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.
There are new sepsis definitions! Hurrah?
There are new sepsis guidelines. I guess that warrants headline news, and there has been a lot of excitement on the medical internet. However, they are really just the opinions of 19 experts, aren’t backed by any quality prospective data, and probably shouldn’t change your management. If you want to read more, I wrote a full post on the topic: Sepsis 3.0 – No thank you
Bottom line: Talk about qSOFA if you want to sound in the know, but clinically I would ignore this paper
Procedural sedation consent: “Don’t worry, it’s super safe… it’s the Michael Jackson drug.”
Bellolio MF, Gilani WI, Barrionuevo P. Incidence of Adverse Events in Adults Undergoing Procedural Sedation in the Emergency Department: A Systematic Review and Meta-analysis. Academic emergency medicine : official journal of the Society for Academic Emergency Medicine. 23(2):119-34. 2016. PMID: 26801209
What exactly are the risks of procedural sedation? I know them qualitatively, but when having an informed choice conversation, are you able to quote the actual incidence? I know I couldn’t. This is a systematic review and meta-analysis to determine the incidence of adverse events in ED procedural sedation (limited to after 2004). They found 55 articles that covered 9652 procedural sedations. The most common adverse events: hypoxia (40/1000 but only 23/1000 were <90%), vomiting (16/1000), hypotension (15/1000), and apnea (12/1000). The serious adverse events: laryngospasm (4/1000), intubation (1.6/1000), aspiration (1.2/1000). If you are interested, they do break some of these numbers down based on what agent was used. There was a fair amount of heterogeneity in the definitions used in the original studies. Also pediatrics was excluded.
Bottom line: Procedural sedation is safe, but we should have a sense of these numbers for adverse events.
Still not using topical anesthetics for corneal abrasions? Could topical NSAIDs be a better choice?
Calder LA, Balasubramanian S, Fergusson D. Topical nonsteroidal anti-inflammatory drugs for corneal abrasions: meta-analysis of randomized trials. Academic emergency medicine : official journal of the Society for Academic Emergency Medicine. 12(5):467-73. 2005. PMID: 15860701 [free full text]
Most people have heard me rant about the myth that topical anesthetics are harmful in corneal abrasions. (If you haven’t, watch for an upcoming episode of EMCases Journal Jam, or come to the North York General Emergency Medicine Update this year.) However, an essential part of informed choice is reviewing the alternatives. How do topical NSAIDs perform in managing the pain of corneal abrasions? (Hat tip to Nadia Awad @Nadia_EMPharmD for sending me this paper.) This is a systematic review and meta-analysis that identified 11 RCTs (they don’t report the total sample size, but they were all relatively small studies). I find this paper a little hard to follow, because they report 5 high quality studies to be included in the meta-analysis, but then include only 3 in the forrest plot. Looking at just these 3 trials (n=459), topical NSAIDs did decrease pain, with a weighted mean difference of -1.30 (95%CI -1.56 to -1.03) on a 10 point pain scale. There are a few issues with this data. First: it’s hard to interpret a weighted mean difference, but the minimum change on a 10 point pain score generally considered to be clinically important is 1.4. Second: there is a lot of data that could not be included because of the way the original trials were reported. Third: although a formal funnel plot couldn’t be done, the authors admit a possibility of publications bias. Fourth: There is not enough data on safety, but there was at least one recurrent corneal erosion in the NSAID group. Fifth: The funding source of the original trials was not discussed, but it might be important considering that not a single one of the trials had allocation concealment. Finally: the comparison groups were varied, but often just placebo. It might be better to compare to the less expensive oral NSAIDs (or topical anesthetics.)
Bottom line: Topical NSAIDs may decrease pain from corneal abrasions, but I don’t think this data is enough to support using them over other agents (especially considering their cost.)
Xanthrochromia AKA hey Bob, does this look kinda yellow to you?
Chu K, Hann A, Greenslade J, Williams J, Brown A. Spectrophotometry or visual inspection to most reliably detect xanthochromia in subarachnoid hemorrhage: systematic review. Annals of emergency medicine. 64(3):256-264.e5. 2014. PMID: 24635988
This is a systematic review looking at studies (English only) that included patients presenting with a headache who had LPs where the CSF was sent for xanthrochromia. The gold standard for SAH was either angiography or follow up (not perfect). The studies were also highly heterogenous. Not surprisingly, visual inspection, AKA “hey Bob, does this look kinda yellow to you”, was not perfect, with a sensitivity of 84%, specificity of 96%, positive LR of 14.1 and negative LR of 0.35. However, the fancy spectrophotometry was not any better, with a sensitivity of 87%, specificity of 86%, positive LR of 6.6 and negative LR of 0.29. The included studies are not of high enough quality to be sure about any of those numbers. I just don’t understand how we don’t have something better yet – obviously some chemical is turning the fluid yellow – could the makers of super-ultra-sensitive troponins not just create a test that detects whatever this compound is?
Bottom line: Neither method of detecting xanthochromia is perfect, which adds another layer of complexity to the question of who we should be LPing after CT
Foley free pee?
Herreros Fernández ML, González Merino N, Tagarro García A. A new technique for fast and safe collection of urine in newborns. Archives of disease in childhood. 98(1):27-9. 2013. PMID: 23172785
Here is a contribution from Dr. Kate Bingham. You probably know how I feel about getting urines in pediatric patients. (If you don’t, you can read this.) However, for newborns, a urine culture is going to get done. This paper describes a technique to get the urine without a foley. Basically, feed kid, wait 25 min, clean genitals, hold baby under armpits (standing position), tap suprapubic area at 100/min for 30 seconds, then massage low back for 30 seconds. Repeat until pee is produced, and make sure you catch it in specimen bottle. Does it work? Of the 80 patients they tried this on (no comparison group), they were successful in 69 (86%). Median time to sample collection was 45 seconds. My only concern is if I miss the urine and I have to start all over again (maybe after antibiotics). This is interesting, but I so rarely get newborn urines, I will probably stick with a Foley for now.
