Articles of the Month (September 2016)

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

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

Articles of the month (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 (November 2015)

A monthly collection of the most interesting emergency medical literature I have encountered.

Here is this month’s summary of my favorite reads from the medical literature…

Bronchiolitis – it will take your breath away

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

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

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

More bronchiolitis and the need for oxygen

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

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

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

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

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

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

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

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

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

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

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

More shots fired in the continuing Roc versus Sux RSI battle

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

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

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

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

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

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

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

Acute HIV – a diagnosis I am probably missing

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

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

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

1 more: Non specific viral illness or acute HIV?

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

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

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

It’s all about that aVL

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

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

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

If you want to read more about this and see some example ECGs, check out the blog post by senior author Dr Steve Smith:


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

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

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

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

Bottom line: No hypothermia for trauma

Dual antiplatelets for stroke/TIA?

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

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

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

Great ultrasound tip – try using both probes for IUP

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

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

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

Cricoid pressure: the evidence?

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

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

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

Sex is better than flomax!

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

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

Bottom line: Sex is good

When is dementia not dementia?

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

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

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

Dikembe Mutombo is wagging his finger – Block!

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

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

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

From Dikembe Mutombo to Mark Spitz

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Don’t let an endotracheal tube make your patient worse

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

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

Bottom line: Resuscitation before intubation in hypotensive patients

Cheesy Joke of the Month

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


#FOAMed of the month

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

For now, these talks were amazing:

Lessons from the Princess Bride (Amal Mattu)

When to stop resuscitation (Roger Harris)

What is a good death (Ashley Shreves)

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

Dogmalysis and pseudoaxioms (David Newman)

Bouncing back after tragedy (Rob Rogers)

Educational theory for the clinician (Jonathon Sherbino)


Articles of the month (August 2015)

A monthly collection of the most interesting emergency medical literature I have encountered

Here is this month’s summary of my favorite reads from the medical literature.

Simple and brilliant: A pediatric rainbow

Moreira ME, Hernandez C, Stevens AD, et al. Color-Coded Prefilled Medication Syringes Decrease Time to Delivery and Dosing Error in Simulated Emergency Department Pediatric Resuscitations. Ann Emerg Med. 2015;66:(2)97-106.e3. PMID: 25701295

Pediatric resuscitations are stressful at the best of times and pediatric medication doses can be complicated, increasing the risk of medication errors. This group came up with an ingenious solution: single pre-filled syringes that are color-coded in a rainbow pattern that corresponds to the Broselow tape we all know and love. All you have to do is discard down to the color that corresponds to the size of the child and you are sure to be giving the right dose (best explained by looking at a picture).This study assessed the speed and accuracy of medication administration in simulated pediatric resuscitations. 10 teams consisting of physicians and nurses participated in a cross over study, so that they did one simulation with the new syringes and one without. Time to delivery of medications was quicker with the new syringes (47 versus 19 seconds, a difference of 27 seconds; 95%CI 21-33 seconds). Teams were also more accurate using the new color-coded syringes, with dosing errors occurring 17% of the time with the conventional approach and 0% of the time with the new syringes (absolute difference 17%; 95% CI 4-30%). Obviously a simulation based study is not real life – but I would actually expect more stress and therefore more errors during a real resuscitation.

Bottom line: Simple. Brilliant. Worth looking into.

The same group replicated basically the same study with similar results, but this time running the simulations with paramedics:

Stevens AD, Hernandez C, Jones S, et al. Color-coded prefilled medication syringes decrease time to delivery and dosing errors in simulated prehospital pediatric resuscitations: A randomized crossover trial. Resuscitation. 2015. PMID: 26247145

Fingers, toes, nose and hose. The epinephrine myth

Ilicki J. Safety of Epinephrine in Digital Nerve Blocks: A Literature Review. J Emerg Med. 2015. PMID: 26254284

I’ve talked about this before, but possibly not in the articles of the month. This is a systematic review looking at the safety of using epinephrine in digital nerve blocks. They found a total of 39 relevant articles, although only 12 of them were RCTs. They report no cases of necrosis attributable to epinephrine. In total, they found 2797 reported cases of digital nerve blocks using epinephrine without any important complications.

Bottom line: This was a myth. Epinephrine is almost certainly safe in fingers and toes if you think it might help you.

