A Matter of Convenience: Improper Drug Dosing in the ED

Sergey Motov (@smotovmd) sparked an interesting Twitter debate last month with his poster that looked at ketorolac (Toradol) dosing in the ED.


I have previously written about ketorolac in NSAIDs parts one, two and three.

Elisha Targonsky (@ETube) commented that the equi-analgesic and less GI toxic 10 mg ketorolac dose is standard in his EDWhaaaatttt?


But how? I’ve worked in several EDs and have never seen the 10 or 15 mg dose of ketorolac used regularly.  How could it be that 10 mg is used regularly in this ED?  Simple.


Which prompted Sergey and I to say

So simple, yet so brilliant!


This got me thinking, if we change the packaging, we can change the practice!


In most EDs, including mine, the ketorolac vial is 30 mg/mL in a 1 mL vial.  This makes it fairly obvious that convenience is at least part of the reason 30 mg remains standard dosing for ketorolac. If everyone only had 10 mg vial, I’m sure it would become the standard dose in no time.

There are many medications that are commonly dosed incorrectly because the convenience of not opening a second vial or hanging a second bag, etc.

A few examples:


The first dose of vancomycin is often dosed at 1 gram when it should be 15-20 mg/kg or 25-30 mg/kg (up to a maximum dose of 2 grams) in septic shock or meningitis.   Bryan Hayes (@pharmertoxguy) reviews the literature on this subject here at Academic Life in Emergency Medicine.


Various doses of rocuronium will result in paralysis and optimize intubating conditions.  However, for rapid sequence intubation (RSI), the 1.2 mg/kg dose results in more rapid paralysis (Magorian, Flannery, Miller, Anesthesiology 1993), and also provides a greater safe apnea time for intubation prior to hypoxia (Taha SK et al. Anesthesia 2010 and Tang et al. Acta Anaesthesiology Scandinavia 2011).

Unfortunately rocuronium comes in a 50 mg, 1 mL vial.   This frequently leads to inadequate dosing because a 70-80 kg (or more) patient will only be given 50 mg in order to save opening the extra vial.  When dealing with hypotensive ED patients it may be even more important to use the 1.2 mg/kg dose of roc, given potential decreased drug effects due to hypoperfusion and prolonged time to circulation.

These are just three common examples I can think of, but I’m sure there are many more.  What drugs do you find are dosed improperly on a regular basis?  I look forward to your comments.





Anesthesiology. 1993 Nov;79(5):913-8.

Comparison of rocuronium, succinylcholine, and vecuronium for rapid-sequence induction of anesthesia in adultpatients.

Magorian T1Flannery KBMiller RD.


Anaesthesia. 2010 Apr;65(4):358-61. doi: 10.1111/j.1365-2044.2010.06243.x.

Effect of suxamethonium vs rocuronium on onset of oxygen desaturation during apnoea following rapid sequence induction.

Taha SK1, El-Khatib MF, Baraka AS, Haidar YA, Abdallah FW, Zbeidy RA, Siddik-Sayyid SM.


Acta Anaesthesiol Scand. 2011 Feb;55(2):203-8. doi: 10.1111/j.1399-6576.2010.02365.x.

Desaturation following rapid sequence induction using succinylcholine vs. rocuronium in overweight patients.

Tang L1, Li S, Huang S, Ma H, Wang Z.


Vancomycin dosing in the ER from Bryan Hayes @pharmertoxguy


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Calgary EM Journal Club: Therapeutic Hypothermia – Targeted Temperature Management Trial

In the January 2014 instalment of the journal club, the Calgary EM program reviewed the recent practice changing paper on cooling (AKA therapeutic hypothermia) after out of hospital cardiac arrest.  For more discussion of this paper, you can check out TheSGEM Episode 54 and this EMCrit Podcast and EMCrit Wee with Jon Rittenberger.

Read on for our take on this paper.

Targeted Temperature Management After Out of Hospital Cardiac Arrest

Clinical Question:

In out of hospital cardiac arrest patients with presumed cardiac cause, is there benefit of targeted temperature management at 33°C vs 36°C?


N Engl J Med. 2013 Dec 5;369(23):2197-206. doi: 10.1056/NEJMoa1310519. Epub 2013 Nov 17.

PubMed ID:



Unconscious survivors of out-of hospital cardiac arrest of presumed cardiac cause admitted to critical care units in Australia and Scandinavia


Temperature management at 36°C.


Temperature management at 33°C.


