Article of the month (November 2017)

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.

Continue reading “Article of the month (November 2017)”

Articles of the month (April 2016)

My monthly summaries of the best medical literature that I have come across

Every month I select the best medical articles I have read and provide brief summaries and critical appraisals. Here are this month’s articles:

Headline of the month: No benefit from amiodarone in out of hospital cardiac arrest

Kudenchuk PJ et al. Amiodarone, Lidocaine, or Placebo in Out-of-Hospital Cardiac Arrest. NEJM 2016. PMID: 27043165

There is a lot that could be said about this paper. It was a large, randomized, double-blind placebo controlled trial that included 3026 patients in out of hospital cardiac arrest. It compared amiodarone to lidocaine to placebo. The simplistic answer: there was no difference. I am tempted to stop there, because I never thought amiodarone helped, but the data might be a little more granular than that. For the primary outcome of survival to hospital discharge, the numbers were: 24.4% with amiodarone, 23.7% with lidocaine, and 21.0% with placebo. There was no statistically significant difference, as the trial was powered to find a 6.3% difference, but the absolute difference of 3.4% in survival to discharge could be clinically important. Unfortunately, treatment with these antiarrhythmics is not without harm. More patients in both the amiodarone and lidocaine groups were admitted to hospital. That sounds great on the surface, but the last thing any patient wants is to spend their final days as a vegetable in the ICU. If they aren’t going home at the end of that ICU stay, I think this is an important harm to consider.

Bottom line: I will continue not using anti-arrythmics in cardiac arrest. However, I would not be surprised if future research found a subgroup in which they are actually helpful.

Note: Keep an eye open for a future episode of EMCases Journal Jam, as I will be speaking with a few of the authors to see how they interpret this data.


Where to go for that gush of air?

Laan DV et al. Chest Wall Thickness and Decompression Failure: A systematic Review and Meta-Analysis Comparing Anatomic Locations in Needle Thoracostomy. Injury 2015 [Epub Ahead of Print]. PMID: 26724173

This is a systematic review and meta-analysis that looked at a total of 28 studies that attempted to determine the best location for a needle decompression of pneumothorax. 15 studies were imaging based studies that looked at chest wall thickness, and found that the mean total chest wall thickness was 4.3cm in the traditional midclavicular 2nd intercostal space, 4.0 cm in the 5th intercostal space (anterior axillary line), and 3.4 cm in the 5th intercostal space (mid axillary line) (Not statistically different with p=0.08). 13 studies looked at at how frequently a 5cm angiocath failed to reach the pleural space, and the results were: 38% with the traditional mid clavicular 2nd intercostal space approach, 31% with the 5th intercostal space (anterior axillary line), and 13% with the 5th intercostal space (mid axillary line) (p=0.01).

Bottom line: It might be better to try to needle in the same position as you would insert a chest tube, but honestly I avoid this dilemma altogether by going straight to open (finger) thoracostamy if I am concerned about tension pneumothroax.


 Humans aren’t pigs (most of us at least)

White JM, Braude DA, Lorenzo G, Hart BL. Radiographic evaluation of carotid artery compression in patients with extraglottic airway devices in place. Academic emergency medicine : official journal of the Society for Academic Emergency Medicine. 22(5):636-8. 2015. PMID: 25903385

I love LMAs for cardiac arrest. No matter how slick the operator, intubation takes time, can interfere with compressions, and distracts from the real issue. LMAs are quick, easy, and provide everything we need for the initial resuscitation of cardiac arrest patients. However, a pig study in 2012 raised the concern that LMAs might compress the carotid arteries. Luckily, most humans don’t look like pigs. This is a cohort study of 17 trauma patients with supraglottic airway devices in place who were having CT imaging of their neck. None of the patients had any radiographic evidence of compression of their carotid arteries. This isn’t the strongest paper you will ever read, but nor was the study that raised these concerns in the first place.

