First10EM on theSGEM!

I was honoured to be invited on The Skeptics Guide to Emergency Medicine this week to discuss the FLORALI trial with Ken Milne.

The episode is: SGEM#135: The Answer My Friend is Blowin’ in your Nose – High Flow Nasal Oxygen

 

I had previously mentioned this paper in the May 2015 edition of my Articles of the Month.

My Bottom line: High flow nasal oxygen seems to be as good as NIPPV or facemask oxygen (in this select group of patients). This is enough for me to try this with alert pneumonia patients who don’t obviously need intubation.

I personally like high flow nasal oxygen for a lot of these patients, because it seems to be more comfortable, allow for easier communication, and provides the option of oral intake. This study certainly is not enough to justify the expense of purchasing one of these units if you don’t already have one. However, if there is already one in your department, I say give it a trial.

Two major questions remain, in my mind:

  1. In these hypoxic patients, when should we be intubating? Does placing a patient on high flow nasal oxygen simply delay the inevitable intubation? Might that lead to worse outcomes?
  2. Was this study underpowered to show a benefit? They powered the study to show a 20% decrease in intubation and the study was negative. However, the point estimates were better for high flow nasal oxygen in all categories. Also, a secondary outcome of mortality at 90 days was statistically better in the high flow group. We need more trials to determine the real effect of high flow nasal oxygen.

For a proper skeptical take on this paper, go listen to the episode!

 

Reference

Frat JP, Thille AW, Mercat A, et al. High-Flow Oxygen through Nasal Cannula in Acute Hypoxemic Respiratory Failure. N Engl J Med. 2015. PMID: 25981908

Articles of the month (August 2015)

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

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

Simple and brilliant: A pediatric rainbow

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

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

Bottom line: Simple. Brilliant. Worth looking into.

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

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


Fingers, toes, nose and hose. The epinephrine myth

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

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

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


Physicians might not be so great around genitals

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

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

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

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

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

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

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


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

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

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

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


Just in case that wasn’t enough to convince you

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

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

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


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

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

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

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


It just might be safe to pee in the Amazon

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

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

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


Don’t write off those vital signs just yet

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

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

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


Another quick note on measuring asthma severity

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

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

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


Sepsis and the rush to early antibiotics

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

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

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


We should probably just install CT scanners at triage

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

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

Bottom line: Just say no to CT scans for pneumonia


Glue works for abrasions too

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

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

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


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

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

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

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


Diverticulitis is not necessarily a reason to promote antibiotic resistance

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

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

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


Read enough and I might sound like an antibiotic nihilist

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

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

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


When is a clot a clot?

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

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

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


Positive troponins are negative for patients

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

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

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


Less relevant than the pee fish article?

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

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

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


Cheesy Joke of the Month

What is the difference between surgeons and God?

God doesn’t think he is a surgeon


FOAM resource of the month

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

https://www.phenomenaldocs.com/

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


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

Articles of the month (April 2015)

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

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

Troponin is king – why even send an CK?

Le RD et al. Clinical and financial impact of removing creatine kinase-MB from the routine testing menu in the emergency setting. Am J Emerg Med. 2015;33(1):72-5. PMID: 25455047

This is an observational study, looking at a period before and after CK-MB was removed from an automatic order set. Out of 6444 cases included in the study, there were only 17 cases with a positive CK-MB fraction and a negative troponin. All 17 were ultimately determined by the treating physicians to have non-ACS causes (ie, they were false positives). So, CK-MB was not clinically helpful. Removing it from the order set dropped ordering by 80% and saved the hospital about $47,000 a year.

Bottom line: We might want to keep this one in our back pocket for the next time the hospital demands cost savings – dropping the CK helps us and saves money


Speaking of troponin – high sensitivity and the 1 hour rule out

Reichlin T et al. Prospective validation of a 1-hour algorithm to rule-out and rule-in acute myocardial infarction using a high-sensitivity cardiac troponin T assay. CMAJ. 2015 (In Print). PMID: 25869867

This prospective observational study of 1320 chest pain patients attempted to validate a 1 hour rule out protocol. Using high sensitivity troponins, patients ruled out if they had trop of 12ng/L or less and a 1 hour delta of 3mg/L or less. They ruled in with a trop of 52ng/L or more or a 1 hour delta of 5ng/L or more. Everyone else was put in longer observation. It was a relatively high risk cohort, with 17% overall having an acute MI. 60% of patients were able to be ‘ruled out’ at 1 hour, and only one of those patients (0.1%) ultimately had an MI. It ruled in 16% of the patients at 1 hour, with 78% being true positives. The remaining 24% that couldn’t be ruled in or ruled out had an 18% chance of an MI – so the prolonged observation work up makes a lot of sense.

