Category Archives: the short coat

06.14.13
by

House of God’s Law #3 (Revised)

At a cardiac arrest, the first procedure is to take your own pulse...and nobody else's once CPR is begun.

The Gist:  Worldwide resuscitation guidelines de-emphasize pulse checks using palpation due to poor sensitivity and increased no-flow time (1).  Yet, many in-hospital resuscitations still pause compressions for pulse checks, which is associated with poorer survival outcomes (2,3).  New* opportunities exist, taken within the context of the patient, to gauge return of spontaneous circulation (ROSC) including end-tidal CO2 (ETCO2) and ultrasound that may take less interruption in chest compressions.

The Case:  During one of my first shifts in the Emergency Department as a medical student, I participated in a well executed code.  Each individual had a clear role and my task was to feel for a femoral pulse.  I kept my hand glued in the inguinal area throughout the code, frightened that I might erroneously call something that was or wasn't actually present.  Eventually, after buckets of fluid, some epinephrine, and sodium bicarbonate (suspected DKA with profound hyperkalemia, which turned out to be the case),  I felt a bounding pulse in our patient and spoke up, still worried that it was the reverberation of my own heartbeat.

This case brought forth three questions, one of which was easily answered:
1.  What about the significance of the time off the chest?
  • I've seen a great deal of interruption in chest compressions throughout codes, mostly for transfers or provider switches, pulse checks, and defibrillation.  I began noticing these interruptions more frequently after I discovered that there's a 50% decrease in chance of ROSC for every 10 seconds of hands-off time (4).  I addressed defibrillation here, but pulse checks seem like a non-controversial, more intuitive, and easier means for intervention.

2.  Why aren't we following the guidelines?
3.  Was I crazy to be so worried that I would mis-judge the pulse? We're physicians, surely we can feel a pulse, right?

The FOAM (Free Open Access Medical Education):  On a recent Broome Docs podcast, Dr. Matt Dawson provided reassurance that my fear was not unprovoked.  He recounts a pediatric case in which the discrepancy between cardiac echo and palpation for pulse were not aligned and how that changed the resuscitation.

Do people really still stop for pulse checks?  Yes, and more than we think.
  • National guidelines and popular emphasis on uninterrupted CPR may be executed well in the FOAM world, simulation, and many centers; however, chest compressions are still interrupted more than we think. 
    •  A recent article by Souchtchenko et al in the Journal of Emergency Medicine articulates this point and provides some points for intervention.  
  • We often underestimate interruptions in chest compressions.  It's easier to gauge CPR quality on the periphery of a code, where our minds have a lessened cognitive load.  Furthermore, it's difficult to accurately gauge elapsed time in such situations, particularly when even a 5 second pause has deleterious consequences on cerebral perfusion pressure (3).  Also, we often look more kindly upon our own skills and actions when we are closer in proximity to the action.   
    • A study (n=40 resuscitations) by McInnis et al showed a 30% non-compliance with AHA guidelines regarding compressions and also demonstrated that providers often failed to recognize interruptions in chest compressions.  In a survey, the code leaders explained interruptions in compressions mostly as a result of pulse checks (37%) and defibrillation (24%).  
  • Knowledge translation likely plays a role in the discrepancy between what the guidelines recommend and what we practice.  Some community institutions may be more susceptible to slow uptake and implementation of new/changing practices.
  • Equipment/Training.  Capnography and ultrasound are not available in all resuscitation areas, despite what the FOAM world may have one believe.  
Pulse Palpation Literature: During cardiopulmonary resuscitation (CPR), pulse palpation lacks sensitivity and specificity and typically interrupt chest compressions.  According to some studies, only 55% of rescuers can identify a pulse within 60 seconds (6).  Furthermore, most equipment in the hospital allows for rhythm checks during compressions thereby obviating the need for that pause (during which some providers historically integrated a pulse check).

Tibballs et al 2010 (full text) was similar to a studies in adults by Dick et al and Eberle et al.
  • 209 health care professional "rescuers" were asked whether a pulse was palpable or not in a cohort of pediatric patients receiving forms of extracorporeal life support where some forms generated a palpable pulse while others did not.  Information regarding pressures and pulse forms was obscured
  • Pulse palpation: Correct determination 78% of the time.  Rescuer sensitivity 86%, specificity 64%.  Often took up to 30 seconds.
  • Limitations: pediatric population, gold standard, site of pulse check, on ECLS (supposedly blinded)
What now?: Ultrasound and capnography (ETCO2) offer ways to predict ROSC with limited to no interruption of chest compressions.  Dr. Reuben Strayer has a detailed cardiac arrest vector demonstrating resuscitation flow with no pulse checks and an Academic Life in Emergency Medicine post offers insight into achieving successful cardiac arrest outcomes.


Ultrasound: This is well-covered by FOAM sources, especially after an article by Blyth et al.  Highlights include the following posts: BestBets (see for landmark articles), EM Lit of Note, ScanCrit.
If you're an EMRAP subscriber, check out the Jan 2013 discussion.

  • Lack of cardiac activity on point of care limited echo is associated with poor likelihood of ROSC with a pooled negative LR of 0.18 (95% CI = 0.10 to 0.31), and a positive likelihood ratio of 4.26 (95% CI = 2.63 to 6.92).
  • Use the echo in the context of the individual patient/resuscitation. Experts such as Dr. Matthew Dawson suggest that echo be used in two situations: 
    • (1) Rule out reversible causes such as tamponade or massive PE.  
    • (2) After rounds of CPR as an excuse to cease CPR when resuscitation seems futile (3).
  • Limitations:  typically involves interruption in chest compressions, very rare occasions exist when a patient may not have cardiac activity on ultrasound and go on to walk out of the hospital.
  • On the horizon? Transesophageal echo during CPR, which limits interruptions but takes far more skill (Blaivas et al).  

Capnography.  There are excellent posts by St. Emyln's, ScanCrit, and a short PK talk by Jon Schonert of EMChatter on this topic so I won't rehash these.

  • Given consistent ventilation, the partial pressure ETCO2 (PetCO2) correlates well with cardiac output during CPR.  During CPR, the carbon dioxide in the lungs is primary delivered by cardiac output.  
    • A rise in PetCO2 to ~35-40 mmHg or a sudden rise of 10mmHg over baseline during CPR has found to predict ROSC (Pokorna et al).  
    • Similarly, PetCO2 levels <10mmHg have been associated with unlikely ROSC or need to improve CPR quality. 
  • There are limitations to PetCO2 in the context of CPR, especially in predicting ROSC.
    • Cause of cardiac arrest may alter the PetCO2.  A respiratory cause may increase PetCO2 whereas large pulmonary embolism may cause very low PetCO2.
    • Administration of sodium bicarbonate may increase PetCO2.
*Use of "new" is relative, as literature such as Salen et al is over a decade old. 

References:
1.  Berg RA, Hemphill  R, Abella  B, et al.  2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science. Circulation. 2010; 122: S685-S705.
2. Cunningham LM, Mattu A, O'Connor RE, Brady WJ.  Cardiopulmonary resuscitation for cardiac arrest: the importance of uninterrupted chest compressions in cardiac arrest resuscitation.  Am J Emerg Med. 2012 Oct;30(8):1630-8. 
3.  Mattu A, Bond M, Tewelde S, Brady W.  The Cardiac Literature 2010.  Am J Emerg Med.  2012 May;30(4):615-25.  (full text)
4.  Edelson, D. P., Abella, B. S., Kramer-Johansen, Jet al.  Effects of compression depth and pre-shock pauses predict defibrillation failure during cardiac arrest. Resuscitation.   2006.  71(2), 137-145. 
5.  Dawson, M.  Comments on Notes from the Community: Cardiac Ultrasound. .Jan 24, 2013.  Available at http://www.emrap.org/episode/2013/january/notesfromthe Accessed June 13, 2013. 
6.Dick WF, Eberle B, Wisser G, Schneider T. The carotid pulse check revisited: what if there is no pulse?Crit Care Med. 2000 Nov;28(11 Suppl):N183-5
04.11.13
by

Indulging in Intubation – Lessons for the Novice

The Gist:  Learning endotracheal intubation (ETI) is both a privilege and a risky endeavor.  As patient safety is of the utmost importance, some situations may not be appropriate for novice intubators.  Dr. Minh Le Cong posed a question regarding who should intubate, discussed here, and Dr. David Marcus also has posts on this topic here and here. There are some things, however, that a novice intubator can do to maximize their learning process in an efficient and safe manner in this training process.
  • Note:  I'm not an expert and this is not an evidence-based review.  This is essentially a "Tricks of the Trade" post.
Last year, I wrote this post after an anesthesia rotation.  Recently, I completed an airway elective, both in preparation for residency and as a gift to myself after a month of public health research. I realized I had benefited from many things gleaned from Free Open Access Medical education (FOAM) world.  Here are some things that have made an impressive difference..

