There are a lot of recurrent themes in this month’s edition (which has clearly shifted from being a monthly to a bimonthly publication). Podcast over on BroomeDocs.
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 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?”
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
Early HIV infection presents as a mononucleosis-like infection, making it very difficult to diagnose. Although I generally dislike using the emergency department for public health screening, if HIV is not diagnosed during this initial stage, many years may pass before it is diagnosed, not only hurting the patient, but also putting their many contacts at risk. This is a letter to the editor describing a study where they retrospectively took all blood samples that were sent for epstein barr virus at Massachusetts General Hospital and tested them for HIV RNA. They found that 1.2% (7/563) has an acute HIV infection and another 0.8% (4/563) had chronic HIV.
Bottom line: This is well above the threshold for screening for HIV. Perhaps monospot and HIV testing should be paired?
1 more: Non specific viral illness or acute HIV?
Pincus JM, Crosby SS, Losina E, King ER, LaBelle C, Freedberg KA. Acute human immunodeficiency virus infection in patients presenting to an urban urgent care center. Clinical infectious diseases : an official publication of the Infectious Diseases Society of America. 37(12):1699-704. 2003. PMID: 14689354 [free full text]
Sticking with the same topic, these authors tested all patients presenting with viral symptoms and 1 or more HIV risk factors at their urban urgent care centre for HIV. (They were very broad with their HIV risk factors: any sexual contact, any injection drug use, any crack use, or any alcohol use in the last 2 months.) Of the 499 patients included, 5 (1.0%) were diagnosed with an acute HIV infection and another 6 (1.2%) were diagnosed with chronic HIV. They did not have any false positives.
Bottom line: Depending on your work environment, it may be worth screening for HIV in patients with viral illnesses.
It’s all about that aVL
Bischof JE, Worrall C, Thompson P, Marti D, Smith SW. ST depression in lead aVL differentiates inferior ST-elevation myocardial infarction from pericarditis. The American journal of emergency medicine. 2015. PMID: 26542793
Is that Inferior ST elevation indicative of STEMI? Or is it pericarditis? aVL might hold the key. This is a retrospective look at 3 different groups. Of 154 patients with a final diagnosis of inferior STEMI, all 154 had some degree of ST depression in aVL. Of the 49 patients with pericarditis, 49 had some degree of inferior ST elevation, but none had any ST depression in aVL. There was a third cohort with subtle inferior ST elevation (less than 1mm) but confirmed vessel occlusion on cath. Of these 54 patients, 49 had ST depression in aVL. The authors conclude that ST depression is highly sensitive for inferior STEMI and specific for pericarditis.
Bottom line: I will certainly look at aVL, but would love to see this repeated prospectively
If you want to read more about this and see some example ECGs, check out the blog post by senior author Dr Steve Smith: http://hqmeded-ecg.blogspot.ca/2015/11/new-paper-published-on-significance-of.html
Cold – the pure green coffee (ask Dr. Oz) of the brain
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)?
“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:
Crack the chest. Get crucified. (John Hinds) – I know I have recommended this one before, but it is worth more than one watch.