Bottom line: You can make children pee using this technique. Not sure where to fit that into practice.
I never get tired of talking about nerve blocks
Dickman E, Pushkar I, Likourezos A. Ultrasound-guided nerve blocks for intracapsular and extracapsular hip fractures. The American journal of emergency medicine. 2015. PMID: 26809928
One rebuttal I have often encountered when talking about nerve blocks for hip fractures is that the block is less likely to work in certain fracture patterns. This is a secondary analysis of data from a previously conducted prospective RCT looking at 77 patients and comparing the effectiveness of ultrasound guided femoral nerve block in intracapsular versus extracapsular hip fractures. They were the same, and both were good (pain scores from 6.5/10 just under 4/10 at 2 hours).
Bottom line: I will keep using nerve blocks for all hip fractures. I’m not too worried about the location of the fracture.
Diverticulitis – antibiotics, seeds, or exercise
Stollman N, Smalley W, Hirano I, . American Gastroenterological Association Institute Guideline on the Management of Acute Diverticulitis. Gastroenterology. 149(7):1944-9. 2015. PMID: 26453777
This is the new acute diverticulitis guideline from the American Gastroenterological Association Institute (that was as hard to type as it was to read.) I found three of their recommendations interesting:
- “The AGA suggests that antibiotics should be used selectively, rather than routinely, in patients with acute uncomplicated diverticulitis. (Conditional recommendation, low quality of evidence).” (They note that so far the RCTs showing no benefit of antibiotics have been in inpatients with CT proven diverticulitis.)
- “The AGA suggests against routinely advising patients with a history of acute diverticulitis to avoid consumption of nuts and popcorn. (Conditional recommendation,very-low quality of evidence).” This is another one of those myths that we breeze over, but can really ruin patients’ quality of life
- “The AGA suggests advising patients with diverticular disease to consider vigorous physical activity. (Conditional recommendation, very low quality of evidence).” This makes sense, but it has not been part of my discharge script – until now.
People are going to start thinking I have a personal vendetta against antibiotics
Gágyor I, Bleidorn J, Kochen MM, Schmiemann G, Wegscheider K, Hummers-Pradier E. Ibuprofen versus fosfomycin for uncomplicated urinary tract infection in women: randomised controlled trial. BMJ (Clinical research ed.). 351:h6544. 2015. PMID: 26698878 [free full text]
Are antibiotics useful in UTI? I actually think so, but there have been previous studies that illustrate that a lot of UTIs will clear on their own. This was a randomized, double dummy, placebo controlled trial in which 484 women (18-65 years old) received either fosfomycin 3 grams PO or ibuprofen 400mg TID for three days. 69% of the women in the ibuprofen only group had complete resolution of their symptoms, and didn’t use any antibiotics in the next 28 days. That is impressive, but the antibiotics did provide some benefit. The ibuprofen group had more dysuria, based on their definition of ‘non-inferiority’, although the actual numbers for pain look pretty similar. Also there were 5 patients in the ibuprofen group who developed pyelonephritis as compared to only one in the fosfomycin group, although the difference was not statistically significant (p=0.12). I think antibiotics help, but this study reminds us that if you are on the fence, there is no reason to rush the antibiotics. Nearly 7/10 women will clear their UTI without your help. Also, if you call someone back with a positive culture, but they no longer have symptoms, they almost certainly don’t need treatment (assuming they aren’t pregnant).
Bottom line: Antibiotics probably help in UTIs, just not as much as you think
One more time: dex is as good as pred in asthma
Cronin JJ, McCoy S, Kennedy U. A Randomized Trial of Single-Dose Oral Dexamethasone Versus Multidose Prednisolone for Acute Exacerbations of Asthma in Children Who Attend the Emergency Department. Annals of emergency medicine. 2015. PMID: 26460983
I have covered this topic before, but repetition is key in both science and education. This was a randomized, open-label non-inferiority trial comparing a single dose of dexamethasone (0.3mg/kg orally) to prednisolone (1mg/kg PO for 3 days) in 245 children aged 2-16 with known asthma. There was no difference in the primary outcome of PRAM score at day 4 (0.91 versus 0.91; absolute difference 0.005; 95%CI 0.35 to 0.34), although I am not sure this is the most clinically important outcome. There weren’t any differences in the secondary outcomes, such as admission to hospital, length of stay, or return visits.
Bottom line: Once again, dex is great for asthma
Sticking with obvious pediatric topics: ondansetron works
Danewa AS, Shah D, Batra P, Bhattacharya SK, Gupta P. Oral Ondansetron in Management of Dehydrating Diarrhea with Vomiting in Children Aged 3 Months to 5 Years: A Randomized Controlled Trial. The Journal of pediatrics. 169:105-109.e3. 2016. PMID: 26654135
This is another paper I might have skipped because the results seem obvious, but I have recently seen it argued that we use ondansetron too liberally, so I guess it’s worth looking at. This is a well done, double blinded, placebo controlled RCT that enrolled 170 children between 3 months and 5 years of age with acute vomiting and diarrhea and clinical signs of dehydration. Although I worry that the primary outcome of failure of ORT, defined as features of some dehydration after 4 hours of ORT, is a little subjective, the trial was appropriately blinded and placebo controlled. Failure was 31% with ondansetron as compared to 61.5% with placebo, an absolute risk reduction of 30%, or a NNT of about 3. The 30% failure rate does seem high to me though, as I almost never have a kid fail ORT.