My Top 10 List
1.  Know what you're getting into.   Dr. Minh Le Cong has built a #FOAMed airway curriculum.
2.  Do an anesthesia rotation.
  • Allows for controlled, planned control of the airway.  This is part of the PGY-1 curriculum in U.S. EM programs, but it's also helpful as a medical student.  
  • Allows one to see what happens after the tube is secured such as response to pain, duration of medications, ventilator management.  
  • On a non-airway note: excellent for nerve blocks and arterial lines as well.
3.  Verbalize what you see see and do every step of the way during ETI.
  • An attending once told me, "It feels like an eternity when you're not holding the laryngoscope." Attendings get nervous if they can't see what's going on.  Let everyone know when you're "in the vallecula" if you're using a Macintosh blade, when you see cords/arytenoids, or if something (like cricoid) isn't working. 
4.  Know the physiologic responses to induction drugs and laryngoscopy.  Control of an airway isn't just about placing the tube - induction drugs, laryngoscopy, and the patient's underlying medical status do bizarre things to hemodynamics.  When it becomes available, check out the lecture given on the opening day of the Social Media and Critical Care Conference by Dr. Scott Weingart.
  • Post-intubation hypotension (PIH)
    • Heffner et al: 1 year retrospective cohort (~1/2 eligible were excluded) showed that PIH is common (22%, n=66).  The percentage is essentially the same as their prior study (23% with PIH; nearly all intubated with etomidate, often referred to as "hemodynamically stable").
    • Another, more heterogeneous study by Green et al, didn't show any clear associations between PIH and medications but demonstrated that patients with underlying respiratory issues are more likely to have PIH and sustained PIH is associated with badness on the mortality front.
  • In the OR, the induction propofol and fentanyl were always backed by sticks of phenylephrine "just in case."  A recent EMRAP episode (subscription required) featured a debate on this concept between Drs. Amal Mattu and Scott Weingart.
  • Laryngoscopy causes stimulation of the sympathetic and parasympathetic innervation to the hypopharynx, larynx, and trachea.
    • Increased heart rate (~30 bpm) and blood pressure (~25mmHg) thought to be due to release of catecholamines secondary to CN IX,X stimulation and renin-angiotensin aldosterone system (1).  
    • Bronchoconstriction due to parasympathetic stimulation (1).
    • Note: Pediatric patients may have bradycardia, pretreatment with atropine in some infants is of controversial utility (1).

5.  Use airway adjuncts.

  • Video laryngoscopy (VL) devices often require a different skill set in passing the tube through the cords. Some institutions have one start with VL before direct laryngoscopy (DL) but in others, this is not routine practice, so get some experience.
  • Mask ventilation.  Practice the two-handed technique, not the inferior E-C taught in BLS (Hart et al).
  • Get a feel for the bougie - it can be surprisingly difficult to induce memory.

6.  Use a combined VL/DL device if you have one available.  
  • Allows attending to visualize structures to augment safety and correct the learner. 
7.  Know your limits. First-pass success in ETI is important, keep this and the patient in mind.
  • A recent retrospective analysis of ED intubations in Academic Emergency Medicine by Sakles et al demonstrated adverse events (AE) increase with a greater number of ETI attempts.
    • 1st pass success = 14.2% with AE (n=1333; 72.9%)
    • Multiple ETI attempts = 53.1% with AE
    • Note: AEs included esophageal intubation, oxygen desaturation >10% (most common), hypotension, dysrhythmia, laryngospasm, etc.  Some of these are probably more clinically important than others.
  • A multi-center prospective study of n=2616 in Japan by Hasegawa et al demonstrated an adjusted odds ratio of 4.5 (95% CI 3.4 to 6.1) for AE in multiple attempt ETIs.
      8.  Establish an airway plan.  Seemingly easy, straight-forward airways can become surprisingly difficult.
      • Talk through your plan with the attending/team to ensure you have an appropriate plan, communicate the plan, identify any pitfalls, ensure proper materials, and demonstrate knowledge. 
      • In the ED, even if you plan to do DL, bring the VL device to the bedside.  If DL fails, the back up plan is ready.
      9.  Remember that ETI doesn't end with the passing of the tube.  
      • Ensure your patients have sufficient analgesia on board.
      • Ensure ventilator settings are appropriate to the situation.  For example, some patient populations need longer expiratory times (asthmatics) or higher respiratory rates (DKA, salicylate ingestion, acidosis in general).
      • This EMCrit post has some neat checklists at the bottom to help one systematize post-intubation care.
      10. Avoid hypoxia.
      • Use apneic oxygenation (NODESAT).  If the attendings don't use this, it offers an opportunity for discussion (at an appropriate time, away from the patient's bedside).  
      • Recognize pulse oximeter lag and the limitations of the pulse oximeter, as demonstrated by Dr. Rob Bryant.  
      References:
      1.  Ron Walls and Michael Murphy.  Emergency Airway Management. 3rd edition. 2008: Philadelphia, p222-229.
        03.28.13
        by

        What’s the MATTER(s) with Tranexamic Acid?

        The Gist:  The anti-fibrinolytic, tranexamic acid (TXA), may be lifesaving in the context of hemorrhagic trauma without some of the thrombotic complications associated with other agents; however, perfect data is lacking.  Follow the evolving literature on this topic and check out the MATTERs study by Morrison et al.  Although it's not an RCT, it offers additional, if imperfect, data upon which to inform our knowledge and discussions on TXA, especially with regard to which patients may benefit the most from its application.

        Many centers in the United States don't have TXA or incorporate it in a massive transfusion protocol.  Some of this may be the result of skepticism regarding the small absolute mortality benefit in CRASH-2, lack of additional prospective studies, appropriate indications,doses, time frame, and side effect profile.  Yet, many physicians don't know about the drug as the inexpensive drug lacks a marketing campaign from the pharmaceutical industry.  This is where free, open access, medical education (FOAM) may have a role in the knowledge translation gap regarding TXA.

        Much chatter abounds about the CRASH-2 study and subsequent sub-group analyses in the FOAM world (see PulmCCM, St. Emlyn's, Trauma Professional, Resus.Me).  In fact, some even suggest pre-hospital TXA to maximize the apparent benefit of early administration.  Also, a 2012 Cochrane Review (CRASH-2 authors) recommends TXA within 3 hours of injury in the bleeding trauma patient.  Aside from a reference on this EMCrit podcast, other studies on TXA seemed non-existent and drew from the massive cohort in CRASH-2.  In fact, I wrote a post on some of the barriers to TXA knowledge translation last year and initially neglected the MATTERs trial.

        Why does this study matter?
        • Study population:  Actively bleeding patients versus those suspected of actively bleeding in CRASH-2.
          • CRASH-2 had more subjective inclusion criteria, part of which had the uncertainty principle at play.
        • Confirmed results of CRASH-2, showing a mortality benefit with TXA
          • 1.5% ARR in CRASH-2 vs 6.5% ARR in MATTERs
        • Demonstrated that the most severely injured cohort might benefit the most
        Methods
        • Retrospective cohort, single center (military hospital in Afghanistan). 
        • Included: n = 896 patients who received at least 1 unit of PRBCs within 24 hours of admission after combat injury
          • Hospital protocol:  all trauma patients receiving emergency transfusion with evidence of hyperfibrinolysis (rotational thrombelastography) also received a 1g bolus of TXA and additional TXA at the discretion of the physician.
        • n=293 received a mean of 2.3 g TXA within 1 hour of injury (125/293 also had massive transfusion)
        • n=603 didn't get TXA (195/603 had massive transfusion)
        Results
        Overall
        Massive Transfusion
        • Absolute in-hospital mortality reduction in TXA group - 6.5%
        • Absolute reduction in the TXA + massive transfusion (10+ units of blood products in 24 hours) group was 13.7%
        • Sickest patients received TXA
        • More VTE in TXA cohort (n=15 in TXA cohort vs n=3), but too few to assess for
          • Pulmonary embolism - 2.7% (TXA) v 0.3%
          • Deep venous thrombosis: 2.4% (TXA) v 0.2% 
        • No reduction in blood products in TXA cohort
          • Note: This may be due to a survivorship phenomenon.
        Limitations
        • This study was conducted at a single military hospital so generalizability may be limited.
        • No randomization
        • Retrospective cohort
        • Really quick time to administration of TXA
        • Thrombelastography is not regularly used in most EDs in the US
        Things to keep your eye on in the future:
        • CRASH-3 Trial -international, multicenter, pragmatic, double-blind RCT to quantify the effects of the early administration (<8 h of injury) of TXA on death and disability in patients with a traumatic brain injury. (end of follow up in 2017)
        Reference:
        03.17.13
        by

        The Modern Matthew Effect


        The Gist:  In medicine and science, regardless of the medium - traditional or Free Open Access Medical education (FOAM)- the Matthew effect exists, potentially perpetuating knowledge and dogma that doesn't necessarily reflect intrinsic worth.  Question the medical dogma, respectfully and, while it's easy to copy and paste a citation for a quote a popular figure, consider critically evaluating the source of information/primary literature.  In words borrowed from TheSGEM podcast, "Be skeptical of everything you learn..," it's another arrow in the metacognition quiver.

        Conversations on the perils of FOAM at the Social Media and Critical Care Conference (SMACC) spurned the following, something I think is worth reminding ourselves of from time to time:
        While many of us exercise healthy skepticism we can still fall victim to a common phenomenon because, in the words of Daniel Kahneman in Thinking Fast and Slow, we have "almost unlimited ability to ignore our ignorance."  We may think we are fully aware of our biases, but they are worked into the fabric of life.  