Bottom line: Humans aren’t pigs. LMAs are great for the initial resuscitation of cardiac arrest


Experts love to change terminology, just to ensure they sounds smarter than us average Joes

Tieder JS, Bonkowsky JL, Etzel RA et al. Brief Resolved Unexplained Events (Formerly Apparent Life-Threatening Events) and Evaluation of Lower-Risk Infants. PEDIATRICS. 137(5):e20160590-e20160590. 2016. [free full text]

ALTE no longer exists. We now have BRUEs or brief resolved unexplained events. This is a clinical practice guideline from the American Academy of Pediatrics on the topic. Aside from the name change, here are some of my take-aways:

  • A BRUE is an brief event (<1 min) that occurs in infants (<1 year), now resolved, that involved 1 or more of cyanosis, pallor, absent, decreased, or irregular breathing, marked change in tone, or altered level of responsiveness
  • An event doesn’t count as a BRUE if there is a likely explanation (probably the biggest change from ALTE)
  • Choking and gagging are specifically not considered BRUEs because they usually have an explanation such as GERD or URI
  • A low risk BRUE is defined as all of: age >60 days, born ≥ 32 weeks and gestational age ≥ 45 weeks, no CPR by a trained medical provider, event < 1 min, and first event. For these children, they specifically say you should not get blood tests or xrays.

Bottom line: There is a lot of stuff here, and not a lot of it has a high degree of evidence. It is worth a read, but I will still be asking a pediatrician to review all these babies for now


Practically predicting propofol pressure problems

Au AK, Steinberg D, Thom C. Ultrasound measurement of inferior vena cava collapse predicts propofol-induced hypotension. The American journal of emergency medicine. 2016. PMID: 27090394

This is a prospective observational study of a convenience sample of 40 patients getting propofol for induction of anesthesia for elective surgery. They used ultrasound to measure the collapse of the IVC pre-propofol, and calculated the percentage collapse as: (max IVC size – min IVC size)/max IVC size. Patients with IVC collapse >50% had more propofol-induced hypotension than those without (76% versus 39%, p=0.02). This would result in a sensitivity of 67%, a specificity of 77%, a positive predictive value of 71%, and a negative predictive value of 74%. None of those values is enough to rule-in or rule -out on their own, but they might be helpful as part of an overall assessment. Of course, isolated brief hypotension after propofol might not be all that relevant as an outcome. Also, the doses of propofol used here were pretty high (mean of 2.4mg/kg IV push) and these were healthy, elective surgery patients, so there are multiple reasons these numbers might not extrapolate the the ED.

Bottom line: IVC ultrasound has some correlation to propofol-induced hypotension, but its clinical utility in the ED is not clear.


The tomahawk

Silverton N, Youngquist S, Bledsoe J, Mallin M, Barton E. 71: Awake “Tomahawk” Video Laryngoscopy. Annals of Emergency Medicine. 56(3):S24-. 2010. [article]

This paper describes a technique I have found very useful in the past. Talking recently with my friend Dr. Joey Newbigging, I realized this might be new (and hopefully useful) for some people. Basically, while the patient is sitting upright, after providing some topical anesthetic, you insert the glidescope into their mouth using a “tomahawk” grip. Basically that means you hold the handle upside down, so the blade is coming out of the top of your hand. If that descriptions didn’t help, check out this blog post with pictures. I find it very useful for visualizing fish bones, especially when the fiberoptic scope is dirty, but also because it also allows for instrumentation of the airway. Using this approach, these authors were able to get grade 2 views of the cords in 94% of the awake, healthy volunteers.

Bottom line: A useful technique to keep in mind


Lump in your throat? Sorry – glucagon isn’t going to help

Weant KA, Weant MP. Safety and efficacy of glucagon for the relief of acute esophageal food impaction. American journal of health-system pharmacy : AJHP : official journal of the American Society of Health-System Pharmacists. 69(7):573-7. 2012. PMID: 22441787

In this review of IV glucagon for the treatment of esophageal food bolus, they identified only two studies that had a control group. Both were negative, with with dislodgement rate actually being lower (but not statistically so) with glucagon in one of the two trials.

