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….
The best emergency medicine articles that I came across in August 2016
Welcome to another edition of my favorite emergency medicine articles of the month. Once again, there will be an accompanying podcast with the talented and insightful Dr. Casey Parker on the BroomeDocs website where we briefly discuss these articles. Continue reading “Articles of the Month (August 2016)”
It’s an SGEM hot off the press! That means that you can comment on this article, and potentially see your comments published next to the original article in the official version of Academic Emergency Medicine. I am also excited to be joining Ken Milne with Corey Heitz as the official co-hosts of the SGEM HOP AEM sessions.
This week, we discuss a new trial on high sensitivity troponin with the lead author and all round excellent chap Dr. Rick Body. Have a listen to the episode and post any questions or comments you have for Dr. Body on the website. It’s a great way to get involved in post-publication peer review. What to you think? Is a single negative high sensitivity troponin as a rule-out strategy ready for prime time?
Body R, Mueller C, Giannitsis E. The Use of Very Low Concentrations of High-sensitivity Troponin T to Rule Out Acute Myocardial Infarction Using a Single Blood Test. Academic emergency medicine. 2016. PMID: 27178492 [Available free, full text here]
This is a secondary analysis of a large, prospective observational cohort (as part of the TRAPID-AMI trial.) They looked at 1282 adult patients presenting to the emergency department with new onset chest pain or symptoms suggestive of acute coronary syndrome that had peaked in the last 6 hours. The were looking at a high sensitivity troponin T on arrival and the primary outcome was acute MI at admission. The major secondary outcome was MACE (major adverse cardiac events). For the primary outcome of acute MI, using the primary strategy of an initial hs-cTnT below the limit of detection (<5ng/L) and no ECG ischemia, the test characteristics are:
- Sensitivity 99.1% (95%CI 96.7-99.5%)
- Specificity 43.9% (95%CI 40.9-46.9%)
- PPV 26.0% (95% CI 23.0–29.2%)
- NPV 99.6% (95%CI 98.5–100.0%)
- LR+ 1.76 (95%CI1.67 – 1.86)
- LR – 0.02 (95% CI 0.01 – 0.09)
In terms of the secondary outcome of MACE, the total 30 day event rate was 1.3%. The actual numbers were 6 MACE events, including only one death, no AMI and 3 revascularizations. I have always had a problem with considering revascularization as a adverse event, as it is so subjective. We know that revascularization is only helpful in the setting of an MI, so if someone goes for revascularization and didn’t have an MI is that really an important outcome, or is it just over-treatment?
My bottom line: Well, I don’t have high sensitivity troponin available, so I don’t have a use for this yet. There is no such thing as 0% risk. I think this information can be used to start a conversation with your patients. Within the context of shared decision making, I already send many patients home after a single negative troponin.
Another month and another edition of the articles of the month. However, this time I have some very exciting news. I have teamed up with Casey Parker (the brilliant, smooth-talking Australian physician, not the adult film star) to produce an audio version of these summaries. You will be able to find this podcast on http://broomedocs.com/, a great FOAM website that everyone should probably be following anyway. This is the first edition, and we will likely tweak the format with time, so if you have any feedback (hopefully more constructive than, “Justin, you have the perfect voice for silent films”), we would love for you to get in touch. Continue reading “Articles of the month (July 2016)”
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
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
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.
My monthly summary of the best reads from the emergency medicine literature
Welcome to the May 2016 edition of my favourite reads from the medical literature. This will probably be the last post on First10EM for a little while, as I plan to take a summer vacation as well as a prolonged Ireland stay for SMACC.
Gastro game changer
Freedman SB, Willan AR, Boutis K, Schuh S. Effect of Dilute Apple Juice and Preferred Fluids vs Electrolyte Maintenance Solution on Treatment Failure Among Children With Mild Gastroenteritis: A Randomized Clinical Trial. JAMA. 315(18):1966-74. 2016. PMID: 27131100
Kids just want to drink juice, but I’ve been told that if I let kids with gastro drink juice they will die (or something like that). This is a randomized, controlled non-inferiority trial out of the Hospital for Sick Children that compared an electrolyte solution to a combination of half strength apple juice in the ED and the child’s preferred fluid (juice or milk) at home. 647 children aged 6 to 60 months with acute (less than 96 hours) diarrhea or vomiting with mild dehydration were included. For the primary outcome, which unfortunately was a composite of a number of things including IV use, hospitalization, health care contact, and prolonged symptoms, the juice group had a ‘treatment failure’ rate of 16.7% as compared to 25.0% with the electrolyte solution (difference 8.3%; 97.5% CI 2% – infinity). Converting from a non-inferiority analysis to a superiority analysis resulted in a p value of 0.006. In other words, the juice group was statistically better than the electrolyte group. The biggest caveat is that these kids were not sick, so the results could be different in kids with even moderate dehydration.