Physicians might not be so great around genitals

Stewart CM, Schoeman SA, Booth RA, Smith SD, Wilcox MH, Wilson JD. Assessment of self taken swabs versus clinician taken swab cultures for diagnosing gonorrhoea in women: single centre, diagnostic accuracy study. BMJ. 2012;345:e8107. PMID: 23236033 [free full text]

This is a prospective cohort of 3859 women aged 16 and over who presented to a single sexual health clinical in the UK. Before undergoing their consultation, they were asked to perform a vulvovaginal swab on themselves which was sent for nucleic acid amplification (NAAT). They then had the normal examination by the physician, with urethral and endocervical swabs sent, both for NAAT and culture. Overall, 2.5% of women tested positive for gonorrhoea (using a gold standard of either positive culture or two different NAAT markers being positive.) The self swabs were the most sensitive (99%), followed by physician swab for NAAT (96%), with the endocervical culture being the least sensitive (81%). In patients with symptoms suggestive of STI, both physician and self swab NAAT were 100% sensitive, but the endocervical culture was only 84% sensitive.

Bottom line: Self taken swabs were the most sensitive at detecting gonorrheal infection in these women

Schoeman SA, Stewart CM, Booth RA, Smith SD, Wilcox MH, Wilson JD. Assessment of best single sample for finding chlamydia in women with and without symptoms: a diagnostic test study. BMJ. 2012;345:e8013. PMID: 23236032 [free full text]

This is another study by the same group, using essentially the same methods, but this time focusing on Chlamydia. They included a total of 3973 women. Again, the self swab outperformed the physician performed swab with a sensitivity of 97% (95%CI 95-98%) as compared to 88% (95%CI 85-91%). The reported specificity of 100% is essentially meaningless because they were using the test itself as the gold standard. Similarly, the sensitivity of both tests might be lower than reported as they were not compared to any other gold standard.

Bottom line: Women do a better job collecting swabs for Chlamydia than physicians do

Overall Bottom line: If there is not another reason for a speculum exam, it does not have to be performed solely to obtain cervical swabs. Unfortunately urine testing was not included in these studies, so we do not know how it compares to self swabs.

Using tamsulosin for kidney stones? You must not be reading these e-mails.

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

This is a prospective, randomized, double-blind trial of 403 adults with CT confirmed ureteric stones comparing tamsulosin 0.4mg daily to placebo. There was no benefit for the primary outcome of stone expulsion at 28 days, with 87% passed in the tamsulosin group and 81.9% in the placebo group (5.1% difference; 95%CI -3 to 13%). There was a difference in a secondary outcome, distal stones sized 5-10mm, with 83.3% passing as compared to 61%. Of course this is a secondary outcome, so should not affect your practice. More importantly, the vast majority of these people should not being getting imaged, so you will never know the size of the stone, making this information clinically useless. There was no difference in urologic interventions, pain, or analgesia requirements.

Bottom line: Tamsulosin doesn’t help patients with ureteric stones.

Just in case that wasn’t enough to convince you

Berger D, Ross M, et al. Tamsulosin does not increase one-week passage rate of ureteral stones in Emergency Department patients. Am J Emerg Med. 2015. In Print. PMID:

This is yet another paper indicating tamsulosin has no role in ureterolithiasis. (Its too bad we can’t just start with the high quality studies, rather than following the predictable pattern of a handful of garbage studies showing questionable benefit followed by a lot of time and money spent on multiple good trials that prove that there was never any benefit.) This was a prospective, double-blind RCT with 127 adult patients with CT confirmed ureterolithiasis, randomized to either tamsulosin 0.4mg daily or placebo. There was no difference in the number of patients in whom the stone did not pass (tamsulosin 62.1% 95CI 49-75%; placebo 54.4% 95%CI 40-67%.) There was also no difference in pain scores or analgesic use.

Bottom line: There is no reason to be using tamsulosin in renal colic patients.

Sticking with urology: systematic reviews are pointless if there isn’t any original literature

Hulme P and Wylie K. Towards evidence based emergency medicine: best BETs from the Manchester Royal Infirmary. BET 1: tranexamic acid in life-threatening haematuria. Emerg Med J. 2015;32:(2)168-9. PMID: 25605262

They decided to do a review of tranexamic acid use in life-threatening hematuria. They managed to find 3 case reports and 1 prospective observational trial of 8 patients. There were no controls, so its hard to know what to make of the outcomes. It is good to know that none of the patients broke the emergency medicine rule that all bleeding stops… eventually.

Bottom line: For patients peeing blood, you are free to make it up as you go.