        The Matthew Effect (with regard to references):  essentially, the greater number of times a paper is cited, the more citations it will receive.   Coined by Merton in this paper, but initially researched by Harriet Zuckerman, from the Gospel according to St. Matthew “For to all those who have, more will be given, and they will have an abundance; but from those who have nothing, even what they have will be taken away” (Matthew 25:29) (1).  
        • The Matthew effect is partially a byproduct of quality.  A content expert likely becomes trusted and their work becomes highly regarded due to the merit of their prior work(s).  Zuckerman identified this in Nobel Prize winners tended to generate/produce more awards compared with those who had shared equally in the project but were more junior researchers (1).
        How does this manifest in medical literature?
        High Impact Journals.  Impact factor (IF) - The IF is essentially the average number of times an article in the journal is cited within the previous two years.  A journal’s prestige is a function of the quality of the articles appearing in it. 
        • What happens when the exact same article (title, author, etc) is published in two journals with disparate IFs?  This paper by Lariviere and Gingras (full text) took at look at this question and found that duplicate papers (4532 pairs of papers) in high impact journals obtain, on average, twice as many citations as their identical counterparts published in journals with lower IFs.  
        • The intrinsic value of a paper is not the only reason for the citation of a specific paper; there is a Matthew effect attached to journals.  Thus, a paper published in a high impact journal has an added value over its intrinsic quality and will generate more citations.
        High Impact Authors.  A high profile author's paper is likely to carry more weight or gain more recognition.
        • Example:  In the Feb. 2013 edition of Emergency Medical Abstracts (subscription required), there's a little bit of banter about how this paper on incidence of contrast induced nephropathy was referred to.  Pulmonary embolism guru Dr. Jeff Kline is listed on the paper but the first author is actually Dr. AM Mitchell.  
        This sounds like splitting hairs..  Perhaps a little, but not necessarily.
        • Implicit in the concept of the Matthew effect is the notion is that a piece of research is more valuable or important because of its association with an individual rather than the contents, quality, or implications of the research.
        • Without realizing it, we may become susceptible to a cognitive bias secondary to the "Halo Effect," which I first heard about in Thinking Fast and Slow by Daniel Kahnemann.  For example, if an individual is widely regarded in the community for a podcast or publication, their institution may be looked upon more favorably.  
          • Dr. Weingart's tweet at the beginning of this post demonstrates potential implications of the halo effect - a positive/powerful reputation may have undue influence over whether we see that information as important or valid.  If someone we respect says an article is a "must read" or "garbage" we have formed an impression of the article prior to actually reading it.
          • In an era of information overload, especially in medicine, we may deal with this cognitive load by perceiving a reputable person's recommendations as most/more important (known as positional cues).  This may skew our evidence base or perception of prevalence or importance of a medical problem.
        Is FOAM impervious to this effect? No.
        • FOAM has a form of Impact Factor.  This can be quantified in retweets, blog hits, or a spot  in a Life in the Fast Lane Weekly Review.  Again, this is not necessarily a negative thing and can be harnessed "for good," introducing innovative or important ideas quickly and diffusely across the globe.  
        • Example:  
         
        • The social connections and the platforms associated with FOAM are intricate (hospital and professional networks, friends/families (social media), affiliations with societies, etc).  As a result, the Matthew effect may be less like the "Nobel Prize" effect noted by Zuckerman as age, rank, and location may not carry as much weight and the sources are vast.
        • Recently, Google announced that it would drop its RSS aggregating service, GoogleReader. This article discusses how Twitter essentially obviates the need for RSS.  Should Twitter supplant RSS, individuals who use an RSS aggregator to review journals and/or medical blogs may have increased susceptibility to biases associated with a social media/recommendation system based system. 
        So what do we do?
        • Question productively and respectfully.
        • Check sources.  For example, while putting together this post on elevated blood pressure in the ED, I came across a statistic in Tintinalli:  3.8% of headaches in the ED have serious intracranial pathology (Ch. 159).  Initially, I copied this statistic and reference because Tintinalli is one of the core EM texts.  FOAM has inspired me to check things out further, and upon evaluating the study I found it underwhelming to support the rate quoted.  This study was referenced by others as well, including the famous Perry et al article on subarachnoid hemorrhage and others. 
        • Keep the Matthew effect in mind when evaluating articles, watching posts/ideas go "viral", or evaluating the validity of an assertion or claim.
        References:
        1.  Zukerman H.  Scientific Elite:  Nobel Laureates in the United States. 2d ed. (New York:  Transaction Publishers, 1996). 
        03.07.13
        by

        Drinking from the Firehouse – One Sip of FOAM at a Time

        The Gist:  Reading/listening/seeing does not equal understanding.  Take advantage of spaced learning, including that offered by Free Open Access Medical education (FOAM), to create a curriculum from chaos.  FOAM naturally serves as a conduit for spaced repetition - be open to the wide array of material and filter smartly.  

        "Medical school is like drinking from a firehouse.." We hear this refrain from the beginning of med school but the truth is that this will extend beyond our formal medical training.  As a result, we find our ways to cram what we can in, often one subject at a time.

        • Disclaimer:  I'm no expert, but as med school draws to a close, I've reflected on things I wish I'd known earlier and may benefit others and things I hope to develop as I continue training. 

        FOAM seems like it could help with this but the there's an enormous breadth of content and some view FOAM as disorganized or overwhelming.  I, like many, have joked that emergency medicine folks love FOAM because it appeals to our ADD tendencies.  In fact, it is somewhat similar to a shift in the ED - there's no way I can predict my Twitter, podcast, or blog feed upon opening.  Trainees, educators, and seasoned physicians have expressed apparent disorganization, as a concern regarding FOAM.  However, there is another way of framing this input.

        Spaced Repetition - Dr. Chris Nickson of Life in the Fast Lane describes this excellently in Learning by Spaced Repetition and The Magic of Spaced Repetition.  Students, take note.  I merely gleaned over the iTeachEM post as I scrolled through my blog feed to reach the stuff that I thought was actually relevant to me..medicine (I was wrong.  Learners like me often don't value thinking about how we learn.  I have realized, however, that it's actually helpful to understand how I think and learn...regardless of how well I believe I've mastered it). Simply:
        • Over time, we forget things
        • Reminders, especially well timed one, mitigate this forgetfulness
        • Flashcards can work in this fashion but much medical information doesn't lend itself well to this practice (which can be cumbersome in a field like EM that spans...everything).  
          • Tip: I uploaded flashcards via GoogleDocs to a $1.99 iPhone application that had a "smart learning" feature which was really helpful in the first 2 years of med school for exams (and I could then go back to as I prepped for the USMLE).
        There's relevant evidence behind this, too:
        • RCT by Kerfoot et al demonstrating effectiveness of spaced repetition in a urology clerkship and another RCT in urology residency programs.  
        • Kerfoot et al have several publications on this intervention, including this one that demonstrated issues with regard to completion of the intervention by students
        FOAM naturally produces spaced repetition through an almost call and response system, indicating that people are critically thinking about topics (while others of us quickly begin the process of forgetting, ready for an opportune reminder at any time).  Check out this example:
        Twitter debate (February)
        ALiEM post on PE diagnostics in Pregnancy (March)

        What's the key? My thoughts:
        • Dut don't be afraid to go back and listen to old podcast episodes, listen or re-read bits of FOAM you've already experienced - you can build and reflect upon what you've learned.  
        • Remember that FOAM offers far more than cutting edge medicine - Be open to all topics, even the seemingly mundane ones.  
        • Have a method of filtering FOAM topically for when you want to explore something in depth. For example:  search FreeEmergencyTalks, Life in the Fast Lane, EMgoogle, or pose a question on Twitter...Your own syllabus!
          • This can help steer you to literature/texts to read (or supplement/update the ones you have read). 
        • Have a method of saving bits of FOAM.  You can't get through it all.  See a paper tweeted that you should read or an interesting PV card?  Star it in GoogleReader, clip it to Evernote, or save it in Pocket.  It'll be easily searchable when you need it.
        • Shuffle.  Haphazardly download from FreeEmergencyTalks or put your podcast player on shuffle.  This may overcome the desire to listen to the 'latest and greatest' and act as a refresher on things you thought were previously mastered.
        • Relax. FOAM isn't a requirement or a race, it's about learning - a tool.  Given our attention spans, the vast amount of information we have to learn, and the nature of truly understanding/mastering something we will miss things.  Fortunately, we will be reminded of these deficits - by a patient, an attending, or by FOAM. 
        Translation into practice (My wake up call to spaced repetition):
        Patient #1 -  A 29 year old male brought into the ED via ambulance for two witnessed seizures, now in his "typical" post-ictal state - not responding to most question but protecting his airway and maintaining posture.  Vital signs were all stable and blood glucose was 88 mg/dL.  His wife provided most of the history, including an apparent "history of seizures," previously on multiple medications.  The patient began having another apparent tonic-clonic seizure.  While 2 mg of lorazepam was being retrieved, the seizure activity abated.
        • This case occurred during my first month in emergency medicine and I felt slick subtly and calmly helping the off-service resident assess and navigate the situation.   
        • With the patient stabilized, we dug through the hospital and clinics' notes and discovered that the patient was, in fact, diagnosed with pseudoseizures.  I felt so..used and wrong. The seizure seemed so real! I made a note to read on these.
        I read plenty, but forgot to read on pseudoseizures, as exciting as they sounded, and as many seizing patients that I saw.  Weeks later, I heard Dr. Mattu and company discuss psychogenic non-epileptic seizures (PNES) on the EMCast June 2011 episode.   I had been coerced into "reading up" on something I had dismissed as unimportant or boring.  (Note: EMCast episodes older than 6 months are now, or should soon be free).

        The discussion briefly focused on prolactin and I was briefly brought back to my time in the social work field when one of my clients had a letter from her neurologist stating that should she have a particular "episode," the ED should draw a prolactin level within 30 minutes.  Curiosity led me to a quick FOAM search led me to a a discussion on the BroomeDocs blog on prolactin.  

        The next week, I saw a patient with PNES in the ED after getting fooled again (which will happen with PNES).  Good job, FOAM, I got the nudge and read.  I began noticing that there were cases of PNES everywhere.

        Two months or so passed and, EMRAP (subscription required) reminded me again, of PNES.  That week, I was approached with two cases of suspected PNES.

        Ailments are so much more common when we know to look for them and when they're on the forefront of one's mind.  In EM, everything in medicine is on the figurative table.  FOAM has certainly helped me identify gaps in my learning, maintain a broad differential, and refresh my memory.  
        02.19.13
        by

        Metacognition For The Pragmatist

        The Gist: Metacognition and cognitive errors in medicine are not merely fluffy, esoteric ideas. There are concrete steps one can take to mitigate these. Check out the Ten Commandments To Reduce Cognitive Error and Ten Commandments To Reduce Diagnostic Error by Dr. Leo Leonidas.

        As a student, my interests lie in the "meat" (or tofu, as it were) of medicine. Yet, as the breadth (minute as it is) of my clinical experience grows, I've increasingly become more interested and aware of cognitive errors, especially my own. Why? I think it will make me a better future physician. Cognitive bias, previously discussed here, is common in medicine and emergency medicine (EM). Metacognition, discussed in this post, can mitigate cognitive error by evaluating one's thinking. Although this seems esoteric, especially to the trainee, there are some concrete ways to go work though this process.