All cause mortality. (Secondary outcome was a composite of poor neurologic function or death at 180 days)

Authors’ Conclusions:

Our trial does not provide evidence that targeting a body temperature of 33°C confers any benefit for unconscious patients admitted to the hospital after out-of-hospital cardiac arrest, as compared with targeting a body temperature of 36°C.

Quality Checklist:

1. The study population included or focused on those in the ED. Yes

Comment: Although all these patients would be seen in the ED it is important to note that both study populations had to undergo active temperature management to achieve either 33°C or 36°C. Given that active cooling is a process that takes hours, the true practical implications for this paper may be more focused on the patient’s stay in the ICU.

2. The patients were adequately randomized. Yes

3. The randomization process was concealed. No

4. The patients were analyzed in the groups to which they were randomized. Yes

5. The study patients were recruited consecutively (i.e. no selection bias). Yes

6. The patients in both groups were similar with respect to prognostic factors. Yes

7. All participants (patients, clinicians, outcome assessors) were unaware of group allocation. No

8. All groups were treated equally except for the intervention. Yes

9. Follow-up was complete (i.e. at least 80% for both groups). Yes

10. All patient-important outcomes were considered. Yes

11. The treatment effect was large enough and precise enough to be clinically significant. Yes

Key Results:

There was no statistically significant difference in all cause mortality or neurologic outcomes between temperature control at 33°C vs 36°C.

BEEM Commentary:

Treating physicians were not blinded to 33°C or 36°C, however the physician assessing neurologic function was.

Patients in this study had extremely early CPR (mean = 1 minute). Can such a population be generalizable to all out of hospital cardiac arrest patients?

Comments on author’s conclusion compared to BEEM conclusion:

The strong methodology of this paper supports the authors’ conclusion that hypothermia confers no benefit over strict temperature control.

The Bottom Line:

There is no benefit of targeted temperature management to 33°C compared with 36°C for out of hospital cardiac arrest patients of presumed cardiac cause.

Clinical Application:

In post cardiac arrest patients, continue with good critical care, including the maintenance of euthermia, however the induction of true hypothermia may be omitted.

What do I tell my patients?

Not applicable, except potentially for family members.


Michael Szava-Kovats (PGY-3 FRCPC-EM Resident, University of Calgary), Chris Bond, Ken Milne

BEEM – McMaster University Courseware RCT Appraisal © 2013

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Paraspinous Cervical Block for Headache

Previously we have discussed the use of propofol for migraine headache (part 1, part 2).  In this post, we’ll look at another headache treatment that can be added to your armamentarium, the paraspinous cervical block.

There are many standard cocktails for headache management in the ED, but unfortunately, many of these require an IV, fluids, and multiple medications.  This requires a significant amount of nursing time and often ties up a precious bed in the ED.  What if we could perform an injection at the bedside and send the patient home 10-15 minutes later?  Wouldn’t that be awesome?


The majority of literature on the paraspinous cervical block has been published by Larry Mellick, an Emergency Physician in Georgia, and his twin brother, Gary Mellick.  According to them, this can be used for all types of headache, from tension type/migraine headaches, to orofacial/dental pain, to meningitis.  The meningitis part is self-report by Larry, not anything that has been studied.

Tim McCormick and Stuart Swadron have previously written on the subject over at EPMonthly, please read their short article now and then come back here.  It will only take about a minute, I promise.

So how do I perform this?

It’s actually very easy.  The steps are listed here, and below are videos from Larry Mellick and Al Sacchetti on how to perform the technique.

1)Landmark the C7 spinous process, which is usually the most prominent one.

2)Mark a point 1 inch lateral to the spinous process on each side, basically in the belly of the trapezius muscle overlying the transverse process.

3)Clean the area with alcohol swab.

4)Raise a wheal using lidocaine.

5)With patient in a sitting position and head held upright, insert a 25 gauge, 1.5 inch needle angled parallel to the floor.  The needle should be nearly buried.  Aspirate before injecting to ensure you are not in a vessel (more on this below) and slowly inject 1.5 cc of bupivacaine.

6)Remove needle and dress wound.

Are there any risks of this procedure?

I think most people worry about the potential harms of this procedure, particularly the many vascular and nerve structures in the neck.  Rightly so, you should know the relevant anatomy before performing a procedure.

Looking at Netter’s Atlas of Human Anatomy, you can see that this area is pretty much all muscle, with the trapezius, levator scapula, splenius capitis and splenius cervicis all in that area.  If you do hit a vascular structure, it will usually be a vertebral vein, but rarely could be a vertebral artery. However, this is unlikely because it is deeper and protected by the foramen transversarium.  If you are injecting over the transverse process, that will further protect you from hitting a vascular structure.