It just might be safe to pee in the Amazon

Bauer IL. Candiru–a little fish with bad habits: need travel health professionals worry? A review. J Travel Med. 2013;20:(2)119-24. PMID: 23464720

This is one of those really weird medical myths that I heard when I was younger and just stuck with me as a true. Apparently if you urinate in the Amazon river, there are little fish, called Candiru, that are attracted to the urine and will swim up your urethra. Once there, they have small barbs that lock them into place. These authors did an extensive review of both the scientific and non-scientific literature and report that there has never actually been a confirmed case of this occurring. For some reason, that is an amazing relief to me (and I have never even been to South America). Was I the only one raised on this particular myth?

Bottom line: Feel free to pee in the Amazon, if that’s your thing.

Don’t write off those vital signs just yet

Rodrigo GJ, Neffen H. Assessment of acute asthma severity in the ED: are heart and respiratory rates relevant? The American journal of emergency medicine. 2015. PMID: 26233619

This is a retrospective look at data that was collected prospectively as part of 7 other asthma trials done at a single emergency department. In total, 1192 adult patients were included. They compared heart rate and respiratory rate between two predefined groups: severe asthma (defined as an FEV1 31-50% of expected) and life threatening asthma (defined as an FEV1 <= 30% expected). The HR and RR were not different between the groups (mean of 102 and 22 respectively). They then use logistic regression to show that only FEV1 and O2 saturation were related to the outcome of admission to hospital. Based on this, they conclude that HR and RR are not determinants of acute asthma severity. I think this is probably the wrong interpretation. They use FEV1 as their definition of illness severity rather than hard outcomes. The lack of correlation between FEV1 and vital signs in this study might equally indicate that FEV1 is not a good indicator of disease severity. (It is a disease oriented, not a patient oriented outcome.) Although FEV1 was correlated with admission rates at this hospital, I imagine this just represents the local practices of the hospital: they believe in FEV1 and therefore admit you to hospital if your FEV1 is low, even if you had no other indications for admission.

Bottom line: I would still strongly suggest assessing patients clinically, including vital signs. Don’t let surrogate outcomes like the FEV1 or peak flow rates confuse you in asthma.

Another quick note on measuring asthma severity

Huff JS and Diercks DB. Use of Peak Expiratory Flow Rate Monitoring for the Management of Asthma in Adults in the Emergency Department. Revision of: American College of Emergency Physicians. Use of Peak Expiratory Flow Rate Monitoring for the Management of Asthma in Adults in the Emergency Department. Ann Emerg Med. 2001;38:198.

Without going into all the problems with the base literature on the use of peak flow rates in emergency medicine, I thought I would include the ACEP policy statement for reference. This is an update of their previous policy statement from 2001, with 27 new studies identified and reviewed. Their summary: “The use of PEFR monitoring has not been shown to improve outcomes, reliably predict need for admissions, or limit morbidity or mortality when used during the ED management of adult patients with acute exacerbations of asthma.”

Bottom line: Peak flow is a disease oriented outcome. Focus on patient oriented outcomes.

Sepsis and the rush to early antibiotics

de Groot B, Ansems A, Gerling DH. The association between time to antibiotics and relevant clinical outcomes in emergency department patients with various stages of sepsis: a prospective multi-center study. Critical care. 2015;19:194. PMID: 25925412

This is a prospective, multicentre observational cohort study including a total of 1,168 adult patients with sepsis (although their definition was anyone admitted to hospital with an infection who received IV antibiotics.) The overall mortality of their cohort was 10%, so significantly lower than the trials of severe sepsis we are used to. In this cohort, the length of time it took to give antibiotics was not associated with mortality. Much like the prior studies that showed a higher mortality in patients with delays to antibiotics, we must be aware of the mantra: association is not causation. In the current study, the delay to antibiotics might have been because patients had less severe infections. On the other hand, in prior studies in which antibiotic delays were associated with increased mortality, we might guess that patients were misdiagnosed or inappropriately dispositioned, which could be the true cause of increased mortality. Why did this study come to a different conclusion? One possibility is simply the timing of the studies. It is impossible to practice emergency medicine these days without a keen awareness of sepsis. This heightened awareness may lead to over-treatment in general, such that the few patients that don’t get early antibiotics really don’t require them.

Bottom line: Once you know there is a bacterial infection, obviously give antibiotics. However, there are many factors that will affect the timing of antibiotic administration and it should not be used as a quality of care metric.