        Commandments to reduce cognitive and diagnostic errors
        Adapted from Dr. Leo Leonidas (1,2)

        Thou shalt think of serious and treatable conditions and act on them without delay. 

        • This is the crux of EM.  We must be facile with some of the most intense minutes of every specialty - retrobulbar hematoma, subarachnoid hemorrhage, asthma, cardiac arrest, or...anything! 
        • Know the killers and, as I learned from this EMBasic episode, always place a few in the differential.  

        Thou shalt mentally rehearse common and serious conditions that you expect to see in your specialty.
        • Simulation plays an expanding role in medical education, especially in EM where physicians must be skilled in life and limb-saving procedures that are rarely used. Preparation is crucial to making logical decisions under pressure and time constraints. Check out this paper by Dr. Cliff Reid (full text).
        • There is a cornucopia of FOAM procedure videos and tips, available regardless of one's proximity to a fancy simulation center . Examples include: Life In The Fast Lane repository, Procedurettes, EMCrit's Thoracotomy Episode, and so many more out there (use EMgoogle).
        Thou shalt not rely on your memory when making critical decisions.
        • Check the actual vitals, labs, etc when making crucial decisions or talking with consultants. EDs are insanely busy and it's difficult to keep things straight, no matter how sharp the mind.  
          • I overheard a conversation in which a PCP received a call to admit a syncope patient and, when the PCP asked about the patient's blood pressure, stated it was "about 150's systolic." Upon review of the patient's chart, her systolic BP was 90mmHg throughout her ED stay. This misinformation didn't result in harm, but it certainly pointed to potential cause of syncope and a lack of attention to detail.
        Thou shalt consider other possibilities even though you are sure of your first diagnosis.  
        • Always think of a differential, even if it's a "slam dunk" case. This can help avoid anchoring bias as well as diagnostic momentum bias.
        • Continue the debate and questioning even though the data is “in,” this will help mitigate confirmation bias and premature closure (see ALiEM post). 
          Thou shalt maintain a high index of suspicion or uncommon presentations of the common.
          • Know the probability and epidemiology of the diseases in the your differential but, in order to lessen availability bias, also recognize that zebras exist.  Include one in each differential, it's a great thought exercise and the diagnosis doesn't have to be worked up fully solely because it's on the differential.   
          • Patient's often don't present in the "classic" or "textbook" way.  According to Dr. Amal Mattu, "Classic, in medicine, means 15% of the time."  Sound about right.
          Thou shalt be wary of your hunches and intuitions; use Evidence Based Medicine (EBM).  
          • Gestalt plays a huge role in EM.  As discussed in this post, however, this is something that evolves over the course of an entire career and is something that trainees like myself are fiercely trying to cultivate. 
          • Clinical experience and anecdotes play a formative role in the development of a physician yet come at a price.  We are more likely to remember the 1 in 1,000,000 exception than the mundane 999,999.  These make great stories and provide learning points, but we probably shouldn't become reactionary to the outlier.    
          • EBM is not infallible and there are instances in which there is insufficient, applicable evidence to guide decision making.  However, in many cases there is a body of global experience with a particular disease or intervention.  It would be foolish to not capitalize on the best available information to provide the best patient care.
          Thou shalt take time to decide.
          • At the end of a night shift with a packed waiting room, it may be worth pausing for a moment to think about the 55 year old with abdominal pain. Reconstruct the story without segments spent dealing with the combative drunk, the code, and the literal pain in the neck. There are situations in which action is paramount; however, in most cases there's time to think. 
           Thou shalt engage in accountability procedures and follow up for decisions. 
          • Follow patients - it's a myth that emergency physicians can not or should not engage in follow up.
            • Keep a protected list of patients for each shift - using logs, stickers, or lists in the medical record software. 

            Thou shalt request a test only if it will change your plan or help in predicting the outcome.

            • Danger exists in too much information as it can lead one astray.  Think about how a test is relevant and will change management (ALiEM post). The pieces must fit, otherwise an extraneous bit of information could lead to search satisfying bias. 
            • Testing and treatment has associated risks, for a review, see the St. Emyln's posts on this topic.
            • Diagnosis is largely in the history and physical exam, make sure that the data fits with the story and the patient's clinical exam and vice versa.  As trainees, it's crucial to hone the history and physical skills, particularly for short ED encounters. 
            Thou shalt use available databases.

            • Use an iPad, tablet, or iPhone to readily access information. Consult applications, calculators, and pharmacopeias to double check medication dosages and adverse effects.
            • Colleagues often have niches - in ECGs, stroke, toxicology, etc. Pause to run cases by others for a fresh or alternative perspective.  
            • Lucky enough to have an ED pharmacist? Consult with them to reduce error (Patanwala et al, Cohen et al).
            • Electronic medical records systems allow one to view recent hospital visits and lab work, helpful in piecing together a coherent story.
            • Prescription monitoring databases can be a valuable resource. ACEP recommends using them (Level C).

            Thou shalt reflect on how you think and decide.
            • Recognize your own beliefs, biases, prejudices, and thinking style.  This is one of the toughest commandments, as it requires introspection and reflection.  For example, I know that I often have the tendency to mentally apply EBM and literature before fully assessing a patient's nuances.  Knowing this, however, I benefit from a mental pause checkpoint.  
            • Check out talks from FreeEmergencyTalks.net on this by Dr. Croskerry.
            • Heuristics, often cultivated by gestalt, are frequently used in medicine.  Check out these articles by Wegwarth et al and Marewski to see some ways in some ways in which heuristics can be created and tweaked to as a form of decision support.  

            References:

            1.Leonardo Leonidas.  "Ten Commandments to Reduce Diagnostic Errors."  Given to the Class of 2001 Tufts University School of Medicine From Dr. Leonardo Leonidas, Bangor, Maine, 20 May 2001  

            2.Leonardo Leonidas. "Ten Commandments to Reduce Cognitive Errors."  2003.
            02.16.13
            by

            You Want Me To Stick That Tube Where? – Utility of the Nasogastric Lavage

            The Gist:  Upper gastrointestinal bleeds (UGIB) can be serious and scary, so diagnosis and treatment are essential skills in the ED.  Nasogastric tubes (NGT) are uncomfortable and are not necessary in many UGIB or potential UGIB.  A negative nasogastric lavage (NGL) doesn't mean much, but a positive one is pretty specific.  It may not be worth fighting GI over, but think about the patient and utility of the procedure first (is airway a problem? patient uncomfortable?). 

            The Cases:  
            1. 23 y/o female with history of bipolar disorder and recent URI presented after "seeing some blood in my vomit" (further history sounded less like hematemesis and more like a spitting up a small bit of blood after a bout of coughing).  She took 600 mg ibuprofen three times daily for headaches over the past 3 days but had no other symptomatology. Vitals WNL, PE: unremarkable, Hb 13.5 g/dL, chemistry WNL.  

            2. 63 y/o male with a history of atrial fibrillation and COPD presented with two episodes of hematemesis and more shortness of breath than his baseline. He was on warfarin, lisinopril, atorvastatin, carvedilol, furosemide, and a myriad of inhalers.  VS: BP 118/78, P 100, R 18, O2 94% RA.  PE: pale, no diaphoresis, abdomen soft, non-tender.  Hb 7.6 g/dL 

            The attendings asked the nurses to place an NG tube - in Patient #1 to rule out UGIB and in Patient #2, because it's part of their routine for UGIB.

            The outcome: Patient #1 - halted the NGT placement and left AMA.  Patient #2 - difficult passing NGT, NGT abandoned secondary to unsuccessful attempts, increased combativeness, and epistaxis.  His INR then returned at 5.6.  Patient was given vitamin K and admitted to GI for endoscopy.  

            NGT placement, cited as one of the most uncomfortable ED procedures, resulted in patient distress in these two cases.  Many people in the FOAM world likely don't routinely use NGL; however, I found that many emergency physicians do so I opted to explore the utility of this procedure.  

