Articles of the Month (December 2016)

Welcome to the year-end edition of the Articles of the Month (released well into the new year because of the craziness of emergency department holiday schedules). The podcast version of this post with Casey Parker is available through the BroomeDocs podcast.

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

Articles of the month (June 2016)

A monthly summary and brief critical appraisal of the best emergency medicine literature I have encountered

Biggest non-news of the month

ATTACH-2 trial: Qureshi AI, Palesch YY, Barsan WG. Intensive Blood-Pressure Lowering in Patients with Acute Cerebral Hemorrhage. The New England journal of medicine. 2016. PMID: 27276234 [free full text]

To date, all the evidence available has indicated no clinically important benefit to lowering blood pressure in people with head bleeds. However, evidence is never enough to stop people from talking about how much an intervention “makes sense”. This is a large, randomized, multi-center, open-label trial that compared intensive blood pressure management (target systolic 110-139) to standard BP management (target 140-179) in 1000 patients with acute intracranial hemorrhage. To get into the trial, you needed at least one systolic blood pressure measurement over 180. Blood pressure was maintained in the target zone for 24 hours after enrollment. The primary outcome was 90 day death or disability, represented by a modified Rankin score of 4-6, and was the same for both groups (38.7% intensive vs 37.7% standard). There were no important differences in secondary outcomes. Despite the excitement for intensive treatment that somewhat inexplicably sprang from previous negative trials, like INTERACT-2, this negative finding is in keeping with all the evidence on this topic to date. Although both groups here were managed to some target, it’s not clear to me that any blood pressure management is really required. As long as you remember to treat their pain, the blood pressure generally normalizes anyway.

Bottom line: There is no need to aggressively manage blood pressure in patients with head bleeds.

You don’t remember INTERACT-2?

Anderson CS, Heeley E, Huang Y. Rapid blood-pressure lowering in patients with acute intracerebral hemorrhage. The New England journal of medicine. 368(25):2355-65. 2013. PMID: 23713578 [free full text]

This is a multi-center, randomized, partially blinded trial comparing intensive blood pressure control (target of a systolic pressure <140 within 1 hour) to guideline recommended care (to a target systolic <180) in 2794 adult patients with intracerebral hemorrhage within the last 6 hours. It was a negative trial, with the primary outcome of death or disability (modified Rankin score 3-6) at 90 days of 52.0% in the intensive group and 55.6% in guideline group (p=0.06, OR 0.87, 95%CI 0.75-1.01). This is obviously pretty close to statistically significant, and a secondary outcome using the relatively controversial ordinal analysis was statistically significant, so a lot of people seemed to overlook the fact that it was a negative trial. Interpreted in isolation, you might think that this could be a positive result trying to escape our slavish devotion to p values, but in the larger context of the recurrent negative trials, this is just another negative trial.

Bottom line: There is no evidence out there that really supports aggressive blood pressure control in patients with head bleeds.

OK – blood pressure might not help, but surely brains need salt?

Berger-Pelleiter E, Émond M, Lauzier F, Shields JF, Turgeon AF. Hypertonic saline in severe traumatic brain injury: a systematic review and meta-analysis of randomized controlled trials. CJEM. 18(2):112-20. 2016. PMID: 26988719

I have heard hypertonic saline mentioned as a replacement for mannitol for the treatment of intracranial hypertension at numerous conferences since finishing residency. I was under the impression it was becoming the treatment of choice, but there is a reason we practice evidence based medicine. This is a systematic review and meta-analysis that identified 11 RCTs covering 1820 adult patients with traumatic brain injury comparing hypertonic saline to either mannitol (½ the studies) or another solution (often normal saline, or even hypotonic saline.) Hypertonic saline did not decrease mortality (RR 0.96, 95%CI 0.83-1.11). It didn’t lower intracranial pressure (weighted mean difference -0.39, 95%CI -3.78 – 2.99). And it didn’t improve functional outcomes (RR 1.12, 95% CI 0.92-1.36). Having the same outcomes as mannitol may not be bad, but in ½ these studies hypertonic saline was compared to iso or even hypotonic crystalloids (placebo?) and didn’t perform any better. On the other hand, it doesn’t look any worse than mannitol, so there still may be a role somewhere for it in trauma.

Bottom line: We probably shouldn’t be rushing to change to hypertonic saline in the management of traumatic brain injury.

EDIT: Scott Weingart has pointed out that the individual studies included in this review really weren’t designed to make the conclusions these authors make. (See the comments below). I haven’t read the individual studies yet, but once I do, I will provide an updated post on all the evidence for hypertonic saline. 

We desperately need droperidol back

Meltzer AC, Mazer-Amirshahi M. For Adults With Nausea and Vomiting in the Emergency Department, What Medications Provide Rapid Relief? Annals of emergency medicine. 2016. PMID: 27130801

This is a systematic review of RCTs looking at the treatment of nausea and vomiting in the emergency department. They found 8 trials that covered 952 patients. The ONLY medication that demonstrated a statistically significant decrease in nausea at 30 minutes was droperidol. Metoclopramide, ondansetron, prochlorperazine, and promethazine were all statistically nondifferentiable from placebo, and even if you had larger numbers, the magnitude of change with those drugs is likely clinically insignificant (about 0.5/10 on a VAS). Droperidol decreased nausea by 1.6/10 at 30 minutes.