We should probably just install CT scanners at triage

Claessens YE, Debray MP, Tubach F, et al. Early Chest CT-Scan to Assist Diagnosis and Guide Treatment Decision for Suspected Community-Acquired Pneumonia. Am J Respir Crit Care Med. 2015. PMID: 26168322

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

Bottom line: Just say no to CT scans for pneumonia

Glue works for abrasions too

Singer AJ, Chale S, Taylor M. Evaluation of a liquid dressing for minor nonbleeding abrasions and class I and II skin tears in the emergency department. The Journal of emergency medicine. 48(2):178-85. 2015. PMID: 25456777

This is an open label observational trial with no comparison group,using a convenience sample of 40 patients and 50 total wounds. The wounds were either abrasions or skin tears. They used a cheaper skin adhesive that has not been tested for tensile strength (unlike dermabond). If tensile strength was required, a steristrip was applied before the glue. In follow up, there were no infections and only one patient needed anything else: his glue peeled off on day 3 and he had bandage applied. Of course, with no comparison group, all we can say is “Mikey likes it”.

Bottom line: Glue works in skin. Perhaps there is a role for stocking the cheaper liquid bandaid products sold at drug stores?

A simple, life-saving therapy I didn’t know about

Jamtgaard L, Manning SL, Cohn B. Does Albumin Infusion Reduce Renal Impairment and Mortality in Patients With Spontaneous Bacterial Peritonitis? Ann Emerg Med. 2015. PMID: 26234193

I always find it funny that I finished residency with a head full of practices, like PPIs for GI bleeds, that are demonstrably unhelpful, but at the same time there are potentially life saving treatments that I have never heard about. Albumin for spontaneous bacterial peritonitis is one of those treatments. These authors report a systematic review and meta-analysis of RCTs studying albumin for SBP. In total they found 4 studies that include 288 patients with limited heterogeneity and no evidence of publication bias. Only 1 trial was blinded, but with a hard outcome of mortality that might be less important. The administration of albumin (the 2 largest trials made sure to give it within 6 hours, so this might be an ED therapy) was associated with less renal impairment (OR 0.21 95%CI 0.11-0.42) and lower mortality (OR 0.34 95%CI 0.19-0.60). Dosing varied among studies, but the largest trial used 1.5grams/kg IV at the time of diagnosis and 1gram/kg on day 3.

Bottom line: These are small numbers, but I will be giving albumin to SBP patients until we see more.

Diverticulitis is not necessarily a reason to promote antibiotic resistance

Chabok A, Påhlman L, Hjern F, Haapaniemi S, Smedh K; AVOD Study Group. Randomized clinical trial of antibiotics in acute uncomplicated diverticulitis. Br J Surg. 2012 Apr;99(4):532-9. PMID: 22290281

I included the meta-analysis a few months back, but here is a multicentre RCT of 623 adult patients with CT confirmed uncomplicated diverticulitis (defined as lower abdo pain plus fever, an elevated WBC, and CT consistent with diverticulitis but no abscess or free air) randomized to either antibiotics or not. They used pretty big gun antibiotics: either a 2nd/3rd gen cephalosporin plus metronidazole or a carbapenem or piperacillin-tazobactam. There were no statistical differences between the groups. There were 3 perforations in each group. There were 3 abscesses in the no antibiotics group compared to none in the antibiotics group. 10 patients (3.2%) that started with no antibiotics were given antibiotics eventually. There were no differences in length of hospital stays or recurrent diverticulitis.

Bottom line: It may well be that we don’t need antibiotics for diverticulitis, but these patients were all treated as inpatients, so its probably not up to us to make that call.

Read enough and I might sound like an antibiotic nihilist

Matthys J, De Meyere M, van Driel ML, De Sutter A. Differences among international pharyngitis guidelines: not just academic. Annals of family medicine. 5(5):436-43. 2007. PMID: 17893386 [free full text]

I love this article, probably because it hits on two of my favorite soapbox topics: guidelines and antibiotics for sore throats. They searched for any major pharyngitis guidelines and found 10 from different countries and organizations. Two people individually coded each guidelines for all the major recommendations. The key finding of this paper is that despite all of these guidelines being “evidence based”, they arrive at wildly different recommendations. Several guidelines recommend prescribing antibiotics only if the patient is very sick or high-risk, but others suggest treating almost everyone. (If you want to find a guideline that tells you not to give antibiotics, look to Belgium, the Netherlands, England, or Scotland. Interestingly, these were the guidelines that were written by family doctors, as compared to specialists – I knew we had brains.) Not a single publication, including the Cochrane review, was cited by all the guidelines.