Bodkin RP, Weant KA, Baker Justice S, Spencer MT, Acquisto NM. Effectiveness of glucagon in relieving esophageal foreign body impaction: a multicenter study. The American journal of emergency medicine. 2016. PMID: 27038694

This study is retrospective – but given how little evidence we have for glucagon, it might be worth looking at. They retrospectively identified 127 patients who were given 133 doses of glucagon (median dose 1mg IV) for esophageal food bolus, as well as a control group that was not given glucagon. Resolution occurred in 14% of patients given glucagon, which wasn’t statistically different from the 10% resolution seen with nothing. Vomiting occurred in 13% of patients given glucagon.

Bottom line: These patients need scopes, not medicines

You can read more here: A Closer Look at Glucagon for the Foreign Body


Could you ever really have too much ketamine?

Kannikeswaran N, Lieh-Lai M, Malian M, Wang B, Farooqi A, Roback MG. Optimal dosing of intravenous ketamine for procedural sedation in children in the ED—a randomized controlled trial. The American Journal of Emergency Medicine. 2016. [article]

This is a prospective, double-blind, RCT of 125 children aged 3-18 years comparing 3 different doses of ketamine (1, 1.5, and 2mg/kg). Not surprisingly, re-dosing was higher in the 1mg/kg group (16% vs 2.9% and 5%), but I’m not sure that is an important outcome. There weren’t any differences in sedation scores, sedation duration, or adverse events. Physician satisfaction was lower with 1mg/kg (80% vs 94% and 97%). Perhaps the most important numbers were from phone follow-up (although they did lose some patients). Vomiting: 10% with 1mg/kg, 12% with 15mg/kg, and 20% with 2mg/kg. Recall of the painful procedure: 19% with 1mg/kg, 7% with 15mg/kg, and 7% with 2mg/kg.

Bottom line: More vomiting, but less recall with higher doses. 1.5mg/kg seems like a sweet spot.


Game changer for head lice?

Kolber MR, Pierse M, Nickonchuk T. The louse is (no longer) in the house. Canadian family physician Médecin de famille canadien. 62(4):322. 2016. PMID: 27076544 [free full text]

This review looked to answer the question: what is the best treatment for head lice? They found 2 RCTs comparing permethrin with dimeticone (a silicone-based product that suffocates lices). They conclude that dimeticone is superior to permethrin, with 1 extra cure for every 3 to 4 patients treated. Dimeticone also seems to be cheaper.

Bottom line: I am switching to dimeticone 4% applied once for 8 hours (can be repeated at 1 week)


Come on antibodies, leave the NMDA receptor for ketamine

Titulaer MJ et al. Treatment and prognostic factors for longterm outcome in patients with anti-NMDA receptor encephalitis: an observational cohort study. Lancet Neurol. 2013 Feb;12(2):157-65. PMID: 23290630 [free full text]

If you haven’t heard of or seen anti-NMDA receptor encephalitis, this prospective observational trial has some good take away points.

  • This is an autoimmune disease, primarily of young females. It is associated with teratomas
  • It is more common than HSV encephalitis in young patients – so if you are doing an encephalitis workup, it should probably be on your differential
  • There are generally 4 phases: 1.Viral prodrome 2.Psychosis phase with behavioral changes, hallucination, amnesia and seizures in up to 75% of patients 3.Unresponsive phase with catatonia, possible choreiform movements and orofacial dyskinesia and 4.A hyperkinetic phase with autonomic instability.
  • CSF should specifically be sent for anti-NMDA receptor antibodies
  • Treatment is high dose steroids and IVIG. There are usually good outcomes if treated, but the morality is as high as 10%, so you don’t want to miss it

Bottom line: Be sure to have anti-NMDA receptor encephalitis on the differential of young females with altered mental status.


Roids vs Uric acid

Rainer TH, Cheng CH, Janssens HJ. Oral Prednisolone in the Treatment of Acute Gout: A Pragmatic, Multicenter, Double-Blind, Randomized Trial. Annals of internal medicine. 164(7):464-71. 2016. PMID: 26903390

This is a multicenter, double blind RCT of 416 adult patients presenting to the ED with gout, comparing indomethacin to prednisolone. There really weren’t any differences, either in effectiveness or adverse events. Pain was decreased by 2.5/10 at rest and 4.5/10 with activity with both treatments. About 40% of each group had minor adverse events. Unfortunately, many of the side effects that make me want to avoid NSAIDs (primarily in older patients) are also present with steroids, so I am not sure when to choose one over the other. (I would love to see some single dose dexamethasone studies for gout, just for ease of dosing.)