Bottom line: Once again, droperidol is a very valuable drug, that was taken away from us for no good reason.

Single dose dex for asthma – again

Rehrer MW, Liu B, Rodriguez M, Lam J, Alter HJ. A Randomized Controlled Noninferiority Trial of Single Dose of Oral Dexamethasone Versus 5 Days of Oral Prednisone in Acute Adult Asthma. Annals of emergency medicine. 2016. PMID: 27117874

Have I beat this one to death yet? A steroid is a steroid is a steroid. However, the previous papers I have covered on this topic were in children – so I’ll throw this in. This is a randomized, double-blind, non-inferiority trial comparing a single dose of dexamethasone (12mg) to a 5 day course of 60mg of prednisone in 376 adult emergency patients with asthma exacerbations. The primary outcome of recidivism at 14 days was essentially the same (12.1% vs 9.8%, 95%CI -4.1 to 8.6%). However, because they defined non-inferiority as 8%, and the confidence interval is relatively wide, they cannot conclude that dexamethasone is noninferior. Personally, I think based on those numbers it probably is going to be, and that this trial was just under powered – but perhaps we should be giving a second dose of dex the next day.

Bottom line: Single dose dexamethasone is probably just as good as 5 days of prednisone in adults with asthma.

Can’t touch this (Stop. Hammer time.)

Ferguson CM, Swaroop MN, Horick N. Impact of Ipsilateral Blood Draws, Injections, Blood Pressure Measurements, and Air Travel on the Risk of Lymphedema for Patients Treated for Breast Cancer. Journal of clinical oncology : official journal of the American Society of Clinical Oncology.34(7):691-8. 2016. PMID: 26644530

Physiologically speaking, I could never quite understand why I was supposed to avoid drawing blood or measuring blood pressures in the arm that a breast cancer patient had axiallry lymph node dissection on. It is supposed to be a disaster resulting in lymphedema, and patients can get very angry if you try – but what exactly was the mechanism of disaster? Well, maybe there isn’t one. This is a prospective study of postoperative breast cancer patients being screened for lymphadenopathy, comparing patients who had blood draws, blood pressure measurement, injections, trauma, and cellulitis in the affected arm to those who didn’t. They also compared number of times on an airplane. The biggest weakness in this data is that although the lymphedema data was collected prospectively, data about the exposures was based on patient report and is therefore subject to recall bias. None of venipuncture, injection, or blood pressure measurements had any association with lymphedema. For patient information, the number of flights and length of flights were also not associated with lymphedema. This data is not enough to prove safety, but given the dubious physiologic explanation, this is reassuring.

Bottom line: You are unlikely to cause lymphedema by doing simple ED procedures such as injections, blood draws, or blood pressure measurements.

Hippocrates has still got it

St John PD and Montgomery PR. Utility of Hippocrates’ prognostic aphorism to predict death in the modern era: prospective cohort study. BMJ 2014. PMID 25512328 [free full text]

Another gem from the BMJ Christmas edition. One of Hippocrates’s aphorisms was: “It augurs well, if the patient’s mind is sound, and he accepts all food that’s offered him; but, if the contrary conditions do prevail, the chances of recovery are slim”. In other words, good appetite and good cognition make survival more likely. Using data from the Manitoba Study of Health and Aging, a prospective cohort study, these authors tested that theory. Combined, poor appetite and poor cognition predicted death, with a hazard ratio of 2.37. Both components were individually predictive, with poor appetite and cognition having hazard ratios of 1.79 and 2.21 respectively. They conclude, “An aphorism devised by Hippocrates millennia ago can predict death in the modern era.”

Bottom line: Hippocrates was probably a better clinician than all of us. (Also, these are important factors to think about when discussing end of life issues with our patients.)

Reminder: we treat patients, not numbers (times three)

Nakprasert P, Musikatavorn K, Rojanasarntikul D, Narajeenron K, Puttaphaisan P, Lumlertgul S. Effect of predischarge blood pressure on follow-up outcomes in patients with severe hypertension in the ED. The American journal of emergency medicine. 34(5):834-9. 2016. PMID: 26874395

This is a single center prospective observational study looking at 146 consecutive adult emergency department patients with a blood pressure ≥ 180/110 and no acute end-organ damage (the so called “hypertensive urgency”). One exclusion criteria that could be useful to you clinically was if patients had their BP decrease to less than 180 with just 10 minutes of quiet bed rest, which happened in 16/221 (7%) of the patients screened. They compared patients who had a blood pressure less than 180 at the time of discharge (98 patients) to those who still had a pressure over 180 at discharge (48 patients). There were no differences between these two groups. In fact, only 1 patient (0.7%) had a “hypertension related adverse event”, and that was in the group with the lower blood pressure at discharge. (The adverse event was just a patient who returned with an asymptomatic 5cm descending thoracic aortic aneurysm for which no intervention was done.) This trial was nonrandomized, and almost everyone was given antihypertensives, even though we know there is no value and potential harm in asymptomatic patients. Also, it is really hard to draw conclusions from a trial with an event rate of 1. However, we already know that asymptomatic hypertension does not require ED treatment. This study tells you that there is no need to get a lower number recorded on the chart before discharge. The outcomes are the same.