Bottom line: Surprise? Ondansetron does help vomiting kids orally hydrate.
When your heart leaves you speechless
Wasserman JK, Perry JJ, Dowlatshahi D. Isolated transient aphasia at emergency presentation is associated with a high rate of cardioembolic embolism. CJEM. 17(6):624-30. 2015. PMID: 25782453
This is a prospective cohort of 2360 TIA patients, 41 of whom had isolated aphasia at the time of presentation. Patients with isolated aphasia were twice as likely to have a cardiac source of embolism (22.0% vs 10.6%, p=0.037). This is strong, believable data, but I disagree with the authors’ conclusion that “emergency patients with isolated aphasia with a TIA warrant a rapid and thorough assessment for a cardioembolic source”. Non-aphasic patients still had an 11% chance of a cardiac source as compared to 22% with aphasia. Those two numbers clearly necessitate the exact same work up.
Bottom line: This is interesting trivia, but the association of aphasia with cardioembolism is clinically irrelevant.
A Salter Harris Myth Update
Boutis K, Plint A, Stimec J. Radiograph-Negative Lateral Ankle Injuries in Children: Occult Growth Plate Fracture or Sprain? JAMA pediatrics. 170(1):e154114. 2016. PMID: 26747077
Almost everyone has heard my Salter 1 Rant. Here is some more evidence. This is a prospective cohort of 140 children between 5 and 12 years of age with clinically suspected Salter Harris 1 fractures of the ankle. They were all treated with a removable splint (yes – the pediatric tertiary centers are doing this, so you can too). Then all of the children had an MRI at one week. Of the 140 children, 108 had ligamentous injuries on MRI. So take home #1: Despite the old dogma about ligaments being stronger than pediatric bone, children do get ligamentous injuries. Another 27 had isolated bone contusions. Only 4 children (3.0%, 95% CI 0.1-5.9%) actually has Salter Harris 1 fractures, and only 2 of those had any evidence of growth plate injury. And even more important, at 1 month follow up, there was no difference in function between those with MRI confirmed fracture and those without.
Bottom line: Salter Harris 1 fractures are rare and of questionable clinical relevance. Stop casting all these kids.
How important are c-spine precautions in submersion victims?
Watson RS, Cummings P, Quan L, Bratton S, Weiss NS. Cervical spine injuries among submersion victims. The Journal of trauma. 51(4):658-62. 2001. PMID: 11586155
This is a chart review of all submersion victims in the Seattle area between 1974 and 1996. There were a total of 2244 submersion victims, 34% of whom survived until hospital discharge. The prevalence of c-spine injury was 0.49% overall and 0.38% of those who received any medical care (not pronounced dead on scene). All people with c-spine injuries had obvious trauma. (One, for example, was a victim from a plane crash.) The biggest pitfall of this chart review is that someone with a spine injury from submersion might only be coded as a spine injury at discharge, because that was the important injury. These patients would not have been found by the review. However, this isn’t the only reason to be skeptical of cervical collars, so I have no problem removing it if I need better access to a submerged patient’s airway.
Bottom line: A submerged patient is very unlikely to have a c-spine injury if there isn’t obvious signs of trauma
Modified Sgarbossa criteria – now for more than just ECG geeks?
Meyers HP, Limkakeng AT, Jaffa EJ. Validation of the modified Sgarbossa criteria for acute coronary occlusion in the setting of left bundle branch block: A retrospective case-control study. American heart journal. 170(6):1255-64. 2015. PMID: 26678648
This paper is worth a look, if just to review some ECGs. It is a retrospective case-control study looking to validate a modified Sgarbossa rule for diagnosing STEMI in LBBB. This rule uses the ratio of ST elevation to S wave, rather than a set 5mm cut off for the anterior leads. Based on their 258 patients (only 9 with true STEMI), they report a better sensitivity than the original criteria (80% vs 49%, p<0.001) and equal specificity (99% vs 100% p=0.5). I already use these criteria, but I think we should be cautious about the current evidence base. This is retrospective and based on only 9 patients with acute coronary occlusion. More importantly, I wonder about the inter-rater reliability when we are taking multiple measurement in millimetres and dividing them. I already know from reading Dr Smith’s (excellent) blog that he frequently sees small amounts of ST depression that I would have missed or measured differently.
Bottom line: Like many things on the ECG, proportion probably matters, but it isn’t well studied.
How many diseases can you diagnose at 20 feet?
Narayana S, McGee S. Bedside Diagnosis of the ‘Red Eye’: A Systematic Review. The American journal of medicine. 128(11):1220-1224.e1. 2015. PMID: 26169885
I’ll just do a very quick note on this systematic review. because I found two numbers interesting. For ruling in “serious eye disease”, photophobia is good (LR+ = 8.3; 95%CI 2.7 – 25.9), but photophobia by indirect illumination (shining the light in the opposite eye) is amazing (LR+ = 28.8; 95%CI 1.8 – 459). The other number I found interesting is that bacterial conjunctivitis can almost be ruled out by “failure to observe a red eye at 20 feet”, although I am not sure there is huge clinical value of differentiating bacterial from viral conjunctivitis.
Bottom line: Worth a read through if you want to better understand your eye exam.