Bottom line: Steroids are a reasonable alternative to NSAIDs for gout


Opioids cause nausea and vomiting – so we should try to prevent it right?

One of the most common requests I encounter from nursing is for prophylactic anti-emetics when I prescribe opioids. Understandable, considering that by the time the patient vomits, I am generally off somewhere else doing something more exciting. But do they work? Let’s look at a few papers:

Lambie B, Chambers J, Herbison P. The role of prophylactic anti-emetic therapy in emergency department patients receiving intravenous morphine for musculoskeletal trauma. Emerg Med Australas. 11(4):240-243. 1999. [article]

RCT of 214 emergency department patients getting intravenous morphine for analgesia, randomized to either metoclopramide 10mg IV or placebo prior to the morphine. 1.9% of the placebo group vomited as compared to 5.4% in the metoclopramide group (p=0.0009). Yeah – more vomiting in the metoclopramide group!

Bradshaw M, Sen A. Use of a prophylactic antiemetic with morphine in acute pain: randomised controlled trial. Emergency medicine journal : EMJ. 23(3):210-3. 2006. PMID: 16498159 [free open access]

Again, this is a RCT of 259 emergency department patients getting morphine for pain, comparing metoclopramide to placebo. There was no statistically significant difference in nausea and vomiting between the groups (1.6% with metoclopramide and 3.7% with placebo).

Simpson PM, Bendall JC, Middleton PM. Review article: Prophylactic metoclopramide for patients receiving intravenous morphine in the emergency setting: a systematic review and meta-analysis of randomized controlled trials. Emergency medicine Australasia : EMA. 23(4):452-7. 2011. PMID: 21824312

This is a systematic review and meta-analysis looking at whether prophylactic metoclopramide prevents vomiting from opioids. The conclusion is that there was no difference between metoclopramide and placebo.

As far as I am aware, there are no studies looking at prophylactic ondansetron.

Sussman G, Shurman J, Creed MR. Intravenous ondansetron for the control of opioid-induced nausea and vomiting. International S3AA3013 Study Group. Clinical therapeutics. 21(7):1216-27. 1999. PMID: 10463519

This study takes a different approach: it waits for nausea to develop first, before trying to treat it. It is a randomized, double blind, placebo controlled trial comparing placebo, ondansetron 8mg and ondansetron 16mg IV in patients who developed nausea after being given an opioid. Of 2574 patients given opioids, 520 developed nausea/vomiting and were therefore included in the study. Resolution of N/V with ondansetron was significantly better than with placebo (45.7% with placebo, 62.3% with 8mg, and 68.7% with 16mg.)

Overall bottom line: Vomiting after IV opioid administration is actually pretty rare in these studies. We don’t seem to be able to prevent it from happening. It makes sense to monitor for nausea, and give ondansetron only if it occurs.


Patient gone wild? Bring out the horse tranquilizer

Isbister GK, Calver LA, Downes MA, Page CB. Ketamine as Rescue Treatment for Difficult-to-Sedate Severe Acute Behavioral Disturbance in the Emergency Department. Annals of emergency medicine. 2016. PMID: 26899459

This is a subgroup analysis of a prospective RCT comparing droperidol to midazolam. It looks at 49 patients with acute agitation who had already not responded high dose sedatives (most commonly a total of 20mg of droperidol) and were given ketamine. 44 of the 49 were adequately sedated with ketamine, and 4 of the 5 not sedated were given less than 200mg ketamine IM. There were only 3 adverse events: 2 patients vomited, and 1 had his oxygen saturation drop to 90%. This obviously isn’t practice changing in itself, but ketamine is a very interesting option for sedating agitated patients because of its ability to keep respiratory drive and airway reflexes in tact.

Bottom line: Ketamine is an interesting option for managing severely agitated patients


#FOAMed of the month:

I’m going to have to cheat this month – there is just too much excellent stuff out there.