Bottom line: Unfortunately, guidelines are rarely an adequate source of evidence based clinical information. (Also, for most parts of the world, pharyngitis probably doesn’t need antibiotics.)

When is a clot a clot?

Morgan C, Choi H. BET 1: Do patients with a clinically suspected subsegmental pulmonary embolism need anticoagulation therapy? Emergency medicine journal : EMJ. 32(9):744-7. 2015. PMID: 26293150

What is the evidence for treating subsegmental pulmonary emboli? This review identified 2 observational trials that included patients with subsegmental PEs who were not anticoagulated. Of the total of 47 patients with untreated subsegmental PEs, none had recurrent venous thromboembolism at 3 months. It would not be surprising if the harms of anticoagulation outweighed the benefits, but 47 patients can’t give enough information to decide either way.

Bottom line: We still really don’t know what to do, but any treatment benefit is likely to be small.

Positive troponins are negative for patients

Hakemi EU, Alyousef T, Dang G, Hakmei J, Doukky R. The prognostic value of undetectable highly sensitive cardiac troponin I in patients with acute pulmonary embolism. Chest. 2015;147:(3)685-94. PMID: 25079900

This is a retrospective chart review of 298 patients with confirmed PEs looking at the prognostic value of a positive high sensitivity troponin. 45% of the group had a negative troponin and therefore 55% had a positive trop. If the troponin was negative, no patients died, needed CPR, or received lytics. Among those with a positive trop, 6% died and 9% had either CPR or lytics given. For a retrospective study, this one is more likely than usual to give us a correct answer as death, lytics, troponin, and to a lesser extent CPR are objective values that are likely to be accurately recorded on a chart.

Bottom line: It’s not surprising, but a positive troponin is likely a bad prognostic factor for PE patients.

Less relevant than the pee fish article?

Morgenstern J, Hegele RA, Nisker J. Simple genetics language as source of miscommunication between genetics researchers and potential research participants in informed consent documents. Public Underst Sci. 2015;24:(6)751-66. PMID: 24751688

This isn’t directly related to emergency medicine, but I was excited that after a few years of being “in press” the article based on my master’s thesis actually got published in print. This was a study that used qualitative methods to analyze the language of informed consent documents in genetics research. The main finding was that apparently simple, easy to understand language can be a source of miscommunication. This can occur because different people or groups of people will understand words differently. An example would be geneticists conceptualizing “disease” as an entity that may or may not cause actual symptoms in the future based on genetic predispositions, while their research participants may think of a “disease” as something they definitely have and will notice the effects of. Might this be applicable to emergency medicine? I think so, but without any good evidence. However, we know that when patients hear the words “congestive heart failure” they envision something that will kill within days – after all, their heart is failing – but this is not necessarily what we are trying to convey with those words. Similarly, we might talk about “low risk chest pain”, but different people might understand those words to indicate a 2% risk, or a 1 in a thousand risk, or a 1 in a million risk.

Bottom line: Communication is essential in emergency medicine. It is an area that probably deserves more attention.

Cheesy Joke of the Month

What is the difference between surgeons and God?

God doesn’t think he is a surgeon

FOAM resource of the month

A new site and podcast that I think will benefit all emergency physicians is:

Rather than being focused on clinical aspects of care, this site is run by Jason Brooks, a performance enhancement coach, with the goal of improving performance (both in the ED and in life in general) and making it sustainable. High level athletes have coaches, why shouldn’t we? I really enjoyed the first few podcasts.

Enjoy the free open access medical education? Think you know someone else who might? It would help me a lot if you spread the word and shared this resource with just one of your friends or colleagues. Even easier, you could also help by just clicking the like button on Facebook. Thank you so much!

Post-intubation deterioration in asthma

When the intubated asthma patient crashes: A Brief guide to the first 10 minutes of resuscitation


The 16 year old female with severe asthma you resuscitated last week ended up getting intubated. After calling the pediatric ICU you headed back into an overcrowded sea of belly pains and sprained ankles. 30 minutes later you are called overhead because the patient is now severely hypotensive and hypoxic…

Continue reading “Post-intubation deterioration in asthma”

Management of life threatening asthma in the emergency department

An approach to the initial management of the asthma patient presenting to the emergency department in extremis


