 2057 patients looking at the accuracy of emergency physician performed ultrasound for ectopic pregnancy. The sensitivity (patients with an ectopic who had no IUP on ultrasound) was 99.3%, with a negative predictive value of 99.9% in this population with a 7.5% incidence of ectopic pregnancy.

Bottom line: Bedside ultrasound is excellent for ruling out ectopic.


Whats the best way to keep a cast dry?

McDowell M, Nguyen S, Schlechter J. A Comparison of Various Contemporary Methods to Prevent a Wet Cast. J Bone Joint Surg Am. 2014;96:(12)e99. PMID: 24951750

This non blinded trial compared six methods of keeping casts dry. There were 2 commercial products, compared to a plastic bag with duct tape, double plastic bags with duct tape, a plastic bag with a rubber band, or glad cling wrap. The weighed the cast after submerging in water for 2 minutes (so more intense than a shower) to determine water absorption. Plastic wrap and a single bag with duct tape were the least effective. A double bag with duct tape was 100% effective, as were the commercial products.

Bottom line: Of easily available methods, double plastic bags and duct tape are probably the best for showering with a cast.


Everything you could ever want to know about anal fissures

Nelson RL, Thomas K, Morgan J, Jones A. Non surgical therapy for anal fissure. Cochrane Database Syst Rev. 2012;2:CD003431. PMID: 22336789

This cochrane systematic review of the medical management of anal fissures covers 75 trials and 5031 patients of different medical therapies. Topical nitroglycerin increased early cure rates from about 35% to 49% compared to placebo, an NNT of 7, but about half of patients had late relapses. No conclusions can be made about calcium channel blockers or botox, because all studies were severely under-powered. Surgical therapy (which I have never referred for) was significantly better than any medical therapy, but does have a small risk of incontinence.

Bottom line: There is poor evidence for any medical therapy. In patients with chronic problems, surgical therapy should be considered.


Your kid rolled in poison ivy – what do you do?

Stibich AS, Yagan M, Sharma V, Herndon B, Montgomery C. Cost-effective post-exposure prevention of poison ivy dermatitis. Int J Dermatol. 2000;39:(7)515-8. PMID: 10940115

I didn’t know that you could prophylactically treat poison ivy after coming into contact with the plant, but before developing a rash. 20 healthy “volunteer” medical students were used them as their own controls. They exposed the students to poison ivy at 4 different spots. 2 hours later, the applied 0.5ml of either dial dish soap, Tecnu (a commercial product designed to chemically inactivate poison ivy), or Goop (a commercial cleaning product), and then rinsed the skin. They left the 4th area untouched as a control (but for some reason didn’t even rinse it off – just left it covered.) All three products were similar, but seem to decrease severity of the rash as compared to control. Ii was unclear if the study was blinded in any way.

Bottom line: If you touch poison ivy, it may be worth putting dish soap on the area and then cleaning thoroughly.


Lidocaine for limb pain – no, not a nerve block

Vahidi E, Shakoor D, Aghaie Meybodi M, Saeedi M. Comparison of intravenous lidocaine versus morphine in alleviating pain in patients with critical limb ischaemia. Emerg Med J. 2015;32:(7)516-9. PMID: 25147364

Like low dose ketamine, although to a lesser extent, I have heard a lot about using IV lidocaine for pain control this past year. This is a small RCT of 40 patients with ischemic limbs comparing IV morphine (0.1mg/kg) and IV lidocaine (2mg/kg). In patients with pain starting at 7.5/10, pain in the lidocaine group was better at 15 minutes (5.75/10 vs 7/10) and 30 minutes (4.25/10 versus 6.5/10), although those numbers may not be clinically significant.

Bottom line: Intravenous lidocaine may be an option for pain, but I am not sure when or why I would use it.


There is no such thing is a free lunch

Solomon RC. Coffers brimming, ethically bankrupt. Ann Emerg Med. 2012;59:(2)101-2. PMID: 22078890

An older editorial, but worth a read. The summary is that although we make a lot of excuses for why we take money from drug companies, none are any good. As individuals and as a group, we must just stop.

Bottom line: I will say it again. There is no such thing as a free lunch.


Patient with a PE – do you admit, send them home, or get them to the gym?

Lakoski SG, Savage PD, Berkman AM, et al. The safety and efficacy of early-initiation exercise training after acute venous thromboembolism: a randomized clinical trial. J Thromb Haemost. 2015;13:(7)1238-44. PMID: 25912176

A very small randomized, controlled trial that included 19 patients with PE, 9 of whom were randomized to a 3 month program including exercise and weight loss. They commit a cardinal sin by claiming to have multiple primary outcomes, but it looks like the exercise group lost weight and was more fit as compared to the usual care group. Of course, a grain or two of salt is required, but it looks like an interesting area for future research.

Bottom line: In the future, we may seen an equivalent to cardiac rehab for our PE patients. For now, I recommend all my patients exercise.


Completely irrelevant to medicine, but maybe the most useful information of the month: flight delays

When to fly to get there on time? Six million flights analyzed. Decision Science News. 2015.

http://www.decisionsciencenews.com/2014/11/06/flight-delays/

This is a database study that looked at all the flight data in the United States for the year of 2013 to determine when you are most likely to be delayed. Not surprisingly, the later your flight is in the day, the longer a delay you can expect, until about 10pm, when the delays start to fall again. There are some graphs you can look at.

Bottom line: For the next conference you book (like say SMACC in Dublin next year), try to book your flight early in the morning if you don’t want to be delayed.


Cheesy Joke of the Month

Why can’t you tell when a pterodactyl is going to the bathroom?

Because their P is silent


FOAMed of the month

The world of critical care and open access medical education suffered an incredible loss this month with the passing of Dr. John Hinds. He was one of the most inspirational individuals I have encountered in my life, and although I only shook his hand a single time, his words have forever changed me.

It is hard to pick just one of this many incredible talks, but I know both my wife and I were blown away by his keynote speech at the SMACC conference in Chicago: “Crack the chest and get crucified”:

http://intensivecarenetwork.com/hinds-crack-the-chest-get-crucified/