First, no matter what your level of expertise, some ECGs are so important that we need to continuously review examples to maintain our pattern recognition skills. Hyperacute T-waves are an example an essential finding that is easily overlooked without practice. Dr. Steve Smith had 2 great posts on this ECG finding this month: here and here.

Although I am sure that everyone is aware the moment Scott Weingart posts anything, if you haven’t heard his talk on OODA loops yet, it is a must listen to understand clinical reasoning in the resuscitation room.

I had to stop listing SMACC talks in this section, because they would have just dominated every month. Soon, Josh Farkas might be in the same category. For now, he had two amazing posts that immediately impacted my practice: first, he suggests an innovative way of documenting a difficult airway, using the allergy list; second, he provides some really great insight into vasopressor use in septic shock.

Last, but definitely not least, Choosing Wisely Canada has developed a number of useful implementation guides, such as “Bye-Bye, PPI”


Cheesy Joke of the month

I remember the last thing my grandpa said to me before he kicked the bucket.

He said “Hey, how far do you think I can kick this bucket?”

 

Articles of the Month (June 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.

A simple clinical test to rule out PE? (Yeah right)

Amin Q, Perry JJ, Stiell IG, Mohapatra S, Alsadoon A, Rodger M. Ambulatory vital signs in the workup of pulmonary embolism using a standardized 3-minute walk test. CJEM. 2015;17:(3)270-8. PMID: 26034913

I love this study, although unfortunately it isn’t useful for clinical practice. It is a prospective cohort study of 114 patients, either in an ED or a thrombosis clinic, who were suspected of or had newly confirmed PE. They had patients walk for 3 minutes, and then measured heart rate and oxygen saturation. An increase in HR >10 had a sensitivity of 96.6% and a specificity of 31% for PE. A drop in O2 sat ≥2% had a sensitivity of 90.2% and a specificity of 39.3%. The combination of both had a sensitivity of 100% (95% CI 87-100) and a specificity of 11% (95% CI 6-21).

Bottom line: Although vitals signs seem to change in PE patients when walking, this is a pilot study and isn’t ready for prime time. The horrible specificity of this test may render it clinically useless.


We miss very few MIs, no matter what people want to tell you

Weinstock MB, Weingart S, Orth F, et al. Risk for Clinically Relevant Adverse Cardiac Events in Patients With Chest Pain at Hospital Admission. JAMA Intern Med. 2015. PMID: 25985100

A bunch of big names on this one: David Newman, Scott Weingart, Michael Weinstock. This is a retrospective review, with decent methods, looking at 11,230 patients admitted for an ACS rule out, but who had 2 normal troponins in the ED. In total, 20 of those patients (0.18%; 95%CI 0.11-0.27) had any of: an arrhythmia, STEMI, cardiac arrest, or death during their hospitalization. If you exclude patients with abnormal vital signs or abnormal ECGs, only 4 out of 7266 (0.06%; 95%CI 0.02-0.14%) patients had any of those outcomes.

Bottom line: If you are ruled out by biomarkers and ECG, you are probably ruled out as well as we will ever be able to accomplish.


Patient oriented outcomes: PPIs don’t improve any of them

Cabot JC, Shah K. Are proton-pump inhibitors effective treatment for acute undifferentiated upper gastrointestinal bleeding? Ann Emerg Med. 2014;63:(6)759-60. PMID: 24199839

I know we just talked about the use of PPIs in GI bleeds, but I will throw this in as a bit of staged repetition. This is one of the Annal’s systematic review snap shot series, covering the Cochrane review of the same topic. I will quote: “In conclusion, this systematic review does not demonstrate improvement in clinically important outcomes with proton-pump inhibitor treatment before index endoscopy for undifferentiated upper gastrointestinal bleeding”

Bottom line: We need to choose wisely and stop using PPIs for our GI bleed patients


You actually heard a pericardial friction rub! Now what?

Imazio M, Brucato A, Cemin R, et al. A randomized trial of colchicine for acute pericarditis. N Engl J Med. 2013;369:(16)1522-8. PMID: 23992557

An RCT of 240 patients with acute pericarditis, comparing colchicine (0.5mg daily if 70kg) to placebo. All patients got NSAIDs. The primary outcome of incessant or recurrent pericarditis was decreased from 38% with placebo to 17% with colchicine. Colchicine also decreased symptoms at 72 hours, at 1 week, and hospitalizations. Adverse events were not increased in this study, but everyone knows that colchicine can be nasty at higher doses, like those that used to be used for gout.