            The FOAM:
            Does NGL confirm UGIB?
            • If positive, yes.  Specificity 91% (95%CI 83-95%), +LR 11 (Witting et al)
              • It's not always clear "how positive" an aspirate is.
            • Negative aspirate cannot rule out an UGIB due to poor sensitivity 42% (95% CI 32-51%) (Witting et al). Recall that many UGIB occur in the duodenum, out of reach of the NGL.
            • Less invasive indicators in the history, physical, and lab work can point clinicians towards localizing the source.  See the Rational Clinical Exam from JAMA on this topic, demonstrating that melena, hematemesis, high BUN/Cr ratio, history of prior UGIB, and medication use are all good predictors.  So, if a patient clearly has hematemesis or melena, they really don't need an NGL to confirm UGIB.  
            • Counterpoint:  if a sick patient has rectal bleeding and signs/symptoms for UGIB without clear stigmata (ex: hematemesis), NGL may point to a source easily and more quickly controllable with EGD.
            Any other use for NGL in UGIB?
            • Historically, NGL has been used to predicting the severity of the bleed and need for intervention by determining the rate of bleed.  For example, coffee ground aspirate often indicates a slow bleed whereas bright red aspirate may indicate a more brisk bleed.
            • Most cases of UGIB warrant an endoscopy and the question lies in when this procedure takes place - now or within the next day?
              • NGL may predict high risk lesions, but performance of an NGL doesn't change clinical outcomes (Huang et al) 
            • The need or anticipated need to claim the airway of a patient with UGIB may warrant an NGT (EMCrit:  airway in the GI bleeder).
            There are other ways to risk stratify UGIB..
            • The Glasgow-Blatchford Score (GBS) may have utility in risk stratifying patients prior to endoscopy.  The NICE guidelines allow for consideration of discharge for patients with a score of 0 but this isn't the standard yet in the US.   A simpler, modified GBS has also been developed and needs further validation.  Check out EM Lit of Note's perspective on this.  
            Does NGL affect patient oriented outcomes?  No, Huang et al showed NGL made no difference in:
            • Mortality (OR 0.84; 95% CI 0.37-1.92)
            • Length of hospital stay (7.3 vs 8.1 days, P = .57)
            • Surgery  (OR 1.51; 95% CI 0.42-5.43)
            • Transfusions (3.2 vs 3.0 units, P = .94)
            What about to clear the view for the endoscopy?
            • Erythromycin is just as good (ref)
              If an NGT must be placed... do so humanely
              • Topical anesthesia
              • Whit Fisher's  NGT "Hook" technique (haven't tried this myself)
                • Spray phenylephrine/vasoconstrictor in nose and then viscus lidocaine
                • Clamp nose and have patient lie back.
                • Place NGT tip in oropharyngeal airway and dunk that in ice water for ~ 1 minute. 
              The future...Small studies, but some interesting things being done:
              Final Note:  So, the FOAM world is moving away from NGL and the literature also supports this.  The following pieces in key journals call for a move away from routine NGL in UGIB. This is an example of the crux of medical interventions - Are we doing something just to do it or because it will give us meaningful information and change the patient's outcome?
              • Pallin DJ, Saltzman JR. Is nasogastric tube lavage in patients with acute upper GI bleeding indicated or antiquated? Gastrointest Endosc. 2011;74:981–984. PubMed
              • Pitera A, Sarko J.  Just say no:  gastric aspiration and lavage rarely provide benefit.  Ann Emerg Med 2010 Apr;55(4):365-6.  PubMed
              • Anderson RS, Witting MD.  Nasogastric aspiration: a useful tool in some patients with gastrointestinal bleeding.  Ann Emerg Med. 2010 Apr;55(4):364-5.  PubMed
              Major Studies Referenced: NB:  I haven't found any RCTs on NGL in UGIB and the major studies are in patients admitted to the hospital (high suspicion/obvious bleed or sick).
              Witting et al
              • Retrospective records review of patients admitted through the ED with a code for GI bleed
              • n=220
              • Excluded patients with hematemesis
              • Retrospective, cohort of patients admitted to hospital with code consistent with UGIB
              • n=633 
              • Conducted a Propensity analysis (attempt to mitigate selection bias)
              02.01.13
              by

              Three Dirty Words: Do You Remember…

              The Gist:  There's more uncertainty in medicine than most of us would like, especially in emergency medicine.  We are often required to act with limited information and data and, sometimes, we make mistakes.  Good medical students and physicians reflect on these mistakes in order to improve.  EMCrit's Scott Weingart and Cliff Reid of Resus.Me demonstrate an excellent example of the benefit of reflecting upon cases with unfavorable outcomes in this podcast.

              The case:  "I have a sick one for you, do you remember that woman y'all sent home on Tuesday..."  A sinking feeling crept over me as I glanced at the name on the "board" as we rushed to the room.

              Two days prior: A 63 year old female with a history of diabetes came into the ED in the midst of influenza season with a two days of myalgias, subjective fever, dry cough, congestion, nausea, and vomiting.
              • VS: T 99.3F, P 90, R 18, BP 124/78
              • PE: The patient looked somewhat sick.  Nothing focal on physical exam. 
              • Significant Diagnostics: Chemistry and blood counts within normal limits, Glucose 155. CXR - normal
              • I sat down with the patient to discuss options for disposition - observation versus discharge.  After our talk, the patient stated she felt significantly better with the ondansetron and fluids and wanted to go home with an anti-emetic.  She and her significant other promised to return for worsening of symptoms. 
              This visit: The same patient presented with the chief complaint, "I feel like I'm dying," after two syncopal episodes at home.

              • VS T 102F, P 160's, R 22 (actually closer to 30 upon visualization), BP 90/64
              • PE: Gen-Patient pale and diaphoretic, unable to stand under own power.  CV-Tachycardic. Resp-rhonchi in left lower lung. 
              • Significant Diagnostics: ECG-atrial fibrillation with rapid ventricular response, BMP - Cr 1.88, Glucose 160, WBC 13.1
              This case filled me with a sense of unease.  I had been rather confident on the patient's initial presentation that she would improve at home.  Nasty bugs were going around the community and this patient visibly improved in the ED.  I thought back to my thinking two days prior and searched for cognitive errors.  Premature closure and anchoring likely played a role in the case - all diagnostics were negative and the patient didn't even meet SIRS criteria.  Furthermore, she promised me she would return if she felt worse - I felt betrayed.   

              I was reminded of a grand rounds lecture delivered by University of Florida chief resident, Dr. Brandon Allen, entitled "Do You Remember?" in which he shared the following video (very much worth watching!).


              Take Away:
              • Engage in shared decision making.  Empower patients to understand their medical situation, risks and benefits of interventions, and allow them make some decisions for themselves.  Understand that patients don't always do what we want them to do. Wyer et al state it succinctly in this article: 
                • "We should be careful about complacency when it comes to reversion to the paternalistic medical model of decisionmaking. An abundance of evidence attests to the fact that physicians’ decisions on behalf of their patients may be entirely contrary to the decisions the same physicians would make on their own behalf"
                • Inform the patient, in simple language, of their condition, any evidence that may aid them in making a decision (ex using PECARN: fewer than 1 in 2000 kids that have an injury like this would have something that needs be treated picked up on a scan).  Decision aids or instruments, many of which are found on MDcalc may be helpful (just phrase them in a way the patient can understand).
                • Document this process. 
              • Check for cognitive errors when working patients up, especially if the clinical picture doesn't correlate with the diagnostics.  
              • Learn something from each case and carry it forward.  We're not perfect and predicting a patient's future is dangerous; however, discussions with peers and mentors about cases may add another perspective and enable one to hone clinical performance and thinking.  Alternatively, it may affirm your decision making and action.  
              • Beware of a reactionary response. 
                • An attending once told me that I should never send a patient with a DVT home without a CT scan of the chest to look for a PE.  The physician had a bad experience once and had adopted this practice which is really not the standard and potentially detrimental to many patients.  Clinical experiences can be surprising and terrifying.  I certainly have very limited experience, but I think that the cases that weigh on our minds have the potential to alter our clinical practice meaningfully which can be good or deleterious.  Beware.
              Case Conclusion:
              • BP improved in the ED with 3L of IVF.  Patient spontaneously converted into normal sinus rhythm.  Patient treated for sepsis secondary to pneumonia, had a small troponin bump during the hospital course, but had improved and was discharged after a few days in the hospital.
              • I was very thankful that I had documented the shared decision making discussion and return precautions well.
              01.29.13
              by

              Special (Medical) Transfusion Situations

              The Gist:  There are myths and uncertainty surrounding transfusion of packed red blood cells (PRBCs) in certain circumstances.  We've learned that PRBCs carry significant harm and may not benefit many of the patients we've traditionally transfused, hence the move to restrictive transfusion strategies (hb <7.0) in many of the critically ill medical patients.  This philosophy is now creeping into other realms where dogma has traditionally demanded a higher trigger for transfusion (UGIB, ACS..).  

              Lactated Ringer (LR) running during transfusion?  No worries!

              • Cull et al
                • PRBCs diluted with LR or normal saline (NS) in ratios between 5:1 to 1:20 (PRBC to crystalloid) and examined for clot formation at intervals up to two hours at body temperature. Although clotting occurred at dilutions of 1:1 (PRBC to LR) and greater, no clot formation occurred in the clinically relevant dilutions between 5:1 and 2:1
                • No difference in flow rates between PRBC diluted with LR or NS
              • Lorenzo et al Am J Surg
                • PRBC or whole blood (WB) (n=51) mixed with NS, lactate solution and LR solutions
                • No significant differences in infusion time or filter weight using WB or PRBC with NS or LR  
                • No significant difference in clot formation between NS and LR with WB or PRBC


              Does transfusion improve tissue oxygenation?  
              • Rivers surviving sepsis study demonstrated benefit for PRBC transfusion (up to a HCT of 0.30) in an algorithm, which included a goal of achieving a ScVO2 of 70% in study subjects. Patients achieving this goal had better outcomes than did patients who did not reach the goal. The specific effect of transfusion was not evaluated in this study, since the study’s purpose was to evaluate the entire algorithm, and ScVO2 is not a patient-oriented outcome.
              Is old blood bad blood?  It's probably not quite as good as fresh RBCs but this issue is complicated by (1) a changing, unpredictable, and scare supply of PRBCs (2) not knowing a precise, consistent point where benefit outweighs risk (for both the patient and the community served by the blood-bank) (3) patient factors. Lelubre et al did a review and basically couldn't find a solid difference between old blood and fresh blood.
              • Tintinalli says bad blood is associated with poorer outcomes, using a study by Zallen et al (Ch 26).  
                • Microcirculatory changes - laboratory studies have shown that older RBCs may be more fragile and less pliable, resulting in vasoocclusion (ref).
              • Fitzgerald et al, Dietrich et al, and Tsai et al proposed that RBCs a few weeks old may not have the same oxygen carrying capacity.
                • It's proposed that this is secondary to decreased 2,3 DPG. Remember that 2,3 DPG helps facilitate the unloading of O2 into tissues. 

              http://upload.wikimedia.org/wikipedia/commons/8/8a/Oxyhaemoglobin_dissociation_curve.png 
              (Wikimedia commons)

              • A study by Walsh et al demonstrated no difference in measurements of oxygen carrying capacity.
              • A blinded trial in septic patients by Lebiedz et al (2012) found that PRBCs >1 week old were associated with a poorer outcome. 
              • However, this data is sketchy. Check out Flegel 2012 for a counterpoint.
              What about patients with an Upper GI Bleed? This has been all over the FOAM world since Villanueva et al was published in the NEJM in Jan 2013 demonstrating a mortality benefit in a restrictive transfusion strategy in UGIB (<7g/dL). 

