Every month I select the best medical articles I have read and provide brief summaries and critical appraisals. Here are this month’s articles:
Headline of the month: No benefit from amiodarone in out of hospital cardiac arrest
Kudenchuk PJ et al. Amiodarone, Lidocaine, or Placebo in Out-of-Hospital Cardiac Arrest. NEJM 2016. PMID: 27043165
There is a lot that could be said about this paper. It was a large, randomized, double-blind placebo controlled trial that included 3026 patients in out of hospital cardiac arrest. It compared amiodarone to lidocaine to placebo. The simplistic answer: there was no difference. I am tempted to stop there, because I never thought amiodarone helped, but the data might be a little more granular than that. For the primary outcome of survival to hospital discharge, the numbers were: 24.4% with amiodarone, 23.7% with lidocaine, and 21.0% with placebo. There was no statistically significant difference, as the trial was powered to find a 6.3% difference, but the absolute difference of 3.4% in survival to discharge could be clinically important. Unfortunately, treatment with these antiarrhythmics is not without harm. More patients in both the amiodarone and lidocaine groups were admitted to hospital. That sounds great on the surface, but the last thing any patient wants is to spend their final days as a vegetable in the ICU. If they aren’t going home at the end of that ICU stay, I think this is an important harm to consider.
Bottom line: I will continue not using anti-arrythmics in cardiac arrest. However, I would not be surprised if future research found a subgroup in which they are actually helpful.
Note: Keep an eye open for a future episode of EMCases Journal Jam, as I will be speaking with a few of the authors to see how they interpret this data.
Where to go for that gush of air?
Laan DV et al. Chest Wall Thickness and Decompression Failure: A systematic Review and Meta-Analysis Comparing Anatomic Locations in Needle Thoracostomy. Injury 2015 [Epub Ahead of Print]. PMID: 26724173
This is a systematic review and meta-analysis that looked at a total of 28 studies that attempted to determine the best location for a needle decompression of pneumothorax. 15 studies were imaging based studies that looked at chest wall thickness, and found that the mean total chest wall thickness was 4.3cm in the traditional midclavicular 2nd intercostal space, 4.0 cm in the 5th intercostal space (anterior axillary line), and 3.4 cm in the 5th intercostal space (mid axillary line) (Not statistically different with p=0.08). 13 studies looked at at how frequently a 5cm angiocath failed to reach the pleural space, and the results were: 38% with the traditional mid clavicular 2nd intercostal space approach, 31% with the 5th intercostal space (anterior axillary line), and 13% with the 5th intercostal space (mid axillary line) (p=0.01).
Bottom line: It might be better to try to needle in the same position as you would insert a chest tube, but honestly I avoid this dilemma altogether by going straight to open (finger) thoracostamy if I am concerned about tension pneumothroax.
Humans aren’t pigs (most of us at least)
White JM, Braude DA, Lorenzo G, Hart BL. Radiographic evaluation of carotid artery compression in patients with extraglottic airway devices in place. Academic emergency medicine : official journal of the Society for Academic Emergency Medicine. 22(5):636-8. 2015. PMID: 25903385
I love LMAs for cardiac arrest. No matter how slick the operator, intubation takes time, can interfere with compressions, and distracts from the real issue. LMAs are quick, easy, and provide everything we need for the initial resuscitation of cardiac arrest patients. However, a pig study in 2012 raised the concern that LMAs might compress the carotid arteries. Luckily, most humans don’t look like pigs. This is a cohort study of 17 trauma patients with supraglottic airway devices in place who were having CT imaging of their neck. None of the patients had any radiographic evidence of compression of their carotid arteries. This isn’t the strongest paper you will ever read, but nor was the study that raised these concerns in the first place.