Bottom line: I tend to prescribe colchicine for pericarditis based on a NNT of about 5 to decrease recurrence or prolonged symptoms


Speaking of which, the correct colchicine dose is low dose

Terkeltaub RA, Furst DE, Bennett K, Kook KA, Crockett RS, Davis MW. High versus low dosing of oral colchicine for early acute gout flare: Twenty-four-hour outcome of the first multicenter, randomized, double-blind, placebo-controlled, parallel-group, dose-comparison colchicine study. Arthritis Rheum. 2010;62:(4)1060-8. PMID: 20131255 (free full text)

Hopefully anyone using colchicine for gout has already seen this one. This is a double blind, placebo controlled RCT comparing low dose (1.2mg once then 0.6mg 1 hour later) to high dose (4.8mg over 6 hours) colchicine and to placebo. Pain was significantly improved in about 35% of both colchicine groups, but only 15% of placebo. Severe diarrhea and nausea were both increased by the high dose colchicine, but not the low dose.

Bottom line: Colchicine is equally effective at lower doses than traditionally given, but much better tolerated.


Steri-strips for good cosmetic outcomes

Gkegkes ID, Mavros MN, Alexiou VG, Peppas G, Athanasiou S, Falagas ME. Adhesive strips for the closure of surgical incisional sites: a systematic review and meta-analysis. Surg Innov. 2012;19:(2)145-55. PMID: 21926099

This is a systematic review including 12 RCTs of 1317 patients, comparing the use of adhesive strips to sutures in closing surgical wounds. They found no difference in cosmetic results, infection, or dehiscence. Of course, this is in clean surgical wounds.

Bottom line: Almost every paper I read on wounds just reinforces my inherent bias that it doesn’t really matter how you close wounds – within reason.


More of the same

Mattick A, Clegg G, Beattie T, Ahmad T. A randomised, controlled trial comparing a tissue adhesive (2-octylcyanoacrylate) with adhesive strips (Steristrips) for paediatric laceration repair. Emerg Med J. 2002;19:(5)405-7. PMID: 12204985

An RCT of 44 emergency department pediatric patients comparing steri-strips with dermabond. Both a plastic surgeon and the parents judged cosmetic outcomes. There were no differences between the two groups.

Bottom line: Again, just clean it out and get the edges close. Humans have been healing for millennia.


Reading articles about droperidol leaves me in a state that may require some droperidol

Calver L, Isbister GK. High dose droperidol and QT prolongation: analysis of continuous 12-lead recordings. Br J Clin Pharmacol. 2014;77:(5)880-6. PMID: 24168079

I included the much larger study by the same group last month, but it is always nice to explore how many high level decisions in medicine lack a scientific basis. In this prospective observation study, they gave 46 psychiatric patients between 10 and 25 mg of IV droperidol for sedation. All were placed on holter monitors. There were no dysrhythmias. Only 4 patients had any lengthening of their QT and all 4 had other reasons for this, such as methadone.

Bottom line: We should not give up excellent medications based on shoddy science.


Options, for when they take our good drugs away or we run into ‘drug shortages’

Gaffigan ME, Bruner DI, Wason C, Pritchard A, Frumkin K. A Randomized Controlled Trial of Intravenous Haloperidol vs. Intravenous Metoclopramide for Acute Migraine Therapy in the Emergency Department. J Emerg Med. 2015. PMID: 26048068

This is a double-blind RCT of 64 adults with migraines comparing haloperidol 5mg IV to metoclopramide 10mg IV. Both medications offered excellent pain relief, 57/100mm for haloperidol and 49/100mm for metoclopramide (no difference). The metoclopramide group required more rescue medications. There was more restlessness with haloperidol.

Bottom line: Like magnesium (that we discussed a few months ago), Haldol is another option I will keep in mind for the treatment of migraines.