A 16 year old female with a history of severe asthma is brought to your community emergency department after a week of respiratory symptoms that have suddenly become much worse. She has been admitted to hospital 4 times this year, including one visit to the ICU. Her respiratory rate is 45 and she is using every accessory muscle she has, but she doesn’t appear to be moving much air. In fact, her lungs are silent to auscultation. She looks tired and the monitor shows her vitals as a heart rate of 140, blood pressure of 99/60, and an oxygen saturation of 88%…

Continue reading “Management of life threatening asthma in the emergency department”

Articles of the month (February 2015)

A monthly collection of the most interesting emergency medical literature I have encountered

Amoxicillin is the antibiotic of choice in pediatric pneumonia

Williams DJ et al. Narrow vs broad-spectrum antimicrobial therapy for children hospitalized with pneumonia. Pediatrics. 2013 Nov;132(5):e1141-8. PMID: 24167170

This was a retrospective record review of 15,564 admitted but not critically ill pediatric patients with community acquired pneumonia. They used propensity scoring, so the results could mean anything, but kids getting amoxicillin had the same outcomes as those with broad spectrum antibiotics such as cefotaxime or ceftriaxone. In fact, IDSA and peds infectious disease society both recommend narrow spectrum antibiotics, which is contrasted to the 90% of children in this study that were given broad spectrum.

Bottom line: Amoxicillin is probably best in pediatric pneumonia.


Hans and Franz want to pump you up (steroids for pediatric asthma)

Keeney GE et al. Dexamethasone for acute asthma exacerbations in children: a meta-analysis. Pediatrics. 2014;133(3)493-9. PMID: 24515516

A meta-analysis of 6 RCTs of prednisone versus dexamethasone in children with acute asthma exacerbations. There was no difference in relapse at 5 or 30 days. The dexamethasone group was less likely to vomit, both at home and in the ED. (Some studies used 2 doses of dex, some only used 1 versus generally 5 days of prednisone.)

Bottom line: Fewer doses and less vomiting, I am sold on dexamethasone. (My wife adds: “Well Duh! Pediapred tastes like s***. Dex is less volume and way easier to take.”)


The ugly stepchild of papers 1 and 2? Steroids for pneumonia

Blum, CA et al. 2015. Adjunct prednisone therapy for patients with community-acquired pneumonia: a multicentre, double-blind, randomised, placebo-controlled trial. Lancet (January 16). PMID: 25608756

I don’t buy what they are selling here, but I have already heard about this paper from at least 10 different sources, so you will likely hear about it as well. This is a large, multi-center, double blind RCT of 781 community acquired pneumonia patients, randomized to either get or not get prednisone 50mg PO daily for 1 week. It was a positive study, in that the primary outcome “time to clinical stability”, or ‘normal vital signs’, was 3 days in the prednisone group and 4.4 days with placebo. However, as important as vital signs are, are they really a patient oriented outcome? Has a patient ever said, I know I have this pneumonia, but what I really want is for my heart rate to be 95 instead of 105? Side effects: prednisone obviously caused hyperglycemia, but also (non statistically) doubled pneumonia associated complications. Previous studies showed higher recurrence rates with steroids.

Bottom line: Of course steroids make the numbers look better, but we are probably treating the doctor and not the patient here. Not for me.

Bottom line #2: If you are going to design a study, measure outcomes that matter.


Why do we use cervical collars?

Ala’a O et al. 2015. Should suspected cervical spinal cord injury be immobilised?: A systematic review. Injury Journal. (In press). PMID: 25624270

Like many of the things we do, this practice was started based on expert opinion in the pre-EBM era. There are a large number of cadaver and volunteer studies that show that C-collars really don’t prevent movement of the c-spine. What is the clinical evidence? There are a grand total of 8 observational studies ever done. In penetrating trauma, C-collar application was associated with an increase in mortality (OR 8.8), increase scene time, and concealment of neck injuries. In blunt trauma, one study showed that immobilization was associated with worse neurological outcomes. This is balanced by no evidence of benefit. They conclude “there is a clear need for large prospective studies to determine the clinical benefit of prehospital spinal immobilsation.”

Bottom line: I can’t imagine anyone changing their practice, but this does not speak very well to the benefits of cervical spine collars


Where are you drilling? Arm might be better than leg, or go straight towards the heart

Pasely J et al. 2015. Intraosseous infusion rates under high pressure: A cadaveric comparison of anatomic sites. Journal of Trauma and Acute Care Surgery 78(2)295-9. PMID: 25757113

Its a cadaver study, so take that as you will – but I am often drilling into dead people in code situations anyhow, so there might be some external validity here. They tried to infuse saline using a pressure bag, and the rates they could get were: 94ml/min in the sternum, 57ml/min in the humerus, and 30 ml/min in the tibia.