Bottom line: Don’t treat asymptomatic hypertension, even if someone has used the utterly useless label “urgency”

Patel KK, Young L, Howell EH. Characteristics and Outcomes of Patients Presenting With Hypertensive Urgency in the Office Setting. JAMA internal medicine. 2016. PMID: 27294333

This is a retrospective, single-center cohort study of 59,535 patients with hypertensive “urgency” (systolic ≥180 and/or diastolic ≥110 but without symptoms) in an outpatient clinic. Apparently only 426 (0.7%) were referred into the emergency department, which either tells you this database is awful or the physicians are excellent. Major adverse cardiac events (MACE) at 30 days were 0.5% in the patients referred to the ED and 0.2% in those sent home (p=0.23). At 6 months, the numbers were 0.9% and 0.8% (p=0.83) respectively. They conclude: “referral to the ED was associated with increased use of health care resources but not better outcomes.”

Bottom line: There is no such thing as hypertensive “urgency”. Stop using the term. Stop treating the number.

(If any primary care physicians that end up reading this: asymptomatic patients DO NOT need to be sent to the emergency department because of high blood pressure, no matter what the number.)


Driver BE, Olives TD, Bischof JE, Salmen MR, Miner JR. Discharge Glucose Is Not Associated With Short-Term Adverse Outcomes in Emergency Department Patients With Moderate to Severe Hyperglycemia. Annals of emergency medicine. 2016. PMID: 27353284

This is another retrospective, single-center study looking at all patients presenting to the emergency department with a glucose above 22mmol/L (400mg/dL) and subsequently discharged. Patients with type 1 diabetes were excluded. They found 422 patients with 566 encounters for the chart review. Looking at the blood glucose level at the time of discharge, there was no difference in adverse events (primarily re-visits for hyperglycemia, without any consequence) whether you got the glucose level down during the visit or not. In fact, the mean discharge glucose level was lower in patients that had subsequent adverse events than those without (17.6mmol/L vs 18.6mmol/L). Only 2 patients had glucose related adverse events (0.4%), both DKA. Overall, the discharge glucose level was not associated with return visits, ED usages, or hospitalization.

Bottom line: We need to rule out underlying pathology in hyperglycemic patients, but there is no value in temporarily lowering glucose and getting a better number on the chart. These patients just need close follow-up.

How about a shot in the arm?

Kashani P, Asayesh Zarchi F, Hatamabadi HR, Afshar A, Amiri M. Intra-articular lidocaine versus intravenous sedative and analgesic for reduction of anterior shoulder dislocation. Turkish Journal of Emergency Medicine. 16(2):60-64. 2016. [free full text]

This is a randomized, controlled trial of 104 emergency department patients with anterior shoulder dislocations comparing intra-articular lidocaine (20ml of 1% lidocaine, landmark based) to intravenous procedural sedation for reduction. (The biggest weakness of the study is that they used midazolam (0.05mg/kg) and fentanyl (1mcg/kg) as their sedation agents, which most people don’t use any more, and have been shown to have a higher complication rate. The reductions were attempted 15 minutes after the shoulder injection. Pain scores were less during the reduction in the intra-articular lidocaine group (0.3/10 versus 3/10, p<0.001). Pain scores were the same post-reduction (1/10 in both groups). However, there were 9 patients in the injection group who were “completely dissatisfied” with their care, as compared to 0 in the sedation group. Adverse events were higher in the sedation group: there were 0 adverse events with the injections, versus 11% apnea and 10% hypoxia with the sedation. Those numbers are really high, and good reasons not to use the fentanyl/midaz combo. I have used intra-articular lidocaine a number of times, primarily ultrasound guided, and I like it – but I would still personally rather be sedated if my shoulder was out. I had been using this for post-reduction pain, but that was unchanged in this study.

Bottom line: Intra-articular lidocaine can definitely be used to reduce shoulder dislocations, but its exact role as compared to sedation still isn’t clear

Read more here:

LEMONS is a lemon?

Norskov AK, et al. Diagnostic accuracy of anaesthesiologists’ prediction of difficult airway management in daily clinical practice: a cohort study of 188 064 patients registered in the Danish Anaesthesia Database. Anaesthesia 2014. PMID: 25511370 [free full text]

We all know how to assess patients to predict a difficult airway – the classic LEMONS assessment – but are those assessments any good? This is a database study, looking at a cohort of 188,064 Danish anesthesia cases. There were 3391 difficult intubations, and 3154 (93%) were unanticipated. In 929 cases the anesthesiologists predicted difficult intubation, and it was only actually difficult in 229 (25%). Similarly, difficult bag valve mask ventilation was unanticipated in 808/857 (94%) of cases, and predictions of difficulty were only correct in 49/218 (22%).