A classic: The FEAST trial

Maitland K, Kiguli S, Opoka RO, et al. Mortality after fluid bolus in African children with severe infection. N Engl J Med. 2011;364:(26)2483-95. PMID: 21615299 (free open access)

This is a classic RCT that randomized 3170 febrile pediatric patients in resource poor environments to either 20ml/kg NS, 20ml/kg albumin, or no bolus. All patients were severely ill with either impaired consciousness or respiratory distress plus signs of impaired perfusion. 48 hour mortality was significantly worse in the bolus groups than the no bolus group (10.5% versus 7.3%). Mortality was also worse at 4 weeks.

Bottom line: In an African setting, poorly perfused pediatric patients do worse with a fluid bolus. Although these results probably don’t generalize to our population, it does remind us that IV fluids are a drug and should be treated as such.

Bonus: This is a free open access article discussing the mechanisms of increased mortality in FEAST. This paper was discussed a great deal at the SMACC conference, and some experts think FEAST is more applicable to our patients than we have recognized.


Vasopressor? Peripheral line is fine

Loubani OM, Green RS. A systematic review of extravasation and local tissue injury from administration of vasopressors through peripheral intravenous catheters and central venous catheters. J Crit Care. 2015;30:(3)653.e9-17. PMID: 25669592

This systematic review looked for any primary studies or case reports that described local tissue injury from vasopressor extravasation, and includes 85 articles and 270 patients. Although there are reports of tissue injuries after peripheral vasopressor administration, these tend to occur after very long use (the average duration of infusion was 55.9 hours.)

Bottom line: Although data is pretty limited, I would be very comfortable starting vasopressors through a peripheral line. Long term management should probably include central access.


What is a placebo controlled trial of sucrose for pain? You compare sugar pills to sugar pills

Harrison D, Yamada J, Adams-Webber T, Ohlsson A, Beyene J, Stevens B. Sweet tasting solutions for reduction of needle-related procedural pain in children aged one to 16 years. Cochrane Database Syst Rev. 2015;5:CD008408. PMID: 25942496

This Cochrane review identified 8 studies encompassing 808 pediatric patients, examining the utility of sucrose or other sweet tasting solutions in decreasing the pain of needles. The studies were all small and of moderate quality. Overall, sweetened substances did not seem to lower pain scores no matter what scoring system you used. Prior studies have concluded benefit – but always after trying to assess the look on a neonate’s face. Judging pain in neonates may be difficult, but I think there is an inherent flaw in saying that a child smiled more after the sugar, so it must have hurt less.

Bottom line: If you think a child is in pain, please give them a pain medication, rather than the key ingredient of every placebo ever made.


Speaking of placebos, a needle may not be better than pills

Schwartz NA, Turturro MA, Istvan DJ, Larkin GL. Patients’ perceptions of route of nonsteroidal anti-inflammatory drug administration and its effect on analgesia. Acad Emerg Med. 2000;7:(8)857-61. PMID: 10958124

I love this study. For 64 patients presenting to the ED with an MSK injury, they gave everyone a juice drink that actually had 800mg of ibuprofen in it (unknown to the patients). They then randomized them to either get placebo pills that looked liked 800mg of ibuprofen or a placebo IM injection resembling 60mg of ketorolac. The patients and the nurses were all blinded. There were no differences in pain on a visual analog scale in the 2 hours that followed, contradicting prior research that indicated that needle based placebos are ‘stronger’ than pill based placebos.

Bottom line: Don’t give patients IM/IV medications just for the placebo affect. Oral NSAIDs are almost always appropriate.


An expensive placebo made popular by sports stars

Rowden A, Dominici P, D’Orazio J, et al. Double-blind, Randomized, Placebo-controlled Study Evaluating the Use of Platelet-rich Plasma Therapy (PRP) for Acute Ankle Sprains in the Emergency Department. J Emerg Med. 2015. PMID: 26048069

Less relevant to emergency medicine, but I have been asked about platelet rich plasma therapy by patients and friends. This is the (placebo?) therapy of sports stars such as Kobe Bryant, in which your own platelets plus some cytokines are injected back into you to treat tendonitis among other things. This was a double blind RCT comparing platelet rich plasma therapy to placebo for acute ankle sprain in the ED. There was no change in pain or function at day 0, 3, or 8.