              How About Cardiac Disease? Traditional teaching recommends a higher hemoglobin as a "transfusion trigger" than in other patient populations, which is plausible given ischemia and potential pump problems. Recently, some literature has come out that these patients probably don't need automatic transfusions with a hb of 9-10 g/dL, but there is insufficient data to recommend a good trigger point. Perhaps, however, less is more. This is a popular topic and more studies will be out soon!

              Yang et al (2005)
              • n = 85,111 with NSTE ACS, observational study, mean transfusion nadir HCT 26%(8.6 g/dL).  
              • LOS- higher in transfused group 7 days (5.0-11.0) vs. 4 days (2.0-5.0). 
              • Absolute rate of death higher in transfused group (11.5% vs. 3.8%)
              • Death or MI combined higher in transfused group (13.4% vs. 5.8%)
              • Adjustment for patient and hospital characteristics - transfused patients remained 67% more likely to die and 44% more likely to experience either death or MI than those who did not undergo transfusion.
              • Limitations:  observational study, statistical adjustments, records review (data dredge).
              Meta-analysis by Chatterjee et all (2012)
              • Included 10 studies, n=203,665
              • Mortality in transfused vs non-transfused 18.2% vs 10.2% (weighted absolute risk increase of 12% or a number needed to harm of 8)
                • No mortality difference in studies that included patients with STEMI (RR, 2.89; 95% CI, 0.54-15.58; P = .22) 
                • No mortality difference in patients with a baseline hematocrit of less than 30% (RR, 1.72; 95% CI, 0.39-7.63;P = .47). Note: few studies satisfied this.
              • Blood transfusion was also significantly associated with a higher risk for subsequent myocardial infarction (RR, 2.04; 95% CI, 1.06-3.93; P = .03
              • Limitations: almost all were observational studies, only 1 was an RCT. Few reported baseline hemoglobin levels and those that did varied widely (8-11 g/dL).

              Sickle Cell? These patients live with low hb so a 7 g/dL transfusion trigger may not really apply to this population. Patients with sickle cell typically receive many transfusions throughout their life. This increases their risks of adverse effects from transfusions (and can make it more difficult to find usable blood).  These are the recommendations from the NIH and this literature review. There are controversial indications (complicated pregnancy, limb ulcers, refractory priapism), but these are generally outside the realm of EM.

              Transfuse:
              • The bad stuff we see in the ED:
              • Before surgery requiring general anesthesia
              Don't need to transfuse:
              • Clinically stable patients with high reticulocyte count
              • Typical pain crises (there's some data, scant as it is, that transfusions could exacerbate a pain crisis)
              01.29.13
              by

              What’s Your Trigger?

              The Gist: "Permissive _____" is becoming increasing popular in medicine-blood glucose, blood pressure, and oxygen saturation. Hemoglobin is similar. Currently, the best evidence suggests that transfusion of packed red blood cells (PRBCs) should be considered in most critically ill medical patients, in the absence of massive hemorrhage, at a hemoglobin (hb) <7 g/dL. The data show that liberal transfusions don't benefit the patient; however, there are limitations to the data and it and should be interpreted within the context of the individual patient. Use the patient as a guide, not merely the lab value! Prevent iatrogenic anemia, resulting in more transfusions.  Life in the Fast Lane (LITFL) has a good review.

              The case(s): In the ED, transfusion of PRBCs is often clear-cut. Massive hemorrhage with high TASH score? Activate the protocol. Patient with melena, as white as the sheets, with a hemoglobin of 4.0 g/dL? Hang the blood. What about the 60 year old patient with suspected sepsis, resting comfortably without complaints, who has a hemoglobin of 7.8 g/dL (baseline ~8-8.5 g/dL)? What if we know he is undergoing fluid resuscitation due to the sepsis, mild hypotension, and tachycardia, which will likely cause a dilutional drop in hemoglobin?

              I recently encountered similar cases and found the art of medicine plays a large role when patients. While this topic may not be very relevant in the ED, I anticipate fun-filled months in ICUs in the near future as an EM resident. Tintinalli recommends transfusion at 7.0-9.0 g/dL, but our patient, like many, falls within that grey area so any course of action is justified (Ch 146). Can the literature help sort this out?

              I didn't find anything earth shattering in my quest; however, I put some things together for a presentation and I figured I'd share the strengths and weakness of the database that underpins recommendations and decision making.

              What did the FOAM say?
              • The NNT review - 100% saw no benefit, 1 in 18 harmed by pulmonary edema by liberal transfusion.
              • Yasser Sakr's talk offers some skepticism to this practice (note: second author on the SOAP study paper).  
              How About the Society Guidelines?
              Society of Critical Care Medicine.  Suviving Sepsis 2012 Guidelines
              • RBCs when the hemoglobin concentration decreases to < 7.0 g/dL (target a hb 7.0-9.0 g/dL)
              AABB (American Association of Blood Banks) Red Blood Cell Transfusion: A Clinical Practice Guideline From the AABB (full text)
              • Consider transfusion at hb of 7 g/dL or less. 
              • Postoperative surgical patients, consider RBCs at hb of 8 g/dL or less or for symptoms (chest pain, orthostatic hypotension or tachycardia unresponsive to fluid resuscitation, or CHF)
              American College of Critical Care Medicine Clinical practice guideline - Pulm CCM review
              • Transfuse RBCs as single units in the absence of hemorrhage (Level 2 evidence)
              • Cognitive changes seem to occur at <5 g/dL so some asymptomatic, hemodynamically stable patients may not need transfusion with hb 5-7 g/dL. 
              • Symptoms: Cognitive changes, syncope, dyspnea, chest pain, etc-

              The Problems.. (LITFL's superb table and this excellent article by Gould et al)
              • Febrile nonhemolytic reactions (most common)
              • Hemolytic transfusion reaction (type 2 hypersensitivity)
              • Transmission of pathogens (Viral, Bacterial)
              • Pulmonary - TRALI (transfusion-associated lung injury), Pulmonary Edema, ARDS
              • Cardiovascular - Transfusion Associated Circulatory Overload (new respiratory distress and hydrostatic pulmonary edema within 6 hours after RBCs) - associated with renal failure and number of units (ref)
              • Biochemical - may lead to vasocontriction, GFR changes, hyperkalemia (older cells)
              • Hypothermia, coagulopathy (dilutional), thrombocytopenia with massive transfusion.
              • Human error
              • Expensive -Cost to transfuse 1 unit to patient $1600-2400 (ref)
                •  
              Prevention:
              Literature base for society recommendations: 
              • Main trials: TRICC (the only major RCT), ABC, CRIT, SOAP. 
              • These all look at a hemoglobin level as a transfusion trigger, not symptoms.
              • Observational studies have large potential for bias due to variation in a physician's decision to transfuse as well as individual patient factors (despite statistical models to account for this)
              Cochrane review 2012
              • 19 trials (Diverse: 8 surgical, 5 in setting of acute hemorrhage, 1 oncologic, 3 critical care, 1 pediatric), n=6264 patients
              • 30 day mortality - no significant difference (RR 0.85, 95% CI 0.70-1.03)
              • In hospital mortality - lower in restrictive group (RR 0.77, 95% CI 0.62-0.95) 
              • Risk of receiving RBCs - average absolute risk reduction of 34% (95% CI 24%-45%). The volume of RBCs transfused was reduced on average by 1.19 units (95% CI 0.53-1.85 units).
              • Restrictive transfusion strategies did not appear to impact on the rate of cardiac events, myocardial infarction, stroke, and thromboembolism (i.e. appeared as safe from a hemodynamic standpoint).
              • Infection - no significant difference (6 trials)
              • Limitations - Lots of heterogeneity, TRICC study contributed the majority to the review.
              Trial of Transfusion Requirements in Critical Care (TRICC trial) Hebert et al
              • Multicenter RCT, n=838, ICU setting.  Restrictive: transfuse <7.0g/dL; Liberal transfuse <10.0 g/dL
              • 30 day Mortality - no statistical difference between groups: 18.7% vs 23.3% in the restrictive vs. liberal-strategy group (95% CI –0.84-10.2%)
                • Subgroup analysis showed that younger patients (<55 years old) and less sick patients (APACHE II <20) who received transfusion had increased mortality.
              • Mortality rates during hospitalization- lower in the restrictive group 22.2% vs. 28.% (P=0.05)
              • ICU mortality- lower in restrictive group, but not significant 13.9% vs. 16.2% (P=0.29) 
              • 60-day mortality- lower in restrictive group, but not significant 22.7% vs. 26.5% (P=0.23)
              • Limitations:  
                • Study stopped early due to poor enrollment. Physicians hesitant to enroll patients, possibly due to fear of restrictive transfusion.
                • Excluded: chronic anemia, surgical patients, active bleeding.
                • Subgroup analyses: underpowered.
              Anemia and blood transfusion in critically ill patients (ABC study) Vincent et al (2002)
              • Observational study, European ICUs n=3534 patients
              • ICU  mortality =18.5% vs 10.1%, respectively; P<.001, Overall mortality rates =29.0% vs 14.9%, P<.001  had vs had not received a transfusion, respectively
              • For similar degrees of organ dysfunction, patients who had a transfusion had a higher 28-day mortality rate 22.7% vs 17.1% (p =.02) in a matched patients in the propensity analysis
              • Higher mortality in ICU patients receiving PRBC transfusion (OR of death of 1.37).
              • Limitation: observational, although analysis accounted for degree of organ dysfunction, provider discretion played a role in decision to transfuse; thus, the sicker patients likely received more transfusions.
              The CRIT study Corwin et al (2004)
              • Prospective, multi-center, observational study in US ICUs with n = 4,892
              • Upon mulivariate analysis, the number of PRBCs a patient received was independently associated with longer ICU and hospital LOS and an increase in mortality 1.65; 95%CI 1.35–2.03, p <.001). Note: one model showed increased mortality in patients with hb nadir <9.0.
              • Patients who received transfusions also had more total complications.
              • Most common reason for transfusion - low hemoglobin (mean transfusion hb = 8.6 g/dL) not symptoms
              • Excluded: cardiac/burn/neuro/pediatric ICUs, renal failure. Limited by statistical analysis instead of direct comparison.
              SOAP study Vincent et al (2008)
              • Prospective, multi-center, observational. n=3,147 patients
              • Transfused patients had higher ICU LOS (5.9 vs. 2.5 days; P <0.001)
              • Transfused patients had higher ICU mortality rate (23.0 vs. 16.3%; P<0.001)
              • Lower 30-day hazard of death in the transfused group when adjusted (HR 0.73; 95% CI 0.59–0.90; P <0.004)
              • Why the difference from the very similar ABC study?  
                • Used more leuko-depleted blood than the ABC study. This is now standard practice.
                • More knowledge about potential harms of transfusions by this time (ABC, TRICC studies already published) so more likely that sicker patients received the transfusions.