Bottom line: I am no longer forcing kids to drink something they hate. Whatever their preferred liquid is, it will keep them hydrated.
This is another paper that will be featured on EMCases Journal Jam. If you have questions you want the author to answer, let me know.
I’m not so ENCHANTED
I am honestly surprised that I managed to read an entire article that started with the statement: “Thrombolytic therapy with intravenous alteplase (recombinant tissue-type plasminogen activator) at a dose of 0.9 mg per kilogram of body weight is an effective treatment for acute ischemic stroke, despite increasing the risk of intracerebral hemorrhage.” (This is a good reminder that when reading articles, it is often best to just skip the introduction. This section is just a non-systematic review of the topic, aka a statement of the author’s biases and opinions.) Moving beyond that, this was a multi-center, prospective, randomized, open-label, non-inferiority trial comparing usual dose tPA (0.9mg/kg) to low dose tPA (0.6mg/kg) in 3310 patient with acute ischemic stroke within 4.5 hours of onset. (As a reminder of how rarely we use this intervention, they screened 69305 patients to enroll those 3310.) The primary outcome was a composite of disability and death, defined as a modified rankin score of 2 or more. There was no statistically significant difference between the two groups (53.2% low dose and 51.1% usual dose, p=0.51). However, the 95% confidence intervals around this result go beyond a pre-specified definition, therefore they were unable to demonstrate non-inferiority. For the primary harm outcome, there was less intracranial bleeding in the low dose group (1.0% vs 2.1% (p=0.01) by SITS-MOST criteria or 5.9% vs 8.0% (p=0.02) by NINDS criteria). Death at 7 days was lower in the low dose group, but death at 90 days was unchanged. There are a number of problems with this study. I am not going to delve too deeply into the issues of comparing different doses of placebo. (A dose response relationship is generally something we look for in efficacious therapies.) There is really no reason to make a study like this open-label and unfortunately that introduces a number of potential biases. Almost all the follow up was done by phone and the modified Rankin score is notoriously unreliable. Finally, like almost all of this research, the authors have significant conflicts.
Bottom line: High dose, low dose, no dose? I like this line of research. Maybe we can just keep lowering the tPA dose until is diluted by a factor of 10300 and hand care of acute stroke patients over to the homeopaths.
Therapeutics Initiative. Benefits and harms of drugs for “neuropathic” pain. Therapeutics Letter. 2016; 96:1-2. [free full text]
We see a lot of chronic pain. More than a lot. Since I started practicing, the number of people on gabapentin or lyrica for their neuropathic pain has skyrocketed. But just how good are these medications? This therapeutics letter looks at the evidence summarized in 11 different Cochrane reviews, and the best evidence on the topic is:
- The evidence is weak (surprise anyone?) and the available RCTs have a high risk of bias
- At best, about 1/10 patients will achieve any meaningful reduction in pain
- Almost everyone has some side effects from these drugs
- If there is going to be a benefit, you will see in within about 1 week
- There does not seem to be any benefit in higher doses. (I think this is the most important takeaway, as I often see people on crazy escalating doses)
Bottom line: It might be reasonable to try these medicines, but start at a low dose, and recheck at 1 week if benefits outweigh side effects. If they don’t, stop the drug.
Black box on fluoroquinolones
FDA Drug Safety Communication: FDA advises restricting fluoroquinolone antibiotic use for certain uncomplicated infections; warns about disabling side effects that can occur together [available here]
So this isn’t research – it’s a notice of a new black box warning from the FDA. I am often skeptical of these warnings, as in some cases I think they have clearly done more harm than good (droperidol), but I think this one is worth knowing about. They say that “the serious side effects associated with fluoroquinolone antibacterial drugs generally outweigh the benefits for patients with sinusitis, bronchitis, and uncomplicated urinary tract infections who have other treatment options. For patients with these conditions, fluoroquinolone should be reserved for those who do not have alternative treatment options.” I would say this is pretty obvious, as there is no benefit of antibiotics in sinusitis and bronchitis. If a patient has a bad outcome and you are giving them a drug that has no chance of helping them, I would find that hard to defend.