Bottom line: We cannot predict difficult airways. Be prepared and have a set algorithm you are going to follow for every airway, no matter how easy you think it is going to be.

Obsessive twitter users beware

Alim-Marvasti A, Bi W, Mahroo OA, Barbur JL, Plant GT. Transient Smartphone “Blindness”. The New England journal of medicine. 374(25):2502-4. 2016. PMID: 27332920

I just found this case report interesting. They present 2 patients with transient monocular blindness. They had normal workups, but both patients experienced this after looking at their smartphones while lying in bed. They think that the blindness was the result of one eye being blocked by the pillow, so that it was dark-adapted, while the other was looking at the bright screen and therefore became light-adapted. When the phone was turned off, and both eyes were used in the dark room, the light-adapted eye was perceived as being blind for a number of minutes.

Bottom line: Physiology can still be interesting

Chest compressions can’t circulate blood you don’t have

Bowles F, Rawlinson K. BET 3: The efficacy of chest compressions in paediatric traumatic arrest. Emergency medicine journal : EMJ. 33(5):368. 2016. PMID: 27099381

Cardiac arrest means push hard and push fast. That has been branded into our grey matter. However, most trauma experts I have spoken with don’t think that there is much of a role for chest compressions in traumatic cardiac arrest. They just get in the way of what you really need to be doing, if there is any chance of salvage, which is opening the chest. However, my experience in community hospitals is that this distinction between traumatic and non-traumatic arrests is not well known. This is a review looking for evidence of the benefit of chest compressions in pediatric traumatic arrests. There is no evidence, so it’s not much of a paper. They just conclude that you should follow local guidelines. I see no reason that children should be different from adults in this scenario, but there also isn’t great evidence in adults.

Bottom line: We have no idea whether we should be doing chest compressions in traumatic cardiac arrest. Just make sure that your compressions don’t result in injuries to staff trying to perform important procedures.

The authors’ title is best: Docusate: A placebo pill for soft poops

Carbon J and Kolber M. Docusate: A placebo pill for soft poops. Tools for practice. Alberta College of Family Physicians. April 25, 2016. [free full text]

This review looked at whether docusate sodium (Colace) or docusate calcium (Surfak) are effective for prevention or treatment of constipation. They identified 3 RCTs of docusate versus placebo in functional or medication induced constipation, and all were negative. One RCT compared docusate to polyethylene glycol, and the polyethylene glycol resulted in a bowel movement 1-2 days earlier. Biggest limitation: these trials were not in emergency department patients.

Bottom line: There is probably no role for docusate in the management of constipation.

I know a number of people who like to chase their drugs with a good fatty meal – and now we can give it to them intravenously

Lam SH, Majlesi N, Vilke GM. Use of Intravenous Fat Emulsion in the Emergency Department for the Critically Ill Poisoned Patient. The Journal of emergency medicine. 2016. PMID: 26972018

This is a review, but not surprisingly, considering that it is a toxicology paper, they only found 1 RCT. The majority of the ‘evidence’ is from 4 retrospective cohorts, and 79 case reports. In other words, there really is no evidence – but we still need to know what to do, so here is what they suggest. They think intralipid therapy is ‘probably’ beneficial for all local anesthetic toxicity. (I reviewed that topic here.) There is a long list of drugs that they conclude may have a ‘possible benefit’, including amitriptyline, calcium channel blockers, cocaine, and beta-blockers – based entirely off low quality case reports. They suggest it should be used if the patient is hemodynamically unstable and not responding to standard resuscitation, and that the dose is 20% intravenous fatty emulsion as a 1.5 ml/kg bolus, then an effusion of 0.25ml/kg/min for up to 60 minutes. The bolus could be repeated once at 5 minutes.

Bottom line: In the dying tox patient, this might be worth a try. I would definitely use it with local anesthetic toxicity, but otherwise would probably speak with poison control.

Cheesy joke of the month

Doctor: Sir, were you using a condom during the last time you had sex?

Patient: Doctor, what do you mean by “the last time”!?

Thanks for reading. If you find these monthly summaries useful, or you know anyone else who might find them useful, please spread the word. I love doing this, but it is really only valuable if the information reaches people who might use it. On the other hand, if you have any suggestions for improvement or come across any articles that you think should be included, please feel free to contact me.

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 (February 2016)

There are new sepsis definitions! Hurrah?

Singer M, Deutschman CS, Seymour CW. The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA. 315(8):801-10. 2016. PMID: 26903338 [free full text]

There are new sepsis guidelines. I guess that warrants headline news, and there has been a lot of excitement on the medical internet. However, they are really just the opinions of 19 experts, aren’t backed by any quality prospective data, and probably shouldn’t change your management. If you want to read more, I wrote a full post on the topic: Sepsis 3.0 – No thank you

Bottom line: Talk about qSOFA if you want to sound in the know, but clinically I would ignore this paper

Procedural sedation consent: “Don’t worry, it’s super safe… it’s the Michael Jackson drug.”