Hoegberg LC, Bania TC, Lavergne V. Systematic review of the effect of intravenous lipid emulsion therapy for local anesthetic toxicity. Clinical toxicology (Philadelphia, Pa.). 2016. PMID: 26853119
Another quick one: A systematic review of intralipid therapy in local anesthetic toxicity. It might be worth a deep dive, but the quality of the evidence is just so poor that it’s hard to trust any conclusions. For what it is worth, they conclude that intralipid appears effective, but there is no evidence that it is more effective than vasopressors.
My real reason for bringing this up is to lament the quality of toxicology literature in general. I have heard people argue that it would be unethical to randomize these dying patients in order to get good data, but we have to remember that in the absence of good data, the care they are getting is entirely random anyway. The random factor is just the belief of the physician who happens to be on that day. Although these are rare cases, we have the technology to gather data from around the world. We need to do better.
Bottom line: I will probably use intralipid if this comes up, but we really need better science in toxicology.
Osteoarthritis is not an xray diagnosis
This study looks at data from 2 large cohort studies: The Framingham study (in which every patient over 50 got a pelvic x-ray, regardless of symptoms) and the osteoarthritis initiative study (which included 4366 patients thought to be at risk for knee arthritis, and again everyone was imaged.) Xray is not predictive of osteoarthritis. In Framingham, only 15.6% of patients with frequent pain (clinical OA) had radiographic evidence of OA and only 20.7% of those patients whose xray indicated OA actually had clinical symptoms. Likewise, In the osteoarthritis initiative study, only 9.1% of patients with symptoms had xray changes, and only 23.8% of patients with xray changes had symptoms.
Bottom line: Xray cannot provide any valuable information about osteoarthritis of the hip
Should we let residents use Google on shift?
Kim S, Noveck H, Galt J, Hogshire L, Willett L, O’Rourke K. Searching for answers to clinical questions using google versus evidence-based summary resources: a randomized controlled crossover study. Academic medicine : journal of the Association of American Medical Colleges. 89(6):940-3. 2014. PMID: 24871247 [free full text]
Rushing around the emergency department, it is obviously tempting to just google something rather than find a specific medical resource, but how good is google? This is a prospective, randomized, controlled, crossover study in which they took 48 internal medicine residents and asked them to answer a series of medical questions. They were randomized to answer 5 questions, either using Google or using their choice of DynaMed, First Consult, or Essential Evidence Plus. They then ‘crossed over’ and answered another 5 questions using the opposite tool. This was repeated for 48 weeks. There was no difference in time to correct answer, response rate, or accuracy. They found answers for 80% of the questions, but the correct answer in only 60%.
Bottom line: Google doesn’t look worse than these specific medical tools, but I really want my residents to be right more than 60% of the time in an open book test.
Cheesy Joke of the Month
What did the pirate say on his 80th birthday?
#FOAMed of the Month
I often lament the current state of medical science. Data is unreported. Secondary outcomes are reported as primary. Harm outcomes aren’t even mentioned.
COMPare (CEBM Outcome Monitoring Project) is a group of people trying to fix this. You can read a short blog post about it here. In short, they compare publications with the original trial protocol, report discrepancies, write letters to the editors, and report on their progress. It’s an interesting project that is worth checking out.
However, I guess that’s not really education, so I will add a second #FOAMed selection:
Have ever heard of BRASH syndrome? You’ve probably seen it, but if you are like me, you had probably never heard of it before this month:
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.
I am on vacation this month and I am trying hard to make it a real vacation. So I am not reading any medical literature, even if I have a minute while wait in line at the Colosseum (yes, that has happened before.) Instead of my usual articles of the month, covering the most recent papers I have been reading, I am going to summarize a few classic emergency medicine papers. Most people probably know all of these already, but it is good to review the evidence behind our practice occasionally. Enjoy…
ARDSnet: The rise of low tidal volumes
Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. The Acute Respiratory Distress Syndrome Network. N Engl J Med. 2000;342:(18)1301-8. PMID: 10793162
This is an RCT of 861 mechanically ventilated patients with ALI or ARDS, designed as a 2×2 trial (half of which examined ketoconazole, but that arm of the trial was stopped due to lack of efficacy.) They randomized patients to the now famous ARDSnet protocol of low tidal volumes to limit plateau pressures or a traditional ventilation strategy. The ARDSnet protocol resulted in a decrease in mortality (31.0% versus 39.8%, p=0.007).
Bottom line: Follow the protocol for your intubated patients. (Copy available here)
GUSTO II: Cath versus lytics
Andersen HR, Nielsen TT, Rasmussen K, et al. A comparison of coronary angioplasty with fibrinolytic therapy in acute myocardial infarction. N Engl J Med. 2003;349:(8)733-42. PMID: 12930925 [free full text]
This is a substudy of GUSTO II. It is a prospective multicenter RCT that assigned 1138 patients presenting within 12 hours of their STEMI to either primary angioplasty or thrombolytic (t-PA). For their primary outcome, a composite of death, non-fatal reinfarction, and non-fatal stroke at 30 days, angioplasty had better outcomes (8.0% versus 13.7% p<0.001). This effect was entirely from non-fatal re-infarction, as stroke and death were unchanged – a problem with composite outcomes. Interestingly, and something that we don’t tend to talk about a lot, or at least I was never taught, there was no difference in that composite outcome at 6 months (14.1 vs 16.1% statistically insignificant.)
Bottom line: Angioplasty provides some early benefit over fibrinolytics, but we may be over-emphasizing its benefit. For many centers and specific patients, lytics may still be the best option. (See, I am not just totally against t-PA. I am just for evidence.)