Bottom line: Humerus seems twice as fast as the tibia, so maybe that should be our go to spot? I probably wouldn’t suggest drilling sharp things into the sternum, but some people seem to think it’s OK.


Speaking of IOs – they are fine for RSI

Barnard EBG et al. 2014. Rapid sequence induction of anaesthesia via the intraosseous route: a prospective observational study. Emerg Med J (electronic ahead of print). PMID: 24963149

OK, also not really definitive by any means. A prospective observational study, with no controls, in a military setting. 34 patients had their RSI drugs pushed through an IO, first pass success in all but 1 (97%) and that patient was intubated on the second attempt. Although no control, 97% compares well with historical controls.

Bottom line: Go ahead and give RSI drugs through an IO if that is what you have


First RCT of massive transfusion protocol

PROPPR Holcomb et al. Transfusion of Plasma, Platelets, and Red Blood Cells in a 1:1:1 vs a 1:1:2 Ratio and Mortality in Patients With Severe Trauma. The PROPPR Randomized Clinical Trial. JAMA. 2015; 313(5)471-82. PMID: 25647203

After a bunch of theoretical stuff and some observational trials, this was the first ever RCT comparing different ratios of PRBCs, FFP, and platelets in a massive transfusion protocol. They compared 1:1:1 PRBCs, FFP and platelets to 2 units of PRBCs for each 1 unit of FFP and platelet equivalent. This was a negative trial, in that there was no difference in mortality between the two groups. However, some people have argued that their goal of a 10% reduction in mortality was too high, that the non-significant trends (including a 4.3% absolutely mortality reduction) favoured the 1:1:1 group, and secondary bleeding end points also favoured the 1:1:1 group. (This study design makes the inherent assumption that some transfusion ratio is a good thing, in that they did not include a usual care arm. While this has been the trendy thing of late, it is entirely based on flawed observational studies.)

Bottom line: This study will be used to support whatever pre-existing beliefs you had on the subject.


The new AAP bronchiolitis guidelines are very nihilistic (maybe realistic?)

Ralston SL et al. 2014. Clinical practice guideline: the diagnosis, management, and prevention of bronchiolitis. Pediatrics 134(5)e1474-502. PMID 25349312

Quick summary:

Do NOT give ventolin

Do NOT give epinephrine

Do NOT give hypertonic saline (in the ED)

Do NOT give corticosteroids

Diagnosis on Hx/Px, no routine chest xrays

While these guidelines are very evidence based, my EBM self is fighting with my practical self. If there are no treatments, peds is going to have to see 30 kids a day in the ED. Should we just set aside a room for them?

Bottom line: The AAP says don’t do anything for bronchiolitic kids

Two for the price of one: pediatric head injuries aren’t cured by CT

Lee LK et al. (PECARN). Isolated loss of consciousness in children with minor blunt head trauma. JAMA Pediatrics 2014; 168(9)837-43. PMID: 25003654

This is a secondary analysis of the PECARN head injury algorithm. Although overall your chance of clinically important head injury was 2.5% with LOC and only 0.5% without, if you only had LOC and no other PECARN risk factors, your risk of a clinically important injury was the back to baseline at 0.5%.

Bottom line: Loss of consciousness, in the absence of other worrisome findings, has a low risk of clinically important injury and CT scan is unnecessary. (Look at the whole patient, not just one aspect of the history or physical.)

Dayan PS et al. (PECARN). Association of traumatic brain injuries with vomiting in children with blunt head trauma. Annals of Emergency Medicine 2014;63(6)657-65. PMID: 24559605

Another secondary analysis of the PECARN head injury algorithm. Vomiting, without any other PECARN risk factors, had an overall incidence of clinically important injury of 0.2%

Bottom line: Vomiting, in the absence of other worrisome findings, has a low risk of clinically important injury and CT scan is unnecessary. (Look at the whole patient, not just one aspect of the history or physical.)


Start sending those stroke patients to the cath lab?

After multiple negative trials in the past, we get 3 new trials on endovascular treatment of stroke. (Given that we aren’t a stroke center and this isn’t going to be a decision you will make in the ED, it is probably best to just skip to the next section. But they will be talked about at cocktail parties.)