Bellolio MF, Gilani WI, Barrionuevo P. Incidence of Adverse Events in Adults Undergoing Procedural Sedation in the Emergency Department: A Systematic Review and Meta-analysis. Academic emergency medicine : official journal of the Society for Academic Emergency Medicine. 23(2):119-34. 2016. PMID: 26801209

What exactly are the risks of procedural sedation? I know them qualitatively, but when having an informed choice conversation, are you able to quote the actual incidence? I know I couldn’t. This is a systematic review and meta-analysis to determine the incidence of adverse events in ED procedural sedation (limited to after 2004). They found 55 articles that covered 9652 procedural sedations. The most common adverse events: hypoxia (40/1000 but only 23/1000 were <90%), vomiting (16/1000), hypotension (15/1000), and apnea (12/1000). The serious adverse events: laryngospasm (4/1000), intubation (1.6/1000), aspiration (1.2/1000). If you are interested, they do break some of these numbers down based on what agent was used. There was a fair amount of heterogeneity in the definitions used in the original studies. Also pediatrics was excluded.

Bottom line: Procedural sedation is safe, but we should have a sense of these numbers for adverse events.

Still not using topical anesthetics for corneal abrasions? Could topical NSAIDs be a better choice?

Calder LA, Balasubramanian S, Fergusson D. Topical nonsteroidal anti-inflammatory drugs for corneal abrasions: meta-analysis of randomized trials. Academic emergency medicine : official journal of the Society for Academic Emergency Medicine. 12(5):467-73. 2005. PMID: 15860701 [free full text]

Most people have heard me rant about the myth that topical anesthetics are harmful in corneal abrasions. (If you haven’t, watch for an upcoming episode of EMCases Journal Jam, or come to the North York General Emergency Medicine Update this year.) However, an essential part of informed choice is reviewing the alternatives. How do topical NSAIDs perform in managing the pain of corneal abrasions? (Hat tip to Nadia Awad @Nadia_EMPharmD for sending me this paper.) This is a systematic review and meta-analysis that identified 11 RCTs (they don’t report the total sample size, but they were all relatively small studies). I find this paper a little hard to follow, because they report 5 high quality studies to be included in the meta-analysis, but then include only 3 in the forrest plot. Looking at just these 3 trials (n=459), topical NSAIDs did decrease pain, with a weighted mean difference of -1.30 (95%CI -1.56 to -1.03) on a 10 point pain scale. There are a few issues with this data. First: it’s hard to interpret a weighted mean difference, but the minimum change on a 10 point pain score generally considered to be clinically important is 1.4. Second: there is a lot of data that could not be included because of the way the original trials were reported. Third: although a formal funnel plot couldn’t be done, the authors admit a possibility of publications bias. Fourth: There is not enough data on safety, but there was at least one recurrent corneal erosion in the NSAID group. Fifth: The funding source of the original trials was not discussed, but it might be important considering that not a single one of the trials had allocation concealment. Finally: the comparison groups were varied, but often just placebo. It might be better to compare to the less expensive oral NSAIDs (or topical anesthetics.)

Bottom line: Topical NSAIDs may decrease pain from corneal abrasions, but I don’t think this data is enough to support using them over other agents (especially considering their cost.)

Xanthrochromia AKA hey Bob, does this look kinda yellow to you?

Chu K, Hann A, Greenslade J, Williams J, Brown A. Spectrophotometry or visual inspection to most reliably detect xanthochromia in subarachnoid hemorrhage: systematic review. Annals of emergency medicine. 64(3):256-264.e5. 2014. PMID: 24635988

This is a systematic review looking at studies (English only) that included patients presenting with a headache who had LPs where the CSF was sent for xanthrochromia. The gold standard for SAH was either angiography or follow up (not perfect). The studies were also highly heterogenous. Not surprisingly, visual inspection, AKA “hey Bob, does this look kinda yellow to you”, was not perfect, with a sensitivity of 84%, specificity of 96%, positive LR of 14.1 and negative LR of 0.35. However, the fancy spectrophotometry was not any better, with a sensitivity of 87%, specificity of 86%, positive LR of 6.6 and negative LR of 0.29. The included studies are not of high enough quality to be sure about any of those numbers. I just don’t understand how we don’t have something better yet – obviously some chemical is turning the fluid yellow – could the makers of super-ultra-sensitive troponins not just create a test that detects whatever this compound is?

Bottom line: Neither method of detecting xanthochromia is perfect, which adds another layer of complexity to the question of who we should be LPing after CT

Foley free pee?