Bottom line: This could work (if we had the right assay), but I think our rule in rate for MI is way less than 17% – so this strategy could actually increase our testing and admissions without benefit to our patients 


How often to you order pregnancy tests just for medication use?

Goyal MK et al. 2015. Underuse of pregnancy testing for women prescribed teratogenic medications in the emergency department. Academic Emergency Medicine (in print). PMID: 25639672

A retrospective study using the NHAMCS database (notoriously poor data) but still raises an interesting point. Looking at all women who were given or prescribed FDA pregnancy category D or X medications, only 22% had pregnancy testing done. (I will note that this is one area where I don’t trust NHAMCS at all – there was one study where 50% of patients diagnosed with ectopic pregnancies didn’t have a pregnancy test done – but then how did they get diagnosed with ectopic pregnancy?) This also doesn’t tell us how many of these women were actually pregnant, so it is difficult to tell how big an issue this really is.

Bottom line: Are you checking for pregnancy before giving Advil to ankle sprains in ambulatory care? Should we have quicker point of care testing to make this feasible? Does it matter? 


Non-news of the month: there happen to be some bacteria in your blood post CPR

Coba V et al. The incidence and significance of bacteremia in out of hospital cardiac arrest. Resuscitation. 2014 Feb;85(2):196-202. PMID: 24128800

I ignored this one when it first came around a year ago, but I have heard it repeated so many times, with strange conclusions, that I guess it should be included. This is a prospective observational study of 250 adult out of hospital cardiac arrest patients who they drew blood cultures on in the ED, 38% of whom were found to be bacteremic. But come on, you get bacteremic after brushing your teeth. Are you surprised this happened with crash airways, CPR, and broken ribs? They note that mortality was higher in the bacteremic group, but again, in dead people as mucous membranes break down, I expect more bacteremia. This is a silly surrogate outcome, unless someone can show early antibiotics save lives.

Bottom line: Try to ignore this paper when it is mentioned over and over again in the coming years


Another one with strange conclusions

Schuch S et al. Effect of oximetry on hospitalization in bronchiolitis: a randomized clinical trial. JAMA. 2014;312(7):712-8. PMID: 25138332

This is a double blind RCT from Sick Kids, where they took 213 infants with bronchiolitis and randomized them to either have an accurate pulse ox reading, or one that displayed values that were 3 points higher than the actual value. When higher oxygen sats were shown, admissions went down from 41% to 25%. This is obvious – we admit hypoxic patients. I have heard lots of doctor bashing around this, but what this study didn’t show was that it was safe to discharge home babies with borderline sats. I admit a child with a sat of 89% because they are right at top of the steep part of the oxygen desaturation curve, and I am worried they might get worse. Telling me that the sat is 92% might change my mind – but how do we know those kids didn’t go on to have complications? This study certainly didn’t look for it. (I will admit we probably over-rely on the sat – but until someone proves 89% is safe with no treatment or monitoring, I will keep admitting.)

Bottom line: If you lie to doctors about important clinical parameters, their decisions change


Once again, forget about atypicals in the treatment of community acquired pneumonia

Postma DF et al. Antibiotic treatment strategies for community-acquired pneumonia in adults. NEJM. 2015;372(14):1312-1323. PMID: 25830421

Despite the theory of needing to cover for atypical organisms, this study is another in a long line of papers that all say the same thing. This is a large, multi-centre cluster-randomized trial of 2283 adult patients with community acquired pneumonia who did not require ICU care. They randomized months to to either use beta-lactam monotherapy, a beta-lactam plus a macrolide, or a fluroquiolone. The primary outcome was mortality at 90 days, and was statistically the same in all groups (but actually 1.9% higher in the macrolide group.) Secondary outcomes, like length of stay, were also the same. (The authors do note that during the time of the study, there was a low incidence of atypicals. However, multiple previous studies have show atypicals don’t matter, except maybe legionella.)

Bottom line: We already knew this, but are always taught differently: you don’t need to add a macrolide to beta-lactams to treat community acquired pneumonia. (Empiric evidence trumps petri dishes every day.) 