                Next up...select situations (UGIB/ACS) and myths in transfusion

                  01.21.13
                  by

                  Learning to Read (Efficiently)

                  The Gist:  Feed aggregators like GoogleReader can be a great way to browse primary literature and bring journal articles directly to you, all in one place.  It's a great way to stay well read and it's easy to set up.  After assisting other med students and attendings with setting up their feed aggregator with their favorite journals, I figured I'd share this video below, in the event it's useful for anyone else.


                  Advantages:
                  • Abstracts in one place
                  • Accessible from any smart phone, tablet, or computer.  RSS feed applications for smart phones and tablets abound and sync with GoogleReader.  For example, I use the Feeddler app (free), but there are many.

                  • Makes it easy to increase the exposure to primary literature by making journals "scannable"
                    • Note:  I do not endorse just scanning abstracts but some journals may have a lower yield of interesting or relevant articles but one can still scan the abstracts easily to detect papers that are worth checking out the full text.  
                  • The "Articles in Press" RSS feed option available from many journals makes the newest literature available (less wait time because there's often a good bit of lag time until the article is published in the journal).
                  • FOAM is eco-friendly -No paper! 
                  Disadvantages:
                  • Full text is rarely available.  Most medical school libraries/institutions have an e-journal option on the library web page.  Take advantage of this, if available.
                    • Bookmark commonly visited journals.
                    • Use Evernote to save and store full-text articles for easy accessibility.  The Google Chrome browser has a free "web clipper" application available for Evernote, making it easy to save articles.  There's an Evernote application for smart phones, as well. 

                  • Information overload.  Choose what's important or valuable for you so the process is still meaningful and not overwhelming.  Here are some excellent tips from Chris Nickson.
                  01.14.13
                  by

                  Mercury Rising – Severely Elevated Blood Pressure in the ED

                  The Gist:  Hypertension is common within the ED population but the workup and treatment of the asymptomatic patient with a scary high blood pressure (BP) is variable.  Evaluate each patient independently but patients with asymptomatic, severely elevated BPs do not routinely need investigations (lab, ECG, UA) or urgent medication. If an anti-hypertensive is used in this population, use oral medications and avoid hydralazine, clonidine, and nitrates.  Arrange good follow up with a PCP.

                  Depending on the ED and attending I'm working with, high BPs in the ED is managed in a different fashion.  At one institution, labetalol, hydralazine, and clonidine were liberally administered despite symptomatology.  In another, we discharged patients without workup or treatment with pressures >190/100.   I've learned that EM practice varies widely, but what's the rationale and evidence behind these disparate approaches?

                  Whenever I have clinical questions, I do some basic review in a core text (i.e. Tintinalli or Rosen).  However, I often first check FOAM sources so that I can get information quickly that may be a little more updated.  It also allows me to study in a relatively uninterrupted fashion, during my cardio time at the gym or a commute.  So in this case, I queried the term on freeemergencytalks.net after my shift and got some great talks:  Dave Karras, Rob Rogers, and Chad Kessler.

                  What are we worried about? (not the focus of this post)
                  Hypertensive emergency - Rapid, progressive decompensation of vital organ, characterized by  evidence of acute dysfunction in cardiovascular, neurologic, or renal systems, caused by an inappropriately increased BP. There is no numerical definition (1).  These are the sick patients who need aggressive treatment.  These are:
                  • Acute pulmonary edema
                  • Aortic dissection
                  • Pre-eclampsia
                  • Subarachnoid hemorrhage
                  • Hypertensive encephalopathy
                  • Acute kidney injury
                  Note:  
                  • Intravenous blood pressure reduction may be indicated in other medical scenarios such as acute coronary syndrome, acute ischemic stroke, and intracerebral hemorrhage.  
                  • Some medical conditions can cause a severely elevated blood pressure, so keep these in mind when evaluating a patient:  thyroid storm, cocaine, autonomic dysreflexia, etc but usually these are accompanied by symptoms and sickness.
                  What do most of the patients actually have?
                  Severe Asymptomatic Hypertension -  previously known as "Hypertensive Urgency" (SBP > 180 mmHg or DBP > 110 mmHg), is more appropriately an outpatient term - they need their blood pressure controlled urgently (borrowed from this great Emergency Board Review podcast).

                  • Hypertension diagnosis requires repeated measurements over time, so a better term in the ED may be severely elevated blood pressure (from EMA 08/08).  
                  Limitations:
                  • The ED is not the ideal place to gauge an individual's baseline blood pressure
                    • Can be elevated due to pain, stress, anxiety.  This retrospective, observational study by Svenson demonstrates that 40% of the pediatric patients had blood pressure readings that qualified as hypertensive...do 40% of kids have hypertension?  Maybe soon in the United States.  In fact, about half of patients may not have hypertension in the outpatient setting (Tanable et al). 
                  • The patient may unknowingly live with this blood pressure.  As mentioned in the Tanable study above, the other half of patients in the ED with elevated blood pressures may have persistently elevated blood pressures in the outpatient setting.  This point seems to be born out across many studies, where the numbers range from 25-50% depending on the rigor of follow up and methodology (2).  

                  But don't they have symptoms if they're in the ED?
                  • Some providers refer patients to the ED for very high BPs or the patient may be scared of the number at home BP checks and desire further evaluation.  
                  • What about headaches, dizziness and epistaxis?  Ok, the epistaxis caused by hypertension myth has been debunked and most people know this.  
                    • Which came first, the symptom or the elevated blood pressure?  Pain, discomfort, or stress may engender an elevated blood pressure.  On other occasions, serious pathology may result from high blood pressure, causing symptoms.
                    • Height of blood pressure does not correlate with symptoms often ascribed to blood pressure, such as dizziness, headache, etc (Karras 2005).   
                    • Headaches in the ED patient with severely elevated blood pressure seem to cause the most concern amongst practitioners.  Emergency Physicians must detect the badness - things like subarachnoid hemorrhage and hypertensive encephalopathy.  However, headache is a common patient complaint in the ED, accounting for 1-4% of ED visits (2), elevated blood pressure is also common in the ED, and the majority do not have intracranial pathology (2, 3).  This is gray, non-evidence based area but history and physical probably play a big role in differentiating whether a patient's headache is concerning for hypertensive "end-organ" pathology.  Is the patient on anti-coagulants?  Do they have a neuro deficit?  Altered mental status?  Do they look sick?  What does dizzy really mean?  Perhaps one could even check for increased ICP with a quick bedside ultrasound.   