Herreros Fernández ML, González Merino N, Tagarro García A. A new technique for fast and safe collection of urine in newborns. Archives of disease in childhood. 98(1):27-9. 2013. PMID: 23172785

Here is a contribution from Dr. Kate Bingham. You probably know how I feel about getting urines in pediatric patients. (If you don’t, you can read this.) However, for newborns, a urine culture is going to get done. This paper describes a technique to get the urine without a foley. Basically, feed kid, wait 25 min, clean genitals, hold baby under armpits (standing position), tap suprapubic area at 100/min for 30 seconds, then massage low back for 30 seconds. Repeat until pee is produced, and make sure you catch it in specimen bottle. Does it work? Of the 80 patients they tried this on (no comparison group), they were successful in 69 (86%). Median time to sample collection was 45 seconds. My only concern is if I miss the urine and I have to start all over again (maybe after antibiotics). This is interesting, but I so rarely get newborn urines, I will probably stick with a Foley for now.

Bottom line: You can make children pee using this technique. Not sure where to fit that into practice.

I never get tired of talking about nerve blocks

Dickman E, Pushkar I, Likourezos A. Ultrasound-guided nerve blocks for intracapsular and extracapsular hip fractures. The American journal of emergency medicine. 2015. PMID: 26809928

One rebuttal I have often encountered when talking about nerve blocks for hip fractures is that the block is less likely to work in certain fracture patterns. This is a secondary analysis of data from a previously conducted prospective RCT looking at 77 patients and comparing the effectiveness of ultrasound guided femoral nerve block in intracapsular versus extracapsular hip fractures. They were the same, and both were good (pain scores from 6.5/10 just under 4/10 at 2 hours).

Bottom line: I will keep using nerve blocks for all hip fractures. I’m not too worried about the location of the fracture.

Diverticulitis – antibiotics, seeds, or exercise

Stollman N, Smalley W, Hirano I, . American Gastroenterological Association Institute Guideline on the Management of Acute Diverticulitis. Gastroenterology. 149(7):1944-9. 2015. PMID: 26453777

This is the new acute diverticulitis guideline from the American Gastroenterological Association Institute (that was as hard to type as it was to read.) I found three of their recommendations interesting:

  • “The AGA suggests that antibiotics should be used selectively, rather than routinely, in patients with acute uncomplicated diverticulitis. (Conditional recommendation, low quality of evidence).” (They note that so far the RCTs showing no benefit of antibiotics have been in inpatients with CT proven diverticulitis.)
  • “The AGA suggests against routinely advising patients with a history of acute diverticulitis to avoid consumption of nuts and popcorn. (Conditional recommendation,very-low quality of evidence).” This is another one of those myths that we breeze over, but can really ruin patients’ quality of life
  • “The AGA suggests advising patients with diverticular disease to consider vigorous physical activity. (Conditional recommendation, very low quality of evidence).” This makes sense, but it has not been part of my discharge script – until now.

People are going to start thinking I have a personal vendetta against antibiotics

Gágyor I, Bleidorn J, Kochen MM, Schmiemann G, Wegscheider K, Hummers-Pradier E. Ibuprofen versus fosfomycin for uncomplicated urinary tract infection in women: randomised controlled trial. BMJ (Clinical research ed.). 351:h6544. 2015. PMID: 26698878 [free full text]

Are antibiotics useful in UTI? I actually think so, but there have been previous studies that illustrate that a lot of UTIs will clear on their own. This was a randomized, double dummy, placebo controlled trial in which 484 women (18-65 years old) received either fosfomycin 3 grams PO or ibuprofen 400mg TID for three days. 69% of the women in the ibuprofen only group had complete resolution of their symptoms, and didn’t use any antibiotics in the next 28 days. That is impressive, but the antibiotics did provide some benefit. The ibuprofen group had more dysuria, based on their definition of ‘non-inferiority’, although the actual numbers for pain look pretty similar. Also there were 5 patients in the ibuprofen group who developed pyelonephritis as compared to only one in the fosfomycin group, although the difference was not statistically significant (p=0.12). I think antibiotics help, but this study reminds us that if you are on the fence, there is no reason to rush the antibiotics. Nearly 7/10 women will clear their UTI without your help. Also, if you call someone back with a positive culture, but they no longer have symptoms, they almost certainly don’t need treatment (assuming they aren’t pregnant).

Bottom line: Antibiotics probably help in UTIs, just not as much as you think

One more time: dex is as good as pred in asthma

Cronin JJ, McCoy S, Kennedy U. A Randomized Trial of Single-Dose Oral Dexamethasone Versus Multidose Prednisolone for Acute Exacerbations of Asthma in Children Who Attend the Emergency Department. Annals of emergency medicine. 2015. PMID: 26460983

I have covered this topic before, but repetition is key in both science and education. This was a randomized, open-label non-inferiority trial comparing a single dose of dexamethasone (0.3mg/kg orally) to prednisolone (1mg/kg PO for 3 days) in 245 children aged 2-16 with known asthma. There was no difference in the primary outcome of PRAM score at day 4 (0.91 versus 0.91; absolute difference 0.005; 95%CI 0.35 to 0.34), although I am not sure this is the most clinically important outcome. There weren’t any differences in the secondary outcomes, such as admission to hospital, length of stay, or return visits.