Here are a few videos of this being performed by Drs. Mellick and Sacchetti.

Larry Mellick performing block (7:33)

Al Sacchetti video (3:25)


Mellick LB, McIlrath ST, Mellick GA. Treatment of headaches in the ED with lower cervical intramuscular bupivacaine injections: a 1-year retrospective review of 417 patients. Headache. 2006 Oct;46(9):1441-49.


Chris Bond


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Calgary EM Journal Club: Dual Anti-Platelet Therapy for Stroke (The CHANCE Trial)

Hi all,

Today is the first installment of a new addition to the site, the Calgary Emergency Medicine Journal Club!

Click here to open the page in full screen width.  It will make the tables much easier to read.

You can check out the Calgary EM Journal Club page here, and this will serve as a resource for residents who couldn’t attend the most recent JC, as well as another FOAM resource to those across the globe.

These will be published once per month, and hopefully we can also get some live Twitter involvement going in the future, much like the TempleEM and St. Emlyns JCs.

Without further ado, here is the November 2013 installment of the Calgary EM JC.

Dual Anti-Platelet Therapy for Stroke

Article: Clopidogrel with Aspirin in Acute Minor Stroke or Transient Ischemic Attack

N Engl J Med 2013;369:11-19.  DOI: 10.1056/NEJMoa1215340

PICO Question:

In patients with TIA or minor stroke, should combination anti-platelet therapy with ASA+Clopidogrel be used in favor of ASA alone?

Bottom Line:

Combination anti-platelet therapy should be considered in patients with TIA/minor stroke, but more evidence is needed for generalization to a North American population. We also felt this should be reserved for patients with rapidly resolving motor symptoms lasting <5min who would otherwise not be admitted, and only pending urgent outpatient neurologic opinion/workup.


The CHANCE (Clopidogrel with Aspirin in Acute Minor Stroke or Transient Ischemic Attack) trial is a multicenter placebo controlled RCT comparing the use of ASA+Clopidogrel with ASA alone after TIA/stroke.

In patients with previous MI or stroke, daily ASA is an excellent therapy, with a NNT = 200 for secondary prevention of stroke.  This study asks if the addition of clopidogrel (Plavix) can improve upon this stroke prevention and if there is an increased bleeding risk with combination therapy.

Overall it was felt that this was an excellent study, with a fantastic NNT of 29 to prevent a stroke at 90 days when comparing A+C with ASA alone.

The key limitation was external validity and the ability to generalize to a North American population was questionable. (See “Are the results clinically applicable” below)  It is also unclear as to why ASA was only used for the first 21 days in the ASA+Clopidogrel arm, with placebo ASA on days 22-90.  It was surmised by the group that this may reduce the bleeding risk of combination therapy, while capturing the benefits of dual anti-platelet therapy in the period of highest risk (immediately post stroke/TIA).

The follow-up period of 90 days was felt to be too short by some, as 1 year follow-up in other studies has shown no difference in stroke rate.  However, those studies did not have as acute an enrolment period (<24 hours) as CHANCE.

Finally, many attendees felt that there was no benefit to starting combination therapy if this would only be stopped by the neurology service a short time later.  Though I can understand their sentiment, previous trials enrolling patients in the sub-acute (1-2 week) period post stroke/TIA showed less or no benefit than CHANCE, and thus I would argue the opposite.  That is, if we are to start dual anti-platelet therapy, it should be done in the ED, as early therapy (<24 hours) has greater potential benefit than delayed initiation of therapy.