Bottom line: Humans aren’t pigs. LMAs are great for the initial resuscitation of cardiac arrest
Experts love to change terminology, just to ensure they sounds smarter than us average Joes
Tieder JS, Bonkowsky JL, Etzel RA et al. Brief Resolved Unexplained Events (Formerly Apparent Life-Threatening Events) and Evaluation of Lower-Risk Infants. PEDIATRICS. 137(5):e20160590-e20160590. 2016. [free full text]
ALTE no longer exists. We now have BRUEs or brief resolved unexplained events. This is a clinical practice guideline from the American Academy of Pediatrics on the topic. Aside from the name change, here are some of my take-aways:
- A BRUE is an brief event (<1 min) that occurs in infants (<1 year), now resolved, that involved 1 or more of cyanosis, pallor, absent, decreased, or irregular breathing, marked change in tone, or altered level of responsiveness
- An event doesn’t count as a BRUE if there is a likely explanation (probably the biggest change from ALTE)
- Choking and gagging are specifically not considered BRUEs because they usually have an explanation such as GERD or URI
- A low risk BRUE is defined as all of: age >60 days, born ≥ 32 weeks and gestational age ≥ 45 weeks, no CPR by a trained medical provider, event < 1 min, and first event. For these children, they specifically say you should not get blood tests or xrays.
Bottom line: There is a lot of stuff here, and not a lot of it has a high degree of evidence. It is worth a read, but I will still be asking a pediatrician to review all these babies for now
Practically predicting propofol pressure problems
Au AK, Steinberg D, Thom C. Ultrasound measurement of inferior vena cava collapse predicts propofol-induced hypotension. The American journal of emergency medicine. 2016. PMID: 27090394
This is a prospective observational study of a convenience sample of 40 patients getting propofol for induction of anesthesia for elective surgery. They used ultrasound to measure the collapse of the IVC pre-propofol, and calculated the percentage collapse as: (max IVC size – min IVC size)/max IVC size. Patients with IVC collapse >50% had more propofol-induced hypotension than those without (76% versus 39%, p=0.02). This would result in a sensitivity of 67%, a specificity of 77%, a positive predictive value of 71%, and a negative predictive value of 74%. None of those values is enough to rule-in or rule -out on their own, but they might be helpful as part of an overall assessment. Of course, isolated brief hypotension after propofol might not be all that relevant as an outcome. Also, the doses of propofol used here were pretty high (mean of 2.4mg/kg IV push) and these were healthy, elective surgery patients, so there are multiple reasons these numbers might not extrapolate the the ED.
Bottom line: IVC ultrasound has some correlation to propofol-induced hypotension, but its clinical utility in the ED is not clear.
Silverton N, Youngquist S, Bledsoe J, Mallin M, Barton E. 71: Awake “Tomahawk” Video Laryngoscopy. Annals of Emergency Medicine. 56(3):S24-. 2010. [article]
This paper describes a technique I have found very useful in the past. Talking recently with my friend Dr. Joey Newbigging, I realized this might be new (and hopefully useful) for some people. Basically, while the patient is sitting upright, after providing some topical anesthetic, you insert the glidescope into their mouth using a “tomahawk” grip. Basically that means you hold the handle upside down, so the blade is coming out of the top of your hand. If that descriptions didn’t help, check out this blog post with pictures. I find it very useful for visualizing fish bones, especially when the fiberoptic scope is dirty, but also because it also allows for instrumentation of the airway. Using this approach, these authors were able to get grade 2 views of the cords in 94% of the awake, healthy volunteers.
Bottom line: A useful technique to keep in mind
Lump in your throat? Sorry – glucagon isn’t going to help
Weant KA, Weant MP. Safety and efficacy of glucagon for the relief of acute esophageal food impaction. American journal of health-system pharmacy : AJHP : official journal of the American Society of Health-System Pharmacists. 69(7):573-7. 2012. PMID: 22441787
In this review of IV glucagon for the treatment of esophageal food bolus, they identified only two studies that had a control group. Both were negative, with with dislodgement rate actually being lower (but not statistically so) with glucagon in one of the two trials.
Bodkin RP, Weant KA, Baker Justice S, Spencer MT, Acquisto NM. Effectiveness of glucagon in relieving esophageal foreign body impaction: a multicenter study. The American journal of emergency medicine. 2016. PMID: 27038694
This study is retrospective – but given how little evidence we have for glucagon, it might be worth looking at. They retrospectively identified 127 patients who were given 133 doses of glucagon (median dose 1mg IV) for esophageal food bolus, as well as a control group that was not given glucagon. Resolution occurred in 14% of patients given glucagon, which wasn’t statistically different from the 10% resolution seen with nothing. Vomiting occurred in 13% of patients given glucagon.