Analgesics for abdominal pain
Mahadevan M, Graff L. Prospective randomized study of analgesic use for ED patients with right lower quadrant abdominal pain. Am J Emerg Med. 2000;18:(7)753-6. PMID: 11103723
I only know the medical world after this study was published, but many people probably still remember the days when surgeons wouldn’t let us treat patients’ pain because it would ruin the abdominal exam. This is a randomized, double blind trial of 68 adult patients suspected of appendicitis, given either tramadol or placebo. Of course, pain was lower in the group that received pain medication (although not by a lot). Not only was the analgesic group examinable, but actually had more specific exams for appendicitis.
Bottom line: If patients are in pain, doctors treat it. I am not sure what surgeons do.
NEXUS: A pain in the neck?
Hoffman JR, Mower WR, Wolfson AB, Todd KH, Zucker MI. Validity of a set of clinical criteria to rule out injury to the cervical spine in patients with blunt trauma. National Emergency X-Radiography Utilization Study Group. N Engl J Med. 2000;343:(2)94-9. PMID: 10891516 [free full text]
Jerry Hoffman. Nexus. This is classic emergency medicine. We should all know the criteria:
- No midline cervical tenderness
- No focal neurological deficit
- Normal alertness
- No intoxication
- No painful, distracting injury
This was a prospective, multi-centre observational study that included 34,069 patients who had imaging of the cervical spine after blunt trauma and found 818 cervical spine injuries. The decision instrument was 99% sensitive (95%CI 98-99.6%) with a negative predictive value of 99.8% (95%CI 98.0-99.6%). Of course, you do have to accept the specificity of 12.9%. Only 1 of the 8 patients missed had a clinically significant injury that required a surgical intervention.
Bottom line: You can remove c-collars quickly and safely in many patients. If you are EMS, you can probably even prevent them from going on in the first place.
Cage match: NEXUS versus the Canadian C-spine rule
This is a prospective cohort of 8283 alert trauma patients comparing NEXUS and Canadian c-spine rule (CCR). There were 169 (2%) clinically important c-spine injuries. Unfortunately, in 10% of patients physicians did not properly apply the CCR – they did not assess range of motion as defined. Of course, if a decision instrument is easily misinterpreted (even with the Hawthorne effect of a study) that will affect its utility in practice. How you interpret this study depends entirely on what you do with those patients. If you exclude them, the CCR looks great (sensitivity of 99.4% and specificity of 45.1%). However, if you include them, the sensitivity drops to 95.3% and specificity is 50.7%. This compares with NEXUS with a sensitivity of 90.7% and a specificity of 36.8%. Obviously, neither test performed quite as well as we would hope in this cohort.
Bottom line: It is important to know the specifics of clinical decision instruments, including inclusion and exclusion criteria. I still use a combination of both these tools in clinical practice.
Dexamethasone for croup
This is a multi-centre, double-blind, RCT that included 720 children with mild croup who were randomized to either dexamethasone 0.6mg/kg to a max dose of 20mg or placebo. The children receiving dexamethasone had less “return to medical care” – 7.3% versus 15.3%, p<0.001. The dexamethasone group also had slightly lower croup scores and slept about 1 hour a day more than the placebo group.
Bottom line: A NNT of 14 to prevent further visits is your primary benefit in mild croup.
Dexamethasone for croup: But what dose?
Geelhoed GC, Macdonald WB. Oral dexamethasone in the treatment of croup: 0.15 mg/kg versus 0.3 mg/kg versus 0.6 mg/kg. Pediatr Pulmonol. 1995;20:(6)362-8. PMID: 8649915
This is an RCT of admitted pediatric patients with croup comparing dexamethasone at doses of 0.15mg/kg, 0.3mg/kg, and 0.6mg/kg. There was no difference in length of hospital stay, use of epinephrine, croup scores, or representations for medical care.
Bottom line: Dexamethasone at 0.15mg/kg is probably just as good as the 0.6mg/kg we have all been taught.
Rehydration – isn’t that what the GI tract was designed for?
Fonseca BK, Holdgate A, Craig JC. Enteral vs intravenous rehydration therapy for children with gastroenteritis: a meta-analysis of randomized controlled trials. Arch Pediatr Adolesc Med. 2004;158:(5)483-90. PMID: pubmed
This is a meta-analysis of 16 RCTs involving 1545 children comparing enteral to intravenous rehydration in the treatment of gastroenteritis. (Unfortunately, I have been told by medical-legal types that I am never allowed to make the diagnosis of “gastroenteritis”, so I am not sure who I will apply this study to.) Oral rehydration has significantly fewer adverse events including death and seizure (relative risk 0.36 95%CI 0.14-0.89) and significantly reduced hospital stay (mean decrease of 21 hours). There was no difference in the treatment effect or weight gain. The failure rate for enteral therapy was 4%.
Bottom line: You should almost never place an IV in a pediatric gastroenteritis patient.
Steroids for meningitis
de Gans J, van de Beek D; European Dexamethasone in Adulthood Bacterial
Meningitis Study Investigators. Dexamethasone in adults with bacterial
meningitis. N Engl J Med. 2002 Nov 14;347(20):1549-56. PMID: 12432041 [free full text]
This is a multi-centre, prospective RCT of 301 adult patients suspected of having meningitis and having either cloudy CSF, bacteria on CSF gram stain, or a CSF white count >1000. Patients were randomized to either placebo or dexamethasone 10mg IV q6h for 4 days, with the first dose give 20 minutes before or concurrently with antibiotics (initial antibiotics treatment was with amoxicillin alone). 7% of the steroid group died as compared to 15% of placebo (p=0.04; relative risk 0.48 95%CI 0.24-0.96). There was no difference in hearing loss or focal neurologic abnormalities. Note that steroids and antibiotics were given only after waiting for the CSF results.