Bottom line: Don’t use fluoroquinolones first in uncomplicated UTIs. Don’t use antibiotics at all in sinusitis or bronchitis.
But can we change our bad antibiotics habits?
Meeker D, Linder JA, Fox CR. Effect of Behavioral Interventions on Inappropriate Antibiotic Prescribing Among Primary Care Practices: A Randomized Clinical Trial. JAMA. 315(6):562-70. 2016. PMID: 26864410
We know that antibiotics don’t help for the vast majority of acute respiratory tract infections, but for some reason people just can’t help themselves. Every patient I see in the ED with a cough for 3 days is already on azithromycin or amoxicillin. They come to the ED because they can’t understand why they aren’t getting better on antibiotics. They think they need something stronger. This is a randomized controlled trial trying to get doctors to smarten up. In a total of 243 different clinicians, they tried three different interventions: 1) automated reminders that antibiotics are inappropriate and alternate treatment suggestions 2) the requirement of an ‘antibiotic justification note’ as part of the permanent record, and 3) intermittent e-mails comparing the performance of various doctors. Each clinician was exposed to anywhere from 0 to 3 of the interventions. The control group (no intervention) decreased their prescribing rate by 11% – a good demonstration of the Hawthorne effect. The reminders did nothing. Requiring a justification and being compared to peers decreased inappropriate antibiotic use.
Bottom line: Sadly, simply giving physicians information is not enough to change their practice. We need to be shamed into change. Maybe I should stop writing about the evidence and instead walk around personally shaming people?
Again – we don’t listen to good advice
Rosenberg A, Agiro A, Gottlieb M. Early Trends Among Seven Recommendations From the Choosing Wisely Campaign. JAMA internal medicine. 175(12):1913-20. 2015. PMID: 26457643
I love the choosing wisely campaign – except that we know doctors love to ignore good advice. This is a retrospective look at a billing database (so not necessarily the most reliable data, although the conclusions are believable.) They looked at 7 items that were listed by choosing wisely as being of minimal or no benefit (such as pre-op chest x-ray in the absence of concerning history, or imaging of low back pain without red flags) and looked to see if the number billed for changed over a 3 year period after the recommendations. They didn’t. (OK, imaging for headache went down from 14.9% to 13.4% – not exactly a clinically important change). Horrendously, the use of antibiotics for sinusitis remained at 84%!
Bottom line: Physicians just don’t change their practice when presented with good evidence or advice. It does makes me wonder if I should stop sending these e-mails – as they are probably not accomplishing anything.
Police officer: “Sir, How high are you?” Pothead: “No officer, its ‘Hi, how are you’”
Tefft BC et al. Prevalence of Marijuana Involvement in Fatal Crashes: Washington, 2010 – 2014. May 2016. Washington, DC: AAA Foundation for Traffic Safety. [free full text]
This is a report by the AAA Foundation for traffic safety. It retrospectively looked at a database from the Washington State Traffic Safety Commission. In Washington State, as many will know, marijuana became legal in December of 2012. This study looked at all motor vehicle collisions that resulted in death and the proportion who had THC (delta-9-tetrahydrocannabinol) in their blood on autopsy. They compared collisions in the 2 years before the new law to the 2 years after the law. Out of the total of 3031 fatal MVCs over 4 years, 303 (10%) involved drivers testing positive for THC. The percentage rose from 8.9% in 2013 (before the law) to 17% in 2014. Of the individuals with positive tests for THC, 39% also had alcohol on board, 16% had other drugs, and 10% had alcohol and other drugs (leaving 34% with only THC detected). There are some problems with this data, the biggest probably being that we don’t know what levels of THC correlate with being impaired. THC wasn’t measured in every case, and sometimes measurement was delayed. Also, the total number of fatalities didn’t increase, just the number with THC on board, so the marijuana could be a bystander rather than a cause of the collisions. However, the issue of impaired driving, and our lack of science to guide us, remains a huge issue as this popular legalization movement continues forward.
Bottom line: Don’t smoke and drive
Would you be surprised if this patient died?