Bottom line: Once again, dex is great for asthma

Sticking with obvious pediatric topics: ondansetron works

Danewa AS, Shah D, Batra P, Bhattacharya SK, Gupta P. Oral Ondansetron in Management of Dehydrating Diarrhea with Vomiting in Children Aged 3 Months to 5 Years: A Randomized Controlled Trial. The Journal of pediatrics. 169:105-109.e3. 2016. PMID: 26654135

This is another paper I might have skipped because the results seem obvious, but I have recently seen it argued that we use ondansetron too liberally, so I guess it’s worth looking at. This is a well done, double blinded, placebo controlled RCT that enrolled 170 children between 3 months and 5 years of age with acute vomiting and diarrhea and clinical signs of dehydration. Although I worry that the primary outcome of failure of ORT, defined as features of some dehydration after 4 hours of ORT, is a little subjective, the trial was appropriately blinded and placebo controlled. Failure was 31% with ondansetron as compared to 61.5% with placebo, an absolute risk reduction of 30%, or a NNT of about 3. The 30% failure rate does seem high to me though, as I almost never have a kid fail ORT.

Bottom line:  Surprise? Ondansetron does help vomiting kids orally hydrate.

When your heart leaves you speechless

Wasserman JK, Perry JJ, Dowlatshahi D. Isolated transient aphasia at emergency presentation is associated with a high rate of cardioembolic embolism. CJEM. 17(6):624-30. 2015. PMID: 25782453

This is a prospective cohort of 2360 TIA patients, 41 of whom had isolated aphasia at the time of presentation. Patients with isolated aphasia were twice as likely to have a cardiac source of embolism (22.0% vs 10.6%, p=0.037). This is strong, believable data, but I disagree with the authors’ conclusion that “emergency patients with isolated aphasia with a TIA warrant a rapid and thorough assessment for a cardioembolic source”. Non-aphasic patients still had an 11% chance of a cardiac source as compared to 22% with aphasia. Those two numbers clearly necessitate the exact same work up.

Bottom line: This is interesting trivia, but the association of aphasia with cardioembolism is clinically irrelevant.

A Salter Harris Myth Update

Boutis K, Plint A, Stimec J. Radiograph-Negative Lateral Ankle Injuries in Children: Occult Growth Plate Fracture or Sprain? JAMA pediatrics. 170(1):e154114. 2016. PMID: 26747077

Almost everyone has heard my Salter 1 Rant. Here is some more evidence. This is a prospective cohort of 140 children between 5 and 12 years of age with clinically suspected Salter Harris 1 fractures of the ankle. They were all treated with a removable splint (yes – the pediatric tertiary centers are doing this, so you can too). Then all of the children had an MRI at one week. Of the 140 children, 108 had ligamentous injuries on MRI. So take home #1: Despite the old dogma about ligaments being stronger than pediatric bone, children do get ligamentous injuries. Another 27 had isolated bone contusions. Only 4 children (3.0%, 95% CI 0.1-5.9%) actually has Salter Harris 1 fractures, and only 2 of those had any evidence of growth plate injury. And even more important, at 1 month follow up, there was no difference in function between those with MRI confirmed fracture and those without.

Bottom line: Salter Harris 1 fractures are rare and of questionable clinical relevance. Stop casting all these kids.

How important are c-spine precautions in submersion victims?

Watson RS, Cummings P, Quan L, Bratton S, Weiss NS. Cervical spine injuries among submersion victims. The Journal of trauma. 51(4):658-62. 2001. PMID: 11586155

This is a chart review of all submersion victims in the Seattle area between 1974 and 1996. There were a total of 2244 submersion victims, 34% of whom survived until hospital discharge. The prevalence of c-spine injury was 0.49% overall and 0.38% of those who received any medical care (not pronounced dead on scene). All people with c-spine injuries had obvious trauma. (One, for example, was a victim from a plane crash.) The biggest pitfall of this chart review is that someone with a spine injury from submersion might only be coded as a spine injury at discharge, because that was the important injury. These patients would not have been found by the review. However, this isn’t the only reason to be skeptical of cervical collars, so I have no problem removing it if I need better access to a submerged patient’s airway.

Bottom line: A submerged patient is very unlikely to have a c-spine injury if there isn’t obvious signs of trauma

Modified Sgarbossa criteria – now for more than just ECG geeks?

Meyers HP, Limkakeng AT, Jaffa EJ. Validation of the modified Sgarbossa criteria for acute coronary occlusion in the setting of left bundle branch block: A retrospective case-control study. American heart journal. 170(6):1255-64. 2015. PMID: 26678648

This paper is worth a look, if just to review some ECGs. It is a retrospective case-control study looking to validate a modified Sgarbossa rule for diagnosing STEMI in LBBB. This rule uses the ratio of ST elevation to S wave, rather than a set 5mm cut off for the anterior leads. Based on their 258 patients (only 9 with true STEMI), they report a better sensitivity than the original criteria (80% vs 49%, p<0.001) and equal specificity (99% vs 100% p=0.5). I already use these criteria, but I think we should be cautious about the current evidence base. This is retrospective and based on only 9 patients with acute coronary occlusion. More importantly, I wonder about the inter-rater reliability when we are taking multiple measurement in millimetres and dividing them. I already know from reading Dr Smith’s (excellent) blog that he frequently sees small amounts of ST depression that I would have missed or measured differently.