Bottom line: These patients need scopes, not medicines
You can read more here: A Closer Look at Glucagon for the Foreign Body
Could you ever really have too much ketamine?
Kannikeswaran N, Lieh-Lai M, Malian M, Wang B, Farooqi A, Roback MG. Optimal dosing of intravenous ketamine for procedural sedation in children in the ED—a randomized controlled trial. The American Journal of Emergency Medicine. 2016. [article]
This is a prospective, double-blind, RCT of 125 children aged 3-18 years comparing 3 different doses of ketamine (1, 1.5, and 2mg/kg). Not surprisingly, re-dosing was higher in the 1mg/kg group (16% vs 2.9% and 5%), but I’m not sure that is an important outcome. There weren’t any differences in sedation scores, sedation duration, or adverse events. Physician satisfaction was lower with 1mg/kg (80% vs 94% and 97%). Perhaps the most important numbers were from phone follow-up (although they did lose some patients). Vomiting: 10% with 1mg/kg, 12% with 15mg/kg, and 20% with 2mg/kg. Recall of the painful procedure: 19% with 1mg/kg, 7% with 15mg/kg, and 7% with 2mg/kg.
Bottom line: More vomiting, but less recall with higher doses. 1.5mg/kg seems like a sweet spot.
Game changer for head lice?
This review looked to answer the question: what is the best treatment for head lice? They found 2 RCTs comparing permethrin with dimeticone (a silicone-based product that suffocates lices). They conclude that dimeticone is superior to permethrin, with 1 extra cure for every 3 to 4 patients treated. Dimeticone also seems to be cheaper.
Bottom line: I am switching to dimeticone 4% applied once for 8 hours (can be repeated at 1 week)
Come on antibodies, leave the NMDA receptor for ketamine
Titulaer MJ et al. Treatment and prognostic factors for longterm outcome in patients with anti-NMDA receptor encephalitis: an observational cohort study. Lancet Neurol. 2013 Feb;12(2):157-65. PMID: 23290630 [free full text]
If you haven’t heard of or seen anti-NMDA receptor encephalitis, this prospective observational trial has some good take away points.
- This is an autoimmune disease, primarily of young females. It is associated with teratomas
- It is more common than HSV encephalitis in young patients – so if you are doing an encephalitis workup, it should probably be on your differential
- There are generally 4 phases: 1.Viral prodrome 2.Psychosis phase with behavioral changes, hallucination, amnesia and seizures in up to 75% of patients 3.Unresponsive phase with catatonia, possible choreiform movements and orofacial dyskinesia and 4.A hyperkinetic phase with autonomic instability.
- CSF should specifically be sent for anti-NMDA receptor antibodies
- Treatment is high dose steroids and IVIG. There are usually good outcomes if treated, but the morality is as high as 10%, so you don’t want to miss it
Bottom line: Be sure to have anti-NMDA receptor encephalitis on the differential of young females with altered mental status.
Roids vs Uric acid
Rainer TH, Cheng CH, Janssens HJ. Oral Prednisolone in the Treatment of Acute Gout: A Pragmatic, Multicenter, Double-Blind, Randomized Trial. Annals of internal medicine. 164(7):464-71. 2016. PMID: 26903390
This is a multicenter, double blind RCT of 416 adult patients presenting to the ED with gout, comparing indomethacin to prednisolone. There really weren’t any differences, either in effectiveness or adverse events. Pain was decreased by 2.5/10 at rest and 4.5/10 with activity with both treatments. About 40% of each group had minor adverse events. Unfortunately, many of the side effects that make me want to avoid NSAIDs (primarily in older patients) are also present with steroids, so I am not sure when to choose one over the other. (I would love to see some single dose dexamethasone studies for gout, just for ease of dosing.)
Bottom line: Steroids are a reasonable alternative to NSAIDs for gout
Opioids cause nausea and vomiting – so we should try to prevent it right?