Dental abscesses are like all abscesses – antibiotics don’t help

Tichter AM and Perry KJ. Are antibiotics beneficial for the treatment of symptomatic dental infections? Ann Emerg Med. 2015;65(3):332-3. PMID: 25477181

This systematic review was able to find 2 RCTs comparing antibiotics (both pen-VK) versus placebo for apical perdiodonitis or abscess. There was no difference in pain, swelling, or infection progression at 24, 48, or 72 hours. All patients were given oral analgesics and ultimately had the definitive management – surgical pulpectomy.

Bottom line: Dental infections are one more diagnosis where we give antibiotics but probably shouldn’t


Was this patient’s DVT caused by an unknown cancer?

Robertson L et al. Effect of testing for cancer on cancer- and venous thromboembolism (VTE)-related mortality and morbidity in patients with unprovoked VTE. Cochrane Database Syst Rev. 2015 [Epub ahead of print] PMID: 25749503

We know that cancer is a risk factor for VTE, so we frequently ask ourselves should we be searching for a potential cancer in people with an apparently unprovoked VTE? This is a Cochrane review, but they could only identify 2 studies with a total of 396 patients – so interpret with caution. Using a a specific suite of screening tests post VTE diagnosis, they did make more early diagnoses of cancer than in patients with usual care, but they were unable to find any cancer specific mortality benefit. (They didn’t even measure all cause mortality.)

Bottom line: This fits well with most screening data we have, in that we can always find more cancer if we look, but we are not good at changing mortality or quality of life (for the better)


More is not always better

Minotti V et al. A double-blind study comparing two single-dose regimens of ketorolac with diclofenac in paindue to cancer. Pharmacoptherapy. 1998;18(3):504-8. PMID: 9620101

With recent drug shortages, the topic of the appropriate ketorolac dose was raised a number of times around the department. This is a double blind RCT comparing ketorolac 10mg or 30mg or diclofenac 75mg (all IM) in adults with acute cancer pain. All three provided equal and reasonable relief over 6 hours. I just picked one, but this is consistent with multiple other studies showing 10 mg = 30 mg of ketorolac.

Bottom line: Toradol 10mg is probably identical to 30mg


We know we don’t talk to our patients – but apparently we can’t even talk to each other

Venkatesh AK et al. Communication of Vital Signs at Emergency Department Handoff: Opportunities for Improvement. Annals of Emergency Medicine. 2015 (in press). PMID: 25805116

This was a prospective observational study looking at ED handoffs. Out of 1163 total handoffs observed, 117 patients had episodes of hypotension, and they were not mentioned for 66 patients (42%). There were 156 patients with hypoxia, and 116 (74%) were not mentioned. (These numbers seem unbelievable, and if you look closer, attending docs rarely left this info out, it was primarily residents.)

Bottom line: Handoffs are important. Take a minute to review all the information. And we should probably be emphasizing this in resident education


Should H.pylori be an ED problem?

Meltzer AC et al. Treating Gastritis, Peptic Ulcer Disease, and Dyspepsia in the Emergency Department: The Feasibility and Patient-Reported Outcomes of Testing and Treating for Helicobacter pylori Infection.  Annals of Emergency Medicine. 2015 (in press). PMID: 25805114

This is a prospective cohort study on a convenience sample of ultimately 212 patients. The attending doctor was asked if the patients’ symptoms could be attributed to gastritis, PUD, or dyspepsia, and if so they tested for H.pylori and treated if positive. 23% of the patients tested positive for H.pylori. With treatment, they were able to eradicate H. pylori in 41% of those patients. At 3 weeks, the pain scores seemed to have decreased about the same amount no matter what had happened to you. For me, this could go either way. I worry about the false positives and a potential anchoring bias where we say this pain couldn’t be ACS just because the patient is H.pylori positive. However, our patients may benefit from early treatment (though they didn’t in this study).

Bottom line: H. Pylori is probably the cause of a lot of the symptoms we see, but we currently don’t have any good strategy to address that


The “rocket launcher” hip reduction technique

Dan M et al. Rocket launcher: A novel reduction technique for posterior hip dislocations and review of current literature. Emergency Medicine Australasia. 2015 (in press). PMID: 25846901

This is a case report of 6 patients, so I wouldn’t pay any attention to the EBM side of things. They describe a technique for hip reduction I hadn’t heard of, and may be helpful for some, especially if you are to short to make the Captain Morgan easy. Essentially, you adjust the height of the bed so that you can put the patients knee over your shoulder. The foot faces forward, like you might picture someone holding a bazooka or ‘rocket launcher’. This allows you to use you shoulder as a fulcrum, and lift with your legs.

