The ALiEM Team: Meet some of our all-star cast

aliem teamHappy new year! Over 80 people make the whole ALiEM organization run, often behind the scenes. In the spirit of creativity and building a cohesive team culture, we felt that an “About Us” page with standard professional headshots would be too traditional.  So we made cartoon avatars of our top 30 organizational and project leaders. Take a peek at our all-star cast on our Meet the Team page.

 

Author information

Michelle Lin, MD

ALiEM Editor-in-Chief
Academy Endowed Chair of EM Education
Professor of Clinical Emergency Medicine
University of California, San Francisco

The post The ALiEM Team: Meet some of our all-star cast appeared first on ALiEM.

Trick of the Trade: Quick & Painless Ampule and Filter Needle Technique

Standard technique for transferring a medication from a glass ampule involves swabbing the ampule with isopropyl alcohol and breaking the neck of the ampule with the alcohol pad or gauze. The problem that many can attest to is the glass breaking in a way that punctures through the pad or gauze and cuts into one’s digits.
Not only is this a painful issue, but there are other considerations when a member of the team cuts themselves: leaving the bedside, hemostasis, glove replacement, potential need for a new ampule, infection, and a focus change from the patient's needs to yours.
Ampule assortment of commonly used medications in emergency medicine

TRICK OF THE TRADE

Avoiding glass in your finger(s) when using a filter needle

Detailed step-by-step instructions:
1. Pull a syringe, alcohol pad, and filter needle. Quickly swab the neck of the ampule.
Keep the syringe and needle aseptic and not on a counter

2. Attach the filter needle to the syringe and place the bottom cap of filter needle on to the top of the ampule. Break neck with hands away and out from you. Withdraw the solution from ampule.
Note: Never inject medication back through the filter needle after withdrawing from a glass ampule.

This trick of the trade works for almost every ampule size and may take a few attempts to optimize the aseptic components of the technique (see video above). 

Mark Culver, PharmD, BCPS (@EMdruggist)
Emergency Medicine Pharmacist
Banner - University Medical Center Phoenix
Phoenix, Arizona

Peer reviewed by Nadia Awad, PharmD, BCPS (@Nadia_EMPharmD) 

Las 15 recomendaciones de «NO HACER» en urgencias

En Viletanos nos recuerdan que: “No basta con saber, se debe también aplicar. No es suficiente querer, se debe también hacer “.

Documento de SEMFYC (hacer clic aquí) sobre:

15 recomendaciones de «NO HACER» en urgencias:

Comentario: me siento abochornado por la reprimenda. He infringido todas y cada una de las recomendaciones mencionadas, dejándome llevar en mi actuación, «porque siempre, siempre se han hecho así»(sin el NO), a pesar de su poca evidencia científica, e incluso con evidencia en contra.

Justificarse es de humanos pero mediocre y aburrido.

De nada sirve reconocer la culpa sin el compromiso de no reincidir;

de NO perpetuar la MALA PRÁCTICA: otros pueden copiar lo que yo hago mal.


Your New Year’s Resolution – Undiagnose a Child This Year

If you’re wondering what to do for your New Year’s resolution, don’t give something up or join a gym.  Neither will work out anyway.  This year, do something truly worthwhile - promise yourself that you will undiagnose a child or three.


Paediatrics is particularly prone to the pitfalls of overdiagnosis and overtreatment.  Although this is a problem, the reasons for overdiagnosis are actually good ones:


When there are no good tests available to tell between two possibilities, we sometimes give a therapeutic trial to help answer the question.  That is a strategy which will lead to misdiagnosis if symptoms improve despite our treatment rather than because of it.


With therapeutic trials, it is often best to challenge the assumption that it was the treatment that worked.   The two best examples that I can think of are childhood asthma and cow’s milk protein allergy in infants.