One of the most common requests I encounter from nursing is for prophylactic anti-emetics when I prescribe opioids. Understandable, considering that by the time the patient vomits, I am generally off somewhere else doing something more exciting. But do they work? Let’s look at a few papers:
Lambie B, Chambers J, Herbison P. The role of prophylactic anti-emetic therapy in emergency department patients receiving intravenous morphine for musculoskeletal trauma. Emerg Med Australas. 11(4):240-243. 1999. [article]
RCT of 214 emergency department patients getting intravenous morphine for analgesia, randomized to either metoclopramide 10mg IV or placebo prior to the morphine. 1.9% of the placebo group vomited as compared to 5.4% in the metoclopramide group (p=0.0009). Yeah – more vomiting in the metoclopramide group!
Again, this is a RCT of 259 emergency department patients getting morphine for pain, comparing metoclopramide to placebo. There was no statistically significant difference in nausea and vomiting between the groups (1.6% with metoclopramide and 3.7% with placebo).
Simpson PM, Bendall JC, Middleton PM. Review article: Prophylactic metoclopramide for patients receiving intravenous morphine in the emergency setting: a systematic review and meta-analysis of randomized controlled trials. Emergency medicine Australasia : EMA. 23(4):452-7. 2011. PMID: 21824312
This is a systematic review and meta-analysis looking at whether prophylactic metoclopramide prevents vomiting from opioids. The conclusion is that there was no difference between metoclopramide and placebo.
As far as I am aware, there are no studies looking at prophylactic ondansetron.
Sussman G, Shurman J, Creed MR. Intravenous ondansetron for the control of opioid-induced nausea and vomiting. International S3AA3013 Study Group. Clinical therapeutics. 21(7):1216-27. 1999. PMID: 10463519
This study takes a different approach: it waits for nausea to develop first, before trying to treat it. It is a randomized, double blind, placebo controlled trial comparing placebo, ondansetron 8mg and ondansetron 16mg IV in patients who developed nausea after being given an opioid. Of 2574 patients given opioids, 520 developed nausea/vomiting and were therefore included in the study. Resolution of N/V with ondansetron was significantly better than with placebo (45.7% with placebo, 62.3% with 8mg, and 68.7% with 16mg.)
Overall bottom line: Vomiting after IV opioid administration is actually pretty rare in these studies. We don’t seem to be able to prevent it from happening. It makes sense to monitor for nausea, and give ondansetron only if it occurs.
Patient gone wild? Bring out the horse tranquilizer
Isbister GK, Calver LA, Downes MA, Page CB. Ketamine as Rescue Treatment for Difficult-to-Sedate Severe Acute Behavioral Disturbance in the Emergency Department. Annals of emergency medicine. 2016. PMID: 26899459
This is a subgroup analysis of a prospective RCT comparing droperidol to midazolam. It looks at 49 patients with acute agitation who had already not responded high dose sedatives (most commonly a total of 20mg of droperidol) and were given ketamine. 44 of the 49 were adequately sedated with ketamine, and 4 of the 5 not sedated were given less than 200mg ketamine IM. There were only 3 adverse events: 2 patients vomited, and 1 had his oxygen saturation drop to 90%. This obviously isn’t practice changing in itself, but ketamine is a very interesting option for sedating agitated patients because of its ability to keep respiratory drive and airway reflexes in tact.
Bottom line: Ketamine is an interesting option for managing severely agitated patients
#FOAMed of the month:
I’m going to have to cheat this month – there is just too much excellent stuff out there.
First, no matter what your level of expertise, some ECGs are so important that we need to continuously review examples to maintain our pattern recognition skills. Hyperacute T-waves are an example an essential finding that is easily overlooked without practice. Dr. Steve Smith had 2 great posts on this ECG finding this month: here and here.
Although I am sure that everyone is aware the moment Scott Weingart posts anything, if you haven’t heard his talk on OODA loops yet, it is a must listen to understand clinical reasoning in the resuscitation room.
I had to stop listing SMACC talks in this section, because they would have just dominated every month. Soon, Josh Farkas might be in the same category. For now, he had two amazing posts that immediately impacted my practice: first, he suggests an innovative way of documenting a difficult airway, using the allergy list; second, he provides some really great insight into vasopressor use in septic shock.
Last, but definitely not least, Choosing Wisely Canada has developed a number of useful implementation guides, such as “Bye-Bye, PPI”
Cheesy Joke of the month
I remember the last thing my grandpa said to me before he kicked the bucket.
He said “Hey, how far do you think I can kick this bucket?”