Bottom line: Like many things on the ECG, proportion probably matters, but it isn’t well studied.

Read more on Dr. Smith’s blog here, here, or here.


How many diseases can you diagnose at 20 feet?

Narayana S, McGee S. Bedside Diagnosis of the ‘Red Eye’: A Systematic Review. The American journal of medicine. 128(11):1220-1224.e1. 2015. PMID: 26169885

I’ll just do a very quick note on this systematic review. because I found two numbers interesting. For ruling in “serious eye disease”, photophobia is good (LR+ = 8.3; 95%CI 2.7 – 25.9), but photophobia by indirect illumination (shining the light in the opposite eye) is amazing (LR+ = 28.8; 95%CI 1.8 – 459). The other number I found interesting is that bacterial conjunctivitis can almost be ruled out by “failure to observe a red eye at 20 feet”, although I am not sure there is huge clinical value of differentiating bacterial from viral conjunctivitis.

Bottom line: Worth a read through if you want to better understand your eye exam.

Intralipid review

Hoegberg LC, Bania TC, Lavergne V. Systematic review of the effect of intravenous lipid emulsion therapy for local anesthetic toxicity. Clinical toxicology (Philadelphia, Pa.). 2016. PMID: 26853119

Another quick one: A systematic review of intralipid therapy in local anesthetic toxicity. It might be worth a deep dive, but the quality of the evidence is just so poor that it’s hard to trust any conclusions. For what it is worth, they conclude that intralipid appears effective, but there is no evidence that it is more effective than vasopressors.

My real reason for bringing this up is to lament the quality of toxicology literature in general. I have heard people argue that it would be unethical to randomize these dying patients in order to get good data, but we have to remember that in the absence of good data, the care they are getting is entirely random anyway. The random factor is just the belief of the physician who happens to be on that day. Although these are rare cases, we have the technology to gather data from around the world. We need to do better.

Bottom line: I will probably use intralipid if this comes up, but we really need better science in toxicology.

Osteoarthritis is not an xray diagnosis

Kim C, Nevitt MC, Niu J. Association of hip pain with radiographic evidence of hip osteoarthritis: diagnostic test study. BMJ (Clinical research ed.). 351:h5983. 2015. PMID: 26631296 [free full text]

This study looks at data from 2 large cohort studies: The Framingham study (in which every patient over 50 got a pelvic x-ray, regardless of symptoms) and the osteoarthritis initiative study (which included 4366 patients thought to be at risk for knee arthritis, and again everyone was imaged.) Xray is not predictive of osteoarthritis. In Framingham, only 15.6% of patients with frequent pain (clinical OA) had radiographic evidence of OA and only 20.7% of those patients whose xray indicated OA actually had clinical symptoms. Likewise, In the osteoarthritis initiative study, only 9.1% of patients with symptoms had xray changes, and only 23.8% of patients with xray changes had symptoms.

Bottom line: Xray cannot provide any valuable information about osteoarthritis of the hip

Should we let residents use Google on shift?

Kim S, Noveck H, Galt J, Hogshire L, Willett L, O’Rourke K. Searching for answers to clinical questions using google versus evidence-based summary resources: a randomized controlled crossover study. Academic medicine : journal of the Association of American Medical Colleges. 89(6):940-3. 2014. PMID: 24871247 [free full text]

Rushing around the emergency department, it is obviously tempting to just google something rather than find a specific medical resource, but how good is google? This is a prospective, randomized, controlled, crossover study in which they took 48 internal medicine residents and asked them to answer a series of medical questions. They were randomized to answer 5 questions, either using Google or using their choice of DynaMed, First Consult, or Essential Evidence Plus. They then ‘crossed over’ and answered another 5 questions using the opposite tool. This was repeated for 48 weeks. There was no difference in time to correct answer, response rate, or accuracy. They found answers for 80% of the questions, but the correct answer in only 60%.

Bottom line: Google doesn’t look worse than these specific medical tools, but I really want my residents to be right more than 60% of the time in an open book test.

Cheesy Joke of the Month

What did the pirate say on his 80th birthday?

Aye Matey


#FOAMed of the Month

I often lament the current state of medical science. Data is unreported. Secondary outcomes are reported as primary. Harm outcomes aren’t even mentioned.

COMPare (CEBM Outcome Monitoring Project) is a group of people trying to fix this. You can read a short blog post about it here. In short, they compare publications with the original trial protocol, report discrepancies, write letters to the editors, and report on their progress. It’s an interesting project that is worth checking out.


However, I guess that’s not really education, so I will add a second #FOAMed selection:

Have ever heard of BRASH syndrome? You’ve probably seen it, but if you are like me, you had probably never heard of it before this month:

BRASH syndrome on PulmCrit