Bottom line: Steroids decreased mortality, but did not affect neurologic outcomes
However, although this study is considered a classic, it is at odds with the bulk of the literature.
Brouwer MC, McIntyre P, Prasad K, van de Beek D. Corticosteroids for acute bacterial meningitis. The Cochrane database of systematic reviews. 6:CD004405. 2013. PMID: 23733364
This review covers 25 studies involving 4121 participants. Steroids did NOT provide a statistically significant mortality advantage (RR 0.90, 95%CI 0.80-1.01). However, steroids did results in less hearing loss (RR 0.74 95%CI 0.63-0.87).
Bottom line: Unfortunately steroids will probably not save any lives. Given the potential delay to antibiotics if steroids are used as they were in the de Gans study, it is unclear how important the hearing changes are. The steroids for meningitis question is not definitively answered, but any benefits are likely to be small.
Sepsis: early goal directed therapy
This paper is now infamous and certainly created its share of controversy. It was a randomized trial of 263 patients with severe sepsis who were randomized to a specific treatment protocol or standard care. Rivers was able to show a significant mortality benefit, 30.5% versus 46.5% (p=0.009). However, we now know that the specifics of his protocol were mostly irrelevant, you just need to care for your sepsis patients.
Bottom line: Dr. Rivers pushed sepsis care forward around the world, but there is no reason to be using this protocol anymore.
Restrictive transfusion policy
Hébert PC, Wells G, Blajchman MA, et al. A multicenter, randomized, controlled clinical trial of transfusion requirements in critical care. Transfusion Requirements in Critical Care Investigators, Canadian Critical Care Trials Group. N Engl J Med. 1999;340:(6)409-17. PMID: 9971864 [free full text]
This is a multi-centre RCT based in Canada that included 838 adult ICU patients with anemia Hb≤ 90 (excluding chronic anemia and patients with active blood loss.) They were randomized to either a restrictive transfusion strategy (transfuse with a Hb <70; target 70-90) or a liberal strategy (transfuse with a Hb < 10; target 100-120). There was not a statistical significance in 30 day mortality (18.7% in restrictive versus 23.3% in liberal). The liberal group had higher in-hospital mortality and cardiac events (secondary outcomes.)
Bottom line: This was the first of many studies showing we give too much blood.
OPALS: What is the value of ACLS?
This is a prospective multicenter before and after trial that compared outcomes with basic life support paramedic crews (who had defibrillators) to advanced crews with full ACLS training including medications. 5638 adult patients with out of hospital cardiac arrest were included. The advanced life support paramedics resulted in more ROSC (12.9% vs 18%) and more admissions to hospital (10.9% vs 14.6%), but without any change in survival to hospital discharge (5.0 vs 5.1%).
Bottom line: This is one of the many studies that indicate ACLS and particularly the use of medications in cardiac arrest don’t work, but might actually be harmful.
Cheesy joke of the month
Why didn’t skeleton cross the road?
He has no guts
A brief review of the management of the child with severe airway obstruction from croup in the emergency department
Another night shift in the emergency department and you are 25 minutes into the history of a patient with 17 chief complaints when your phone rings. “You are needed in resus 3”. Initially, it feels good to be called away for a ‘real emergency’. However, when you lay eyes on the little girl, you kick yourself for that thought. Her mother says she has had a mild cough and runny nose for a few days, but tonight she developed a very harsh, barking cough and noisy breathing. Now she is barely making noise at all. The one year old in front of you is using every accessory muscle she has, breathing at least 60 times a minute, and the monitor shows an oxygen saturation of 88%.
A monthly collection of the most interesting emergency medical literature I have encountered
Amoxicillin is the antibiotic of choice in pediatric pneumonia
Williams DJ et al. Narrow vs broad-spectrum antimicrobial therapy for children hospitalized with pneumonia. Pediatrics. 2013 Nov;132(5):e1141-8. PMID: 24167170
This was a retrospective record review of 15,564 admitted but not critically ill pediatric patients with community acquired pneumonia. They used propensity scoring, so the results could mean anything, but kids getting amoxicillin had the same outcomes as those with broad spectrum antibiotics such as cefotaxime or ceftriaxone. In fact, IDSA and peds infectious disease society both recommend narrow spectrum antibiotics, which is contrasted to the 90% of children in this study that were given broad spectrum.
Bottom line: Amoxicillin is probably best in pediatric pneumonia.
Hans and Franz want to pump you up (steroids for pediatric asthma)
Keeney GE et al. Dexamethasone for acute asthma exacerbations in children: a meta-analysis. Pediatrics. 2014;133(3)493-9. PMID: 24515516
A meta-analysis of 6 RCTs of prednisone versus dexamethasone in children with acute asthma exacerbations. There was no difference in relapse at 5 or 30 days. The dexamethasone group was less likely to vomit, both at home and in the ED. (Some studies used 2 doses of dex, some only used 1 versus generally 5 days of prednisone.)
Bottom line: Fewer doses and less vomiting, I am sold on dexamethasone. (My wife adds: “Well Duh! Pediapred tastes like s***. Dex is less volume and way easier to take.”)