George N, Phillips E, Zaurova M, Song C, Lamba S, Grudzen C. Palliative Care Screening and Assessment in the Emergency Department: A Systematic Review. Journal of pain and symptom management. 51(1):108-19.e2. 2016. PMID: 26335763
I really hate adding work for our overly taxed triage nurses, who end up doing a lot of our screening. However, we are awful at recognizing patients with palliative care needs. This is a review, and I don’t think it is strong enough to completely overhaul triage systems, so I won’t go into the details, but they do conclude that palliative care screening is feasible. My favorite screening question is “would you be surprised if this patient died during this visit or in the coming month?” If no, they should probably have palliative care involved. Of course, the harder part of this equation is actually having adequate palliative resources for all the patients who need them.
Bottom line: Emergency medicine is all about dying patients. Palliative care should be an essential part of our mindset. You can have a much bigger impact by starting palliative care than you ever will handing out antibiotics for sore throats.
Epinephrine is safe in fingers – is that old news by now?
Ilicki J. Safety of Epinephrine in Digital Nerve Blocks: A Literature Review. The Journal of emergency medicine. 49(5):799-809. 2015. PMID: 26254284
This is a systematic review looking at the use of epinephrine in digital blocks. It should be stated up front that the conclusions are only good as the original studies – and they aren’t great. In a total of 30 studies, they identify 2797 blocks performed with epinephrine without any complications. They conclude that epinephrine is safe to use in digital nerve blocks in healthy patients. (Although, to be fair, it probably doesn’t help most of the time.)
Bottom line: This is probably another classic myth, although the data isn’t actually strong enough to definitely conclude safety.
CT first for the scaphoid?
Yin ZG, Zhang JB, Gong KT. Cost-Effectiveness of Diagnostic Strategies for Suspected Scaphoid Fractures. Journal of orthopaedic trauma. 29(8):e245-52. 2015. PMID: 25756914
I hate cost-effectiveness studies. The results hinge on a huge number of assumptions that really can’t be confirmed. However, sometimes they provide some insight that can be interesting. In this study they compared the cost of working up scaphoid fractures using a number of different strategies, such as immediate CT, immediate MRI, MRI on day 3, bone scan on day 3, and x-ray at 2 weeks. Maybe counterintuitively, the immediate CT was the most cost effective approach followed by the immediate MRI. I am not sure that you can take these results to the bank, but it is a good reminder that there a number of costs that we often forget about. Although immediate CT seems expensive, to come to a follow-up visit the patient must miss work, pay for parking, and see another physician. Additionally, being in an unnecessary cast for 2 weeks could result in 2 weeks unnecessarily off work. It’s not time to change yet, but I wouldn’t be surprised if immediate definitive testing for the scaphoid became the standard in the future.
Bottom line: CT first for scaphoid fracture might actually be cheaper than standard practice.
Compassion and the good Samaritan study
Darley JM, Batson CD. “From Jerusalem to Jericho”: A study of situational and dispositional variables in helping behavior. Journal of Personality and Social Psychology. 27(1):100-108. 1973. [article]
This is a classic study from the psychology literature. It is a study of seminary students. Half were told they had to give a talk on the parable of the good Samaritan. The other half were told they had to give a talk on routine seminary jobs. Some students were told they were late for the talk and had to hurry, whereas others were told that they were on time. There was a plant on the way to the lecture hall: a man slumped in a doorway who moaned twice as the students walked by. Whether or not they had been thinking about the parable of the good Samaritan made no difference in whether or not they stopped. The only thing that influenced their decision to help was how hurried they felt. I see a clear connection to emergency medicine. Our job requires an incredible amount of compassion. However, simply thinking about compassion doesn’t seem to help. If we are rushed, we are less likely to be compassionate, whereas if we have time, we will use it. Unfortunately – how many people feel like they have a lot of free time in the emergency department? Managing our departments so physicians are not constantly run off their feet is probably a really good idea. (Of course, that is quite a reach from this research scientifically speaking – but it makes a lot of sense to me.)
Bottom line: Ensuring that physicians aren’t rushed might be crucial in increasing our ability to be compassionate on the job.
Cheesy Joke of the Month
I was sitting in a bar the other night when the waitress yelled out “does anyone know CPR?!”
I yelled back, “yeah, and I know the rest of the alphabet too.”
Everyone laughed. Well, except one guy.
#FOAMed of the month
How is it that one develops mastery? Cliff Reid provides some insight into deliberate practice in the context of getting his ass kicked.
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.
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?
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!
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?”