Bottom line: Despite the huge amount of money being spent on this by rich athletes, it is unlikely to benefit your patients.


Placebos may not help, but medications can actually hurt you

Fralick M, Macdonald EM, Gomes T, et al. Co-trimoxazole and sudden death in patients receiving inhibitors of renin-angiotensin system: population based study. BMJ. 2014;349:g6196. PMID: 25359996 (Free open access)

This is another great massive case control study from David Juurlink and his group looking at the Ontario drug benefit database. They identified all patients who died suddenly and were treated with either an ACEi or an ARB. Those patients who had been on antibiotics within the 7 days before their death were matched to controls who hadn’t received antibiotics. There were 1027 sudden deaths after antibiotics (out of 38879 total sudden deaths.) Using amoxicillin as the baseline, there was an increased risk of sudden death with co-trimoxazole (OR 1.38 95% CI 1.09-1.76) and ciprofloxacin (OR 1.29 95% CI 1.03-1.62). Risk was not increased with nitrofurantoin or norfloxacin. Of course, all standard problems with database observational studies apply.

Bottom line: A tiny absolute risk in the greater scheme of things, but you might want to consider if your UTI patients are on an ACEi or ARB and all else is equal.


Raising a skeptical eyebrow at the literature

White T, Mellick LB. Debunking medical myths: the eyebrow shaving myth. Emerg Med Open J. 2015; 1(2): 31-33. (Free open access)

I love medical myths, so although this myth has never affected my practice in the emergency department, I thought that I would include it. These authors did a systematic review of the literature to determine if shaving of the eyebrows causes problems with eyebrow regrowth. They did not find a single case report or study that would support this myth. There is one tiny study in which they shaved the eyebrows of volunteers and followed them for 6 months, and they all grew back fine.

Bottom line: I don’t know. If you want to shave some eyebrows, go for it.


Steroids for low back pain?

Balakrishnamoorthy R, Horgan I, Perez S, Steele MC, Keijzers GB. Does a single dose of intravenous dexamethasone reduce Symptoms in Emergency department patients with low Back pain and RAdiculopathy (SEBRA)? A double-blind randomised controlled trial. Emerg Med J. 2015;32:(7)525-30. PMID: 25122642

The idea of using corticosteroids for low back pain seems to pop up every once in a while. Although I have never seen it used, I understand there are a number of people who use this regularly. This was a double-blind RCT of 58 patients with acute low back pain in the ED comparing dexamethasome 8mg IV (1 dose) to placebo. At 24 hours, the dexamethasone group averaged 1.86/10 lower pain scores on a visual analogue scale. At 6 weeks pain scores and function were identical. (They report that the dexamethasone group had a lower ED length of stay, but the length of stay in the placebo group was almost 19 hours, which is incomprehensible to me.)

Bottom line: Like steroids for a lot of MSK conditions, there seems to be short term, but not long term improvement in pain.


We now know the evidence. How do you provoke change? Through shame

Yeh DD, Naraghi L, Larentzakis A, et al. Peer-to-peer physician feedback improves adherence to blood transfusion guidelines in the surgical intensive care unit. J Trauma Acute Care Surg. 2015;79:(1)65-70. PMID: 26091316

This trial attempted to address the slow uptake of evidence based guidelines surrounding more restrictive transfusion targets for post-op patients. It was a before and after study in a single tertiary surgical ICU. In the intervention period, if physicians ordered a transfusion in a stable patient that didn’t adhere to the guidelines, they received a follow-up email and education from a colleague. The rate of ‘inappropriate transfusions’ went from 25% to 2%. 30 day readmission rates and mortality were unchanged.

Bottom line: If you want physicians to change their behavior, you shouldn’t just teach them. You should provide peer to peer feedback, aka shame.


Cheesy Joke of the Month

Why was the Kleenex dancing?

Because it had a little boogie in it


FOAMed of the month

Why should we be giving fentanyl IN at triage? Check our this rant via the SGEM and Dr. Anthony Crocco:

https://www.youtube.com/watch?v=bDghbN7I_SM&sns=tw