Study #1 Clopidogrel with Aspirin in Acute Minor Stroke or Transient Ischemic AttackN Engl J Med 2013;369:11-19.  DOI: 10.1056/NEJMoa1215340
Objective: To determine whether combination anti-platelet therapy with ASA + Clopidogrel is superior to ASA alone in the secondary prevention of stroke.
Study Design: Double blind, randomized, placebo controlled trial of 5170 patients with minor stroke (NIHSS ≤ 3) or high-risk TIA (ABCD2 score ≥ 4) at 114 Chinese centers. Patients were randomized to receive either ASA/Clopidogrel  (ASA was for the first 21 days in this group, with placebo ASA given on days 22-90) or ASA alone for 90 days.  Primary outcome was stroke at 90 days (hemorrhagic or ischemic). Secondary outcomes included moderate-severe hemorrhage as defined by the GUSTO classification (*see below), and secondary efficacy outcomes including anew clinical vascular event (ischemic stroke, hemorrhagic stroke, myocardial infarction, or vascular death), analyzed as a composite outcome and also as individual outcomes.
Are the results valid? Risk of Bias: Very Low
  1. Was randomization described in enough detail as to permit replication? Yes. Randomization was done centrally, using a double-blind, double-dummy design, with site investigators calling into a computer random number generator to be assigned a number corresponding to a medication kit at their site.
  2. Was there sufficient concealment of treatment allocation? Yes
  3. Were the 2 groups similar at the start of the trial? Yes, table 1 appears equal in many known predictors of outcome.
  4. Were health care workers and patients blind to the treatment allocation? Yes
  5. Were those assessing the outcome blind to treatment allocation? Yes
  6. Did the authors report an intention to treat protocol? Yes
  7. Was follow up complete? Yes, of the 5170 randomized patients, 36 were lost to follow up, 20 in the ASA/Clopidogrel group and 16 in the ASA only group.
What are the results?                                    A+C                ASA only               HR (95% CI)Stroke                        8.2%              11.7%           0.68 (0.57-0.81,p<0.001)

MI/stroke/CV death      8.4%              11.9 %          0.69 (0.58-0.82,p<0.001)

Ischemic stroke            7.9%             11.4%           0.67 (0.56-0.81,p<0.001)

Bleeding events            2.3%             1.6%              1.41 (0.95-2.10,p=0.09)

All individual secondary efficacy outcomes (Hemorrhagic stroke, MI, CV death, all-cause mortality, TIA, mild/moderate/severe bleeding) differences were non-statistically significant between the two groups.

Are the results clinically applicable? This trial had excellent methodology with a NNT=29 for preventing stroke at 90 days for the A+C group compared with ASA alone.The biggest question with this study is external validity, ie: can these results be translated into our North American patient population?The baseline characteristics show that this is a much higher risk population than ours, with median age =62, 23% having had a previous stroke or TIA, and 42.7% smokers/ex-smokers.  Also, these patients were all minor stroke (NIHSS ≤ 3) or high-risk TIA (ABCD2 score ≥ 4.  This raises the question of benefit in the less severe TIA group.  Furthermore, this population has more uncontrolled co-morbidities, putting them at higher risk for stroke.
Author’s conclusion:  The authors concluded that “among patients with high-risk TIA or minor ischemic stroke who are initially seen within 24 hours after symptom onset, treatment with clopidogrel plus aspirin for 21 days, followed by clopidogrel alone for a total of 90 days, is superior to aspirin alone in reducing the risk of subsequent stroke events. The combination of clopidogrel with aspirin did not cause more hemorrhagic events in this patient population than aspirin alone”.

*GUSTO bleeding classification: Moderate = bleed requiring transfusion but not hemodynamic compromise; Severe = fatal bleed or bleed requiring transfusion and causing hemodynamic compromise or requiring surgical intervention.

Final Question: Will this change your practice?  Let us know in the comments section.



Thanks for reading.  As this is the first Calgary EM Journal Club post, feedback and comments are greatly appreciated.


Chris Bond (@socmobem)

Special thanks to Mike Betzner, FRCPC-EM and Ken Milne of TheSGEM.com for their peer-review.







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SOCMOB How To: Using the Ventilator for DSI with Dave Lendrum

Hi all,

Today we have a guest post from Dr. David Lendrum, an ER physician at the Foothills Hospital in Calgary.  Dave is a super brilliant doc, and this post will outline how to perform BIPAP using a ventilator, as opposed to bringing an extra BIPAP machine into an already crowded resus area.  This is particularly useful for delayed sequence intubation (DSI) or prior to intubating the severe metabolic acidosis patient.