Let me give you a case to illustrate what I mean:

A 3 month old has been treated unsuccessfully for symptoms of gastro-oesophageal reflux disease (GORD).  A clinician suspects non-IgE Cow’s Milk Protein Allergy (CMPA) because first and second line treatment for GORD has been unsuccessful and because they notice that the baby has quite significant eczema.  (Click here to see a guide to diagnosing feeding problems in this age group)  The clinician decides to trial an extensively hydrolysed feed.  Over the next few weeks, the child’s symptoms of being unsettled and bringing back feeds improve considerably.  The eczema is responding to topical treatment.

In this situation, it is easy to assume that the change of milk was what made the difference.  Often, this is simply confirmation bias.  Colic, reflux and other symptoms of infancy have a tendency to self-resolve.  Of course the treatment may have been what worked but at this point in time, we genuinely have no idea.

This is the time to stop the hydrolysed formula and reintroduce a standard formula.  (Only do this for Non-IgE CMPA.  IgE CMPA is the kind that has urticaria and wheeze etc.  The children with this type of allergy need to be referred to an allergoligist.)   If the original symptoms of being unsettled and vomiting lots return in the next couple of weeks, the diagnosis is now more robust.  If the child remains well despite a return to standard formula, you have undiagnosed a thing.  Marvellous.


The second clinical scenario is the 7 year old with a nuisance cough.  The cough has been there for somewhere around 2-3 months.   There are no associated symptoms such as wheeze or altered exercise tolerance, but the cough is waking the family up at night.  The chest is clear on examination.

So, what is the likely diagnosis?  Surprisingly, in research land, coughs like this turn out to be caused by pertussis infection more often than asthma or reflux disease. (1,2)  It seems that although the pertussis vaccination is successful, infection is still relatively common.  Instead of causing a more significant respiratory illness, what we see in vaccinated children is often just the cough that lasts 100 days.  There are other, similarly benign reasons for chronic cough in children.  Also, there are plenty of significant pathological causes of chronic cough that are not asthma.

Diagnosing ‘cough variant asthma’ is possibly the biggest reason for the current debate about overdiagnosis of asthma in children, fuelled by an article in the BJGP earlier this year. (3)   Many children in the UK are prescribed inhaled steroids for chronic cough symptoms.  If they get better, this is taken as evidence that they had asthma, but there are other possible reasons for this resolution of symptoms.  The evidence suggests that the most likely thing is that the cough has resolved with time rather than with treatment.

This is therefore another opportunity to undiagnose a thing.  As well as stopping inhaled steroids after (Snelson makes up a number quickly…) three months it is probably a good idea to get some sort of objective assessment before, during and after the therapeutic trial.  Peak flows are great if you can get the child to do these well.  In many cases a symptom score (4) is more achievable.  If the only complaint was cough, then a symptom diary is all that is required.

If when you stop the steroids, the child’s cough is still resolved, you have a winner.  Your New Year's resolution is fulfilled.  Of course, once you start, undiagnosing an become a bit addictive.  If you find it becomes a problem, why not join a gym instead?

Edward Snelson
Diagnosectomist
@sailordoctor

Disclaimer: My New Year's resolution is to get a better disclaimer.

References:
  1. Marchmont et al, Evaluation and Outcome of Young Children With Chronic Cough, Chest Journal, May 2006, Vol 129, No. 5
  2. Wang et al, Whooping cough in school age children presenting with persistent cough in UK primary care after introduction of the preschool pertussis booster vaccination: prospective cohort study, BMJ, 2014;348:g3668
  3. Looijmans-van den Akker et Al, Overdiagnosis of asthma in children in primary care: a retrospective analysis, BJGP, 1 March 2016
  4. Asthma.com, Child Asthma Control Test




N=1 Principle in ARDS and esophageal pressure directed mechanical ventilation. #FOAMed, #FOAMcc

So i recently came across a review on esophageal pressure-guided ventilation in ARDS, which is in fact a technology I’ve had in my shop since 2008, but rarely use.