MR CLEAN Berkhemer OA et al. A randomized trial of intraarterial treatment for acute ischemic stroke. N Engl J Med. 2015;372:(1)11-20. PMID: 25517348

RCT comparing intra-arterial treatment versus usual care in stroke patients. Good neurological outcome (MRS 0-2 at 90 days) in intra-arterial group was 32% versus only 19% in the usual care group. (These are both way worse outcomes than other stroke trials, like NINDS)

EXTEND-IA Campbell BC et al. Endovascular Therapy for Ischemic Stroke with Perfusion-Imaging Selection. N Engl J Med. 2015. (Ahead of print) PMID: 25671797

RCT (phase II trial) of patients getting TPA within 4.5 hours with a middle cerebral or internal carotid clot AND evidence of salvageable brain tissue plus or minus endovascular therapy. Was stopped early after only 70 patients (they had to screen over 7,000 patients at 10 hospitals over 2 years to find these 70 patients – so they are highly selected to say the least). There were multiple primary outcomes (bad) but importantly if you got treated 80% had good neurological improvement at 3 days, versus only 37% of those without the endovascular treatment.

ESCAPE Goyal M et al. Randomized Assessment of Rapid Endovascular Treatment of Ischemic Stroke. N Engl J Med. 2015. (Ahead of print) PMID: 25671798

RCT of patients up to 12 hours with proximal anterior circulation occlusions and evidence of good collateral flow plus or minus endovascular therapy. Also stopped early, with a total of 316 patients (wanted 500 originally). They also only managed to recruit about 1 patient a month at each of the 22 hospitals involved – so also very highly selected patients. Functional independence (MRS 0-2) at 90 days was 53% in the endovascular arm and 29% in the usual care arm.

Overall bottom line: The benefit described in these trials is impressive. They are small and all have some flaws (stopping them early probably exaggerates the benefit), but I think it is likely they represent a true benefit. However, the number of eligible patients was tiny. Maybe they have finally found the subset of stroke patients that will benefit from revascularization – like the STEMI patient in a sea of chest pains.


Dr. Oz Sucks

Korownyk C et al. Televised medical talk shows–what they recommend and the evidence to support their recommendations: a prospective observational study. BMJ 2014;349:g7346. PMID: 25520234

OK, this isn’t really all that valuable or surprising, because anyone that has ever turned on a TV realizes that Dr. Oz rarely has anything credible to say, and seems to be a lot more interested in selling snake oil than actually helping patients. But in case any one was wondering, these authors prospectively evaluated the claims made on Dr. Oz and The Doctors, and even if a single case report was counted as “evidence” only 50% of the claims made on the shows had any evidence based backing, and a full 15% were completely contradictory to available evidence.

Bottom line: Don’t get your medical advice from a TV shill


Let’s review an older one: TTM, putting dead people on ice

Nielsen N et al. Targeted temperature management at 33°C versus 36°C after cardiac arrest. N Engl J Med. 2013 369(23):2197-206. PMID: 24237006

An ‘older’ paper that I am sure everyone has heard about, but it is good to include at least one practice changing quality study every month. After 2 small, low quality studies were published in 2002 (well before I started medical school in case you were wondering), the medical world went nuts for therapeutic hypothermia. But when I started in medicine, there were still some intelligent people (like Jerry Hoffman) who tried to remind us these were small studies, with inherent biases, and that a corner stone of science is replication. (There is a lesson here for so many other topics – but I don’t think I have the balls to mention NINDS and tPA.)

So this was a large, randomized control trial (not blinded) where 950 patients with ROSC after out of hospital cardiac arrest were either brought to 33 or 36 degrees Celsius. There was no difference in outcome.

The comments about this paper have been all over the map. The favorite statement by a lot of very smart people seems to be “this confirms that we desperately need to avoid fever, but 36 degrees is probably good enough.” I would point out, this study says nothing about avoiding fever. In fact, I don’t know of any study that compared fever or no fever post cardiac arrest. So people are either expressing their left over love of hypothermia, or is basing it on animal models, which are – well animal models.

Another approach would be to ask if we have any reason to believe this would work (the beginning of Bayesian reasoning). There were some animal models that support hypothermia, but probably more important is that hypothermia has been tested in humans for a number of conditions other than cardiac arrest – and it doesn’t seem to work.

Bottom line: There is no benefit from hypothermia post cardiac arrest. No one knows much about fever, but many people will talk about it a lot.

Bonus section: This Penn and Teller vaccination video should play continusouly in the waiting room

Cheesy Joke of the Month

It was a cold February so:

What is the difference between snowmen and snowwomen?