These two concepts have been discussed by EM critical care guru Scott Weingart in the podcasts linked below.  If you haven’t heard them, stop reading and go listen now.
Intubating a patient with severe acidosis
Delayed Sequence Intubation
This post is to demonstrate how to actually accomplish this using our ventilators, and thus may be more useful for the local Calgary docs than others.  However, the steps should be applicable to most ventilators.  I also look forward to feedback regarding better, faster, easier ways to do this.
The post contains text and photos, with a video at the end.  You can also link to my other “How To” videos here.
On with the post.
1) To “BIPAP” a patient we are basically talking about providing a patient with an amount of pressure support when they inspire and an amount of PEEP when they exhale.  We almost always ask the RT’s to bring a “BIPAP” machine to the bedside as we don’t seem to use the actual ventilator to do this.  Why is this???  Mainly because these machines do BIPAP really well, the are simple to use and they are also portable, meaning they can be hooked up to an bottle of oxygen and the patient can be transported while being BIPAP’ed where as this can’t be done with the large ventilators.  The downside is that they are really large and take up a lot of real-estate in the trauma bays and such.
2) You may not know that you need to use a special mask with the BIPAP machine!  I don’t mean that it is special in the fact that it is nice and soft and needs to be on the patient really tightly, but there are actually two different masks for non-invasive ventilation.
BIPAP MACHINE: As you can see there is only one tube going to the patient providing air, but no return circuit. As such, where does the patient exhale?  You MUST use a mask with exhalation holes in it with this mask or the patient can’t exhale at all other than leaking around the mask.  The photo below shows the mask the RT’s will put on the patient which has these holes or vents.
3) You most definitely can do non-invasive ventilation with the regular ventilators we have in the department. However, you need to use a special NON-VENTED mask as the ventilator DOES have a exhalation tube that returns to the machine.  As you can see, the NON-VENTED mask has the blue nose looking thing and no holes in it.
4) Bringing a BIPAP machine into a code room when I have every intention of intubating them in the near future makes no sense.  The RT’s agree with me.  As such, I have done some playing with the vent and figured out ONE of the ways of doing this.  I am sure some of you will have lots of comments on other ways of doing this as well.
5) Find a ventilator and let the RT know what you are thinking.  “I want to non-invasively ventilate this patient until I am ready to pass the ETT”.  Perhaps you are doing this for a patient with an ASA overdose or a severe DKA patient and you are really worried that if the patient becomes any more hypercarbic they really aren’t going to do well.  Or, maybe they are wild and crazy and have a severe pneumonia and you feel that they need some sedation and pre-oxygenation prior to intubation.
6) Here is what the ventilator looks like in standby mode.
7) You can attach the ventilator hosing to the the NON-VENTED BIPAP mask if you wish.  Notice I have also hooked up the end-tidal CO2 to this set up which would be helpful as well.  If you can’t find the non-vented mask you could use the vented one, but there is just going to be a big “leak” out the holes.  It wouldn’t be dangerous, whereas doing the opposite (using a non-vented mask on the BIPAP machine would be).
8) I also like this set up as it totally removes any concern of using a special mask and would solve the same problem, but just require someone to maintain a good seal with the patient.  I suspect to do this well you would have to have a obtunded or very cooperative patient.  This is where some Ketamine/Haldol might go a long way.
Here’s a video showing the process.

Agree/disagree?  I look forward to your comments.  Post them here, or tweet @socmobem.

Dave Lendrum


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Propofol for Migraine Part 2



The use of propofol to treat migraine has been previously discussed here at SOCMOB.  Today an interesting paper came to my attention thanks to Reuben Strayer over at EMupdates.


This paper published by Mosier et al. is a four patient case series looking at patients who received 1 mg/kg of propofol over 60 seconds, in contrast to previous papers in which propofol was slowly titrated to achieve pain relief.  One of the major concerns with the approach previously reported was the time and resources necessary to perform a prolonged sedation (up to 60 minutes) during a busy ER shift. This case series addresses that concern, as patients were rousable 5-13 minutes after receiving the propofol.

The authors report shorter ED length of stay and nearly complete resolution of symptoms with this treatment, however there are still a few concerns from my perspective.  This includes but is not limited to:

1)Convenience enrollment based on “failed outpatient therapy” and physician preference, ie: selection bias. However, one of the patients then received compazine and 1 litre of saline prior to the propofol and another had compazine, diphenhydramine, ketorolac and 2 litres of saline after the propofol.

2)They mention a reduced length of stay when compared with other patients presenting with migraine, however, there would almost certainly be some extra special attention and frequency of re-assessment for these patients who were being closely monitored and receiving a relatively novel therapy for migraine.

3)One of their conclusions is that propofol use for migraine may reduce the narcotic dependence that pervades migraine therapy.  As discussed in part 1, I’m not so sure that we want to replace the expectation of narcotics with the expectation of propofol for our migraine patients.  Not exactly a great trade off.

Aside from these limitations and those inherent in a case series, this paper is intriguing in that single dose propofol does have potential for migraine treatment.  It does address the practical concern of avoiding the prolonged sedation and monitoring period documented in previous studies.

I look forward to larger studies using this treatment protocol, as well as further studies on the use of greater occipital nerve and cervical nerve blocks.






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