                      • Note: The 3.8% incidence of intracranial pathology in headache touted in Tintinalli and many papers is from a study in which records from 1739 patients with headache were randomly selected and reviewed (3).  The more recent study had an incidence of ~2% for any pathologic process (of 2.1 million), but is limited by the follow up (2).  
                  Workup - History and physical may yield an easy culprit.  For example, patient's often fail to take their medications, as evidenced by 42% of the hypertensive cohort in this study.
                  No need for testing in truly asymptomatic patients (Kessler talk).  ACEP guidelines and the EMCREG consensus support this recommendation.
                  • Karras et al study demonstrated that in an asymptomatic hypertensive ED cohort subjected to a battery of tests, 52% had abnormal results.  Management was changed in only 6% (n=7) of patients (could have been anything from more testing to ICU admission). 
                    • Limitation:  Small study that excluded patients with acute illness and "emergent" complaints/triage categories.
                  If you know you're going to start an anti-hypertensive, check a BMP (Kessler talk).  This is less evidence based but makes some sense.
                  • Look for creatinine as a surrogate for renal function (relevant to diuretics, ACEIs) and potassium (before starting an ACEI).
                    • Tintinalli suggests that a urinalysis, looking for hematuria and proteinuria, may be used instead of a BMP to check for renal insufficiency (Ch. 61).
                  What about searching for markers of organ damage?
                  • May indicate the complications of chronically elevated BP such as elevated creatinine, proteinuria, or hypertensive heart disease, which may be prevalent in the asymptotic population (Levy study).  As chronic problems, these necessitate chronic treatment. 
                  • CXR and ECG have poor sensitivity and are unlikely to change management (Bartha.  Limitation: study 35 years old, outpatient setting, n=116, changed management in 2/116 cases)
                  Treatment
                  Don't routinely use anti-hypertensives in the asymptomatic ED patient.  This is the meat of the "controversy" in hypertension in the ED.  The evidence base and consensus agree that asymptomatic patients with severely elevated blood pressures don't warrant acute reduction.  The ACEP guidelines (Level B Recommendations, 8 years old) do not recommend treating patients who are lack evidence of end-organ damage.
                  • This can decrease cerebral perfusion pressure in patients who have a chronically elevated blood pressure, which can lead to a stroke/cerebral hypoperfusion.  This is bad. Mechanism:  The cerebral vasculature has amazing autoregulation, maintaining the brain's blood flow despite changes in mean arterial pressure (MAP).  In chronic hypertension, this mechanism is shifted so that auto-regulation occurs at higher MAPs (lost at a higher MAP as well) leaving them unable to tolerate a rapid return to normal blood pressure.
                  • Lowering the blood pressure in the ED doesn't necessarily translate into patient benefit.  It may make us feel better, but does it really help the patient?  
                    • Gallagher editorial points out that the only real evidence that addresses this question stems from a 1967 VA study. 
                  So, why does this practice remain in some areas?
                  • Many patients don't have any other point of contact with the healthcare system.  
                    • Limitation:  This doesn't necessarily mean a patient can fill a prescription or will establish longitudinal care to continue receiving scripts and medical oversight.
                  • Habit.  We practice how we're taught and within the local culture.  Many EM texts still recommend treatment of asymptomatic high BPs in the ED.  
                  • Patient expectation:  One study demonstrates that the likelihood that a patient is more likely to receive an anti-hypertensive if their chief complaint is "high blood pressure" with an OR 5.6 (95% CI 2.0 -15.3).  When busy, it's tempting to easily satiate the patient with a temporizing measure.  
                  Prescribing an anti-hypertensive in the ED:
                  • Use oral anti-hypertensives (Kessler talk)
                    • If patient receives IV anti-hypertensives, they should probably be admitted (Rob Rogers)
                  • Don't give clonidine, hydralazine, nitrates.  These are unpredictable and if you're giving these, your patient is probably sick (and therefore, not suffering from asymptomatic severe hypertension) (Rogers, Kessler)
                  • Drop pressure gradually without an aim to achieve a normal BP (ACEP guidelines)
                  • Hydrochlorothiazide is still first-line per JNC VII for most patients.  JNC VIII should be out soon (preliminary guess = higher recommendation for ACE-I).  
                    • See this ERCast episode for more anti-hypertensive prescribing pearls
                  Refer the patient for outpatient follow up.  The ACEP guidelines give this a level B recommendation for those with persistently elevated BP readings.  
                  • A good idea as literature base show that many (~50% in some studies) will actually have hypertension (Umscheid et al).  
                  • The patient may very well develop (or already have) the sequelae of chronic hypertension, which can cause significant morbidity. 
                  The blood pressure will fall on its own (oftentimes).  
                  • This study by Cienki et al looked at a small sample of ED patients with high blood pressure and took measurements at 10 minute intervals to examine the fall of these values.  They found that the blood pressure did typically fall significantly in the cohort with BP >160/100 (the population we're really talking about here).  
                    • Limitations:  The study was really small and did not include patients who ingested caffeine/stimulants so while the conclusion is reasonable, it's not entirely applicable to the typical ED population.  
                    Other good resources:
                    Hypertension and the Emergency Physician - post by Dr. Reuben Strayer
                    EB Medicine June 2010 review
                    Commentary/Review by Drs. Shayne and Pitts from Emory
                    01.05.13
                    by

                    Emergency Medicine – Variations on a Theme

                    The Gist:  Although emergency medicine has a reputation for being algorithmic, there's a good amount of variation in thinking and practice.  This is necessary (variable resources, different patient populations) and can be excellent (promoting growth, change, and innovation).  The foundation for our practice is built in the training we receive, both in text and from our local educational community.  FOAM has played a role in laying the foundation to what will become my EM practice and I think that FOAM has the ability to lead to improved patient care through discourse on evidence based medicine, updates on current practice, and insight into the thought process and practice of others (shared learning!).  

                    After spending my third year of medical school in rural Alabama and absorbing a good bit of EM FOAM, I thought I should experience the cutting edge, academic side of EM.  Realizing, through heated Twitter debates, that emergency physicians actually approach many situations rather differently, I wanted to lay a broad foundation of practice...knowing I would probably practice most similarly to wherever (and with whomever) I train.  Over the past six months, I had the privilege of training in seven excellent EDs in five states with the smartest people I've met.  Below is a smattering of bread and butter things I found...

                    Apneic oxygenation/high flow nasal cannula during intubation (NODESAT - nasal oxygen during efforts securing a tube).  One institution had adopted and implemented this by the time I rotated through, another started this after a virtual grand rounds lecture with Dr. Scott Weingart.  Pulse ox lag is real and few people talked about it in airway situations, check out this PHARM post on the subject.  

                    Use of droperidol.  Places either use it liberally or refuse to use the drug, as I discussed in this post.  At an institution that no longer uses droperidol, an attending went through the paucity of evidence behind the black box warning as well as the political/economic factors that likely played a role in the downfall of droperidol.
                    Use of ketamine.  FOAM teams with enthusiasm for ketamine (see any tweet by @embasic or @MDAware, this multi-national podcast, or one of many EMRAP episodes), but I saw this drug rarely used outside of pediatrics in all institutions, the most notable exception was to intubate asthmatic patients.  Why does this matter?  Procedural sedation can be tricky and I witness some that were executed well and others that were less than ideal.  In addition to the amnestic properties, ketamine confers some analgesia and has less respiratory depression (clinically relevant, that's uncertain).  Furthermore, one ED I rotated through had absolutely zero etomidate available.  We used whatever was available for RSI (and thus, needed to be familiar with a cornucopia of agents). 
                    Quantitative capnography (ETCO2).  Not routinely used after intubation or for procedural sedation in 5 of 7 institutions, although infrastructure was the limiting issue at one institution, which has since been rectified.  However, the FOAM community has referred to it as a 'standard of care," including Dr. Scott Weingart in his review of NAP4. 
                    Treatment of an abscess.  At nearly all institutions, antibiotics were prescribed following an I&D of an abscess, although almost all attendings mentioned that one could "probably get away without them"  A minority of cases had significant surrounding cellulitis or immunosuppressed states.  Three of six places had me pack abscesses, although this was more attending dependent than institution dependent.  The Skeptics Guide to Emergency Medicine's podcast #13 is a great review (free registration required) of the evidence base behind packing and antibiotics.  Freeemergencytalks.net also has a great talk on the subject.  
                    • Antibiotics - a review, demonstrating that most abscesses don't need antibiotics.  Antibiotics also carry harm, from resistance to Steven-Johnson and diarrhea and this recent article in Pediatrics shows that TMP-SMX adverse effects are on the rise, likely secondary to profound administration for skin and soft tissue infections.  
                      • What about MRSA abscesses?  Here are some EBM guidelines. 
                        • 90% of patients with MRSA abscesses will do just as well without antibiotics (Rajendren).
                      • What about recurrence? Less recurrence by day 10 but no change at 30 days. 
                    • Packing - The NNT summary of a small study, demonstrating no benefit to packing abscesses. Confirmed in this Kessler et al study.  During ICEM 2012, there was much tweeting on packing in an era in which some abscesses undergo primary closure (across the Atlantic).  
                    • NB:  Much of the literature on this topic is from the surgical literature, which is not exactly equivalent; however, the ED literature base on the topic is growing.  
                    Central lines.
                    • Code line of choice:  Subclavian-4, Femoral-3.  
                    • Use of ultrasound in code lines: 0.  
                    • Use of ultrasound in femoral lines: 0.  
                      • Small study: not slower than landmark approach and had better success. 
                    • Use of ultrasound in subclavian lines: 0.
                    • Use of ultrasound in the IJ: 7.
                    Ultrasound.  Each academic center used ultrasound heavily but the community hospital used ultrasound solely for FAST scans and placement of internal jugular central lines.  At the community institution, they often laughed as I dragged the single SonoSite Titan from room to room or enthusiastically discussed what I could do with a linear array probe.  When I diagnosed a SBO in <30 seconds, one of the doctors was sold.   Billing for scans and the practice of ordering confirmation scans seemed to vary the most. Also, utilization of ultrasound seemed more attending dependent than necessarily institution dependent since training and credentialing are still being worked out in many settings.  Listening to this episode may have been beneficial.

                    Observation units.  All but one place I rotated at had an observation/clinical decision unit (CDU) and the one place that did not have one, incorporated one by the time I returned a few months later.  These units provided a monitored setting where patients could have cardiac enzymes drawn for rule-out protocols, receive antibiotics, or receive rehydration, etc.  Anecdotally, these seemed to improve workflow and allow easier disposition, something supported by literature (Trzeciak, Schneider, Gordon).  In the cardiac setting, use of these seemed to buy most people either a stress test or CCTA on the spot, depending on the institution.  Although this practice is supported by the AHA, evidence seems to be mounting that this may be unnecessary and costly (See EMRAP November 2012 with Dr. Scott Weingart and SMART EM summary and podcasts on this topic).

                    Endotracheal intubation.

                    • FOAM conversations often revolve around direct laryngoscopy (DL) versus video laryngoscopy (VL) (ex: PHARM podcast 51 and post, EMRAP 9/12).  DL served as the primary means of intubation across the board and residents and attendings preferred this modality.  Each institution had at least one VL in the ED, predominantly the glidescope (although one had one in the 'resuscitation area,' a slight trek in an unpredictably difficult intubation).  Two of seven places had combined VL/DL devices available but I didn't see these used during my rotations.  
                    • Post-intubation sedation was not always ordered, but was not an institutionally dependent thing.  Attendings at one institution seemed to consistently stress ordering sedation at the time one was ordering the paralytic and induction agents versus waiting until afterward.
                    In EM, there are constants as well:
                    Emergency physicians know how to have fun

                    (EM clerkship wakeboarding and hiking days)

                    Personal thought:  FOAM levels the playing field with regard to access to information, something that can be amazing for community physicians removed from the academic setting or those in more remote locations.  Additionally, I am incredibly interested to see how FOAM can continue to evoke dialogue about these differences in practice to achieve better quality of medicine.  
                    01.05.13
                    by

                    Emergency Medicine – Variations on a Theme