Bottom line: Captain Morgan is still my go to, but its nice to have this as a backup


Another reduction technique: syringe rolling for mandible reduction

Gorchynski J et al. The “syringe” technique: a hands-free approach for the reduction of acute nontraumatic temporomandibular dislocations in the emergency department. J Emerg Med. 2014;47(6):676-81. PMID: 25278137

This technique involves placing a syringe (5 or 10cc) between the posterior molars, and then turning the syringe in the direction that would push the mandible backwards (as if a wheel were rolling forward along the bottom teeth). In this prospective, convenience sample, they were successful in 30/31 attempts, with 24 of those attempts taking less than a minute. You can do this without sedation. In fact, patients can do this for themselves.

Bottom line: I haven’t tried it yet – let me know if you do


Angioedema of the bowel: I’ve probably seen it, but I’ve never diagnosed it

Bloom AS and Schranz C. Angiotensin-Converting Enzyme Inhibitor–Induced Angioedema of the Small Bowel—A Surgical Abdomen Mimic. Journal of Emergency Medicine. 2015 (In Press). PMID: 25886983

Just a case report, but I include it because we probably see this, but I had never really heard of it. We won’t necessarily rule it in, but in recurrent abdo pain, I might consider stopping an ace inhibitor as a trial. They note that CT findings, if you happen to get one, include ascites, small bowel thickening and straightening, and dilatation without obstruction.

Bottom line: Medication side effects should be part of the differential diagnosis for every chief complaint


Old people have high D-dimers – don’t send them if you can avoid it, but if you have to…

Righini M et al. Age-adjusted D-dimer cutoff levels to rule out pulmonary embolism: the ADJUST-PE study. JAMA 2014;311(11):1117-1124. PMID: 24643601

This is a prospective observational study of 3346 patients with suspected PE (the total rule in rate was 19%), of which a total of 331 had D-dimers greater than 500, but less than age x 10. Using the adjusted D-dimer level of age x 10, they would have missed 1 PE out of 331 patients (0.3%). Unfortunately, not everyone got the gold standard test (CTPA), so it is possible they missed a few more that we don’t know about. However, if the test threshold for PE generally is 2%, and the elderly are particularly prone to renal problems from CT contrast, avoiding 331 CTPAs at the cost of one missed diagnoses might be worth it. The other major problem is that D-dimers are not standardized and there are multiple different assays.

Bottom line: If the D-dimer is less than age x 10, the risk is probably low enough to stop further testing. I use this to (and this is crazy, I know) talk to my patients about whether or not to scan


Clowns cause pregnancy; AKA completely irrelevant paper of the month 

Friedler S et al. The effect of medical clowning on pregnancy rates after in vitro fertilization and embryo transfer. Fertility and Sterility. 2011;95(6):2127-2130. PMID: 21211796

This is just too good not to include. Give women IVF, and then let them play with a clown and 36.4% become pregnant. Remove the clown: only 20.2%.

Bottom line: What exactly are they doing with that clown? 


#FOAMed suggestion of the month

If you haven’t come across it yet, Scott Weingart and Steve Smith put together a list of all the reasons for cath lab activation, including the very subtle details. There are 2 podcasts summarizing, and one very handy pdf. Also, Steve Smith is just giving away his amazing ECG textbook. All can be found at:

Cheesy Joke of the Month

Why don’t you ever see Hippos hiding in trees?
Because they are really f***ing good at it.

Articles of the month (February 2015)

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

Amoxicillin is the antibiotic of choice in pediatric pneumonia

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

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

Bottom line: Amoxicillin is probably best in pediatric pneumonia.

 

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

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

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

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

 

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

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

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

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

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

 

Why do we use cervical collars?

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

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

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

 

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

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

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

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

 

Speaking of IOs – they are fine for RSI

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

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

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

 

First RCT of massive transfusion protocol

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

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

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

 

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

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

Quick summary:

Do NOT give ventolin

Do NOT give epinephrine

Do NOT give hypertonic saline (in the ED)

Do NOT give corticosteroids

Diagnosis on Hx/Px, no routine chest xrays

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

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

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

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

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

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

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

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

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

 

Start sending those stroke patients to the cath lab?

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

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

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

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

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

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

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

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

 

Dr. Oz Sucks

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

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

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

 

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

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

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

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

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

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

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

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

http://www.kevinmd.com/blog/2015/01/watch-2-magicians-destroy-anti-vaccine-movement-90-seconds.html

Cheesy Joke of the Month

It was a cold February so:

What is the difference between snowmen and snowwomen?

Snowballs