The ugly stepchild of papers 1 and 2? Steroids for pneumonia
Blum, CA et al. 2015. Adjunct prednisone therapy for patients with community-acquired pneumonia: a multicentre, double-blind, randomised, placebo-controlled trial. Lancet (January 16). PMID: 25608756
I don’t buy what they are selling here, but I have already heard about this paper from at least 10 different sources, so you will likely hear about it as well. This is a large, multi-center, double blind RCT of 781 community acquired pneumonia patients, randomized to either get or not get prednisone 50mg PO daily for 1 week. It was a positive study, in that the primary outcome “time to clinical stability”, or ‘normal vital signs’, was 3 days in the prednisone group and 4.4 days with placebo. However, as important as vital signs are, are they really a patient oriented outcome? Has a patient ever said, I know I have this pneumonia, but what I really want is for my heart rate to be 95 instead of 105? Side effects: prednisone obviously caused hyperglycemia, but also (non statistically) doubled pneumonia associated complications. Previous studies showed higher recurrence rates with steroids.
Bottom line: Of course steroids make the numbers look better, but we are probably treating the doctor and not the patient here. Not for me.
Bottom line #2: If you are going to design a study, measure outcomes that matter.
Why do we use cervical collars?
Ala’a O et al. 2015. Should suspected cervical spinal cord injury be immobilised?: A systematic review. Injury Journal. (In press). PMID: 25624270
Like many of the things we do, this practice was started based on expert opinion in the pre-EBM era. There are a large number of cadaver and volunteer studies that show that C-collars really don’t prevent movement of the c-spine. What is the clinical evidence? There are a grand total of 8 observational studies ever done. In penetrating trauma, C-collar application was associated with an increase in mortality (OR 8.8), increase scene time, and concealment of neck injuries. In blunt trauma, one study showed that immobilization was associated with worse neurological outcomes. This is balanced by no evidence of benefit. They conclude “there is a clear need for large prospective studies to determine the clinical benefit of prehospital spinal immobilsation.”
Bottom line: I can’t imagine anyone changing their practice, but this does not speak very well to the benefits of cervical spine collars
Where are you drilling? Arm might be better than leg, or go straight towards the heart
Pasely J et al. 2015. Intraosseous infusion rates under high pressure: A cadaveric comparison of anatomic sites. Journal of Trauma and Acute Care Surgery 78(2)295-9. PMID: 25757113
Its a cadaver study, so take that as you will – but I am often drilling into dead people in code situations anyhow, so there might be some external validity here. They tried to infuse saline using a pressure bag, and the rates they could get were: 94ml/min in the sternum, 57ml/min in the humerus, and 30 ml/min in the tibia.
Bottom line: Humerus seems twice as fast as the tibia, so maybe that should be our go to spot? I probably wouldn’t suggest drilling sharp things into the sternum, but some people seem to think it’s OK.
Speaking of IOs – they are fine for RSI
Barnard EBG et al. 2014. Rapid sequence induction of anaesthesia via the intraosseous route: a prospective observational study. Emerg Med J (electronic ahead of print). PMID: 24963149
OK, also not really definitive by any means. A prospective observational study, with no controls, in a military setting. 34 patients had their RSI drugs pushed through an IO, first pass success in all but 1 (97%) and that patient was intubated on the second attempt. Although no control, 97% compares well with historical controls.
Bottom line: Go ahead and give RSI drugs through an IO if that is what you have
First RCT of massive transfusion protocol
PROPPR Holcomb et al. Transfusion of Plasma, Platelets, and Red Blood Cells in a 1:1:1 vs a 1:1:2 Ratio and Mortality in Patients With Severe Trauma. The PROPPR Randomized Clinical Trial. JAMA. 2015; 313(5)471-82. PMID: 25647203
After a bunch of theoretical stuff and some observational trials, this was the first ever RCT comparing different ratios of PRBCs, FFP, and platelets in a massive transfusion protocol. They compared 1:1:1 PRBCs, FFP and platelets to 2 units of PRBCs for each 1 unit of FFP and platelet equivalent. This was a negative trial, in that there was no difference in mortality between the two groups. However, some people have argued that their goal of a 10% reduction in mortality was too high, that the non-significant trends (including a 4.3% absolutely mortality reduction) favoured the 1:1:1 group, and secondary bleeding end points also favoured the 1:1:1 group. (This study design makes the inherent assumption that some transfusion ratio is a good thing, in that they did not include a usual care arm. While this has been the trendy thing of late, it is entirely based on flawed observational studies.)
Bottom line: This study will be used to support whatever pre-existing beliefs you had on the subject.
The new AAP bronchiolitis guidelines are very nihilistic (maybe realistic?)
Ralston SL et al. 2014. Clinical practice guideline: the diagnosis, management, and prevention of bronchiolitis. Pediatrics 134(5)e1474-502. PMID 25349312
Do NOT give ventolin
Do NOT give epinephrine
Do NOT give hypertonic saline (in the ED)
Do NOT give corticosteroids
Diagnosis on Hx/Px, no routine chest xrays
While these guidelines are very evidence based, my EBM self is fighting with my practical self. If there are no treatments, peds is going to have to see 30 kids a day in the ED. Should we just set aside a room for them?
Bottom line: The AAP says don’t do anything for bronchiolitic kids
Two for the price of one: pediatric head injuries aren’t cured by CT
Lee LK et al. (PECARN). Isolated loss of consciousness in children with minor blunt head trauma. JAMA Pediatrics 2014; 168(9)837-43. PMID: 25003654
This is a secondary analysis of the PECARN head injury algorithm. Although overall your chance of clinically important head injury was 2.5% with LOC and only 0.5% without, if you only had LOC and no other PECARN risk factors, your risk of a clinically important injury was the back to baseline at 0.5%.