The truth is that I haven’t seen much “ARDS” in the last years, and I believe quite strongly that this reflects simply our hospital’s increased awareness of the nocive effects of over-zealous fluid resuscitation. Although in the ICU we still admit patients who, in our opinion, have received a bit more fluid than they should have, we have become more aggressive with diuresis “despite” the presence of shock, and usually see “ARDS” resolve. This is a direct consequence of actually “looking” at our patients’ volume status using ultrasound (for more see, well…most other posts on this blog!).

However, what seems like genuine ARDS does come around once in a while, and we recently had severe respiratory failure develop in a morbidly obese patient, and all of a sudden, in the presence of an FiO2 of 100%, a PEEP of 14, intra-abdominal pressures between 20 and 25, and on Flo-Lan, it seemed it might be a good idea to tailor ventilation.

Current Practice:

The most common practice currently is the ARDSnet type low volume (5-7ml/kg) lung protective ventilation, using a PEEP/FiO2 scale and aiming for plateau pressures (Pplat) below 30. Generally speaking a good idea, but one has to understand that this is, once again, a one-size-fits-all (except for the per kg) approach, which isn’t ideal if you try to follow  the N=1 Principle.

Why is this?  Because, due to physical characteristics (obesity, chest wall stiffness, etc,) and pathology (increased abdominal pressure, etc), the airway pressure reflects the respiratory system pressure (Prs) rather than the transpulmonary pressure (Ptp), which is the variable most related to volutrauma (which has eclipsed barotrauma as the mechanism for most ventilator-induced lung injury (VILI).  Ptp essentially relates to overdistension, which is what results in pneumothoraces. In terms of parenchymal micro-injury, it seems to be most related to atelectrauma, in essence the opening and closing of alveoli, with the resultant shear forces disrupting surfactant and cell surface. This type of injury relates best to finding optimal PEEP to both recruit and prevent de recruitment – in effect minimizing the amount of lung tissue collapsing and reopening.

 

Esophageal pressure (Pes)-guided Practice:

So Pes is used as a measure of pleural pleural pressure, and:

Ptp = Paw – Pes

That equation is the central tenet to this, and basically, you have to reset your goals to:

a. Ptp (exp) around zero – optimal PEEP – (meaning no over distension and no de-recruitment)

b. Ptp (insp) below 25 – though this is not really individualized as a hard data point, but has been shown to be a reasonable cutoff for volutrauma.

 

How do you do this?

By slipping in a special oro/naso-gastric tube with a balloon connected to the ventilator, one is able to simultaneously measure airway pressure (as is standardly done) and esophageal pressure. This is what it looks like:

img_6207

Here we can see that this patient has a PEEP of 20 (top), a Pes of about the same, and thus a Ptp (bottom) near zero.

We’ll discuss this case hopefully tomorrow, but just to show the mechanics/technique of it.

 

Bottom Line:

So this involves tossing out the ARDSnet charts and trying to individualize and optimize Ptp (insp and exp) instead of plateau pressures and PEEP.  How may it be useful clinically? Well, you may be able to detect unsuspected states of de-recruitment/ateletasis due to excessive chest wall or abdominal pressure, and allow you to increase PEEP “safely.”

When should I use this?

I’m not sure what everyone else is doing, but we are in the process of setting up a protocol where esophageal balloons will be inserted for any patient whose ventilator settings are approaching or exceeding FiO2 70%/PEEP 15, indicative of sufficiently severe respiratory failure warranting this additional level of fine-tuning.

I tend to use it when ventilating two groups: those with (a) elevated intraabdominal pressure, and (b) the obese patients, as they often have elevated Pes (usually due to diaphragmatic displacement. Interestingly, the correlation between obesity and Pes is not very good, so one should not “blindly” feel they can crank up the PEEP to 25 and ignore plateau pressures, as some obese patients have normal Pes (likely due to compliant abdominal walls.

Would love to hear what others do.

 

Here are the relevant articles/references:

talmor-nejm-2008

ajrccm-2014-review

 

Cheers!

 

Philippe