Bottom line: Loss of consciousness, in the absence of other worrisome findings, has a low risk of clinically important injury and CT scan is unnecessary. (Look at the whole patient, not just one aspect of the history or physical.)
Dayan PS et al. (PECARN). Association of traumatic brain injuries with vomiting in children with blunt head trauma. Annals of Emergency Medicine 2014;63(6)657-65. PMID: 24559605
Another secondary analysis of the PECARN head injury algorithm. Vomiting, without any other PECARN risk factors, had an overall incidence of clinically important injury of 0.2%
Bottom line: Vomiting, in the absence of other worrisome findings, has a low risk of clinically important injury and CT scan is unnecessary. (Look at the whole patient, not just one aspect of the history or physical.)
Start sending those stroke patients to the cath lab?
After multiple negative trials in the past, we get 3 new trials on endovascular treatment of stroke. (Given that we aren’t a stroke center and this isn’t going to be a decision you will make in the ED, it is probably best to just skip to the next section. But they will be talked about at cocktail parties.)
MR CLEAN Berkhemer OA et al. A randomized trial of intraarterial treatment for acute ischemic stroke. N Engl J Med. 2015;372:(1)11-20. PMID: 25517348
RCT comparing intra-arterial treatment versus usual care in stroke patients. Good neurological outcome (MRS 0-2 at 90 days) in intra-arterial group was 32% versus only 19% in the usual care group. (These are both way worse outcomes than other stroke trials, like NINDS)
EXTEND-IA Campbell BC et al. Endovascular Therapy for Ischemic Stroke with Perfusion-Imaging Selection. N Engl J Med. 2015. (Ahead of print) PMID: 25671797
RCT (phase II trial) of patients getting TPA within 4.5 hours with a middle cerebral or internal carotid clot AND evidence of salvageable brain tissue plus or minus endovascular therapy. Was stopped early after only 70 patients (they had to screen over 7,000 patients at 10 hospitals over 2 years to find these 70 patients – so they are highly selected to say the least). There were multiple primary outcomes (bad) but importantly if you got treated 80% had good neurological improvement at 3 days, versus only 37% of those without the endovascular treatment.
ESCAPE Goyal M et al. Randomized Assessment of Rapid Endovascular Treatment of Ischemic Stroke. N Engl J Med. 2015. (Ahead of print) PMID: 25671798
RCT of patients up to 12 hours with proximal anterior circulation occlusions and evidence of good collateral flow plus or minus endovascular therapy. Also stopped early, with a total of 316 patients (wanted 500 originally). They also only managed to recruit about 1 patient a month at each of the 22 hospitals involved – so also very highly selected patients. Functional independence (MRS 0-2) at 90 days was 53% in the endovascular arm and 29% in the usual care arm.
Overall bottom line: The benefit described in these trials is impressive. They are small and all have some flaws (stopping them early probably exaggerates the benefit), but I think it is likely they represent a true benefit. However, the number of eligible patients was tiny. Maybe they have finally found the subset of stroke patients that will benefit from revascularization – like the STEMI patient in a sea of chest pains.
Dr. Oz Sucks
Korownyk C et al. Televised medical talk shows–what they recommend and the evidence to support their recommendations: a prospective observational study. BMJ 2014;349:g7346. PMID: 25520234
OK, this isn’t really all that valuable or surprising, because anyone that has ever turned on a TV realizes that Dr. Oz rarely has anything credible to say, and seems to be a lot more interested in selling snake oil than actually helping patients. But in case any one was wondering, these authors prospectively evaluated the claims made on Dr. Oz and The Doctors, and even if a single case report was counted as “evidence” only 50% of the claims made on the shows had any evidence based backing, and a full 15% were completely contradictory to available evidence.
Bottom line: Don’t get your medical advice from a TV shill
Let’s review an older one: TTM, putting dead people on ice
Nielsen N et al. Targeted temperature management at 33°C versus 36°C after cardiac arrest. N Engl J Med. 2013 369(23):2197-206. PMID: 24237006
An ‘older’ paper that I am sure everyone has heard about, but it is good to include at least one practice changing quality study every month. After 2 small, low quality studies were published in 2002 (well before I started medical school in case you were wondering), the medical world went nuts for therapeutic hypothermia. But when I started in medicine, there were still some intelligent people (like Jerry Hoffman) who tried to remind us these were small studies, with inherent biases, and that a corner stone of science is replication. (There is a lesson here for so many other topics – but I don’t think I have the balls to mention NINDS and tPA.)
So this was a large, randomized control trial (not blinded) where 950 patients with ROSC after out of hospital cardiac arrest were either brought to 33 or 36 degrees Celsius. There was no difference in outcome.
The comments about this paper have been all over the map. The favorite statement by a lot of very smart people seems to be “this confirms that we desperately need to avoid fever, but 36 degrees is probably good enough.” I would point out, this study says nothing about avoiding fever. In fact, I don’t know of any study that compared fever or no fever post cardiac arrest. So people are either expressing their left over love of hypothermia, or is basing it on animal models, which are – well animal models.
Another approach would be to ask if we have any reason to believe this would work (the beginning of Bayesian reasoning). There were some animal models that support hypothermia, but probably more important is that hypothermia has been tested in humans for a number of conditions other than cardiac arrest – and it doesn’t seem to work.
Bottom line: There is no benefit from hypothermia post cardiac arrest. No one knows much about fever, but many people will talk about it a lot.
Bonus section: This Penn and Teller vaccination video should play continusouly in the waiting room
Cheesy Joke of the Month
It was a cold February so:
What is the difference between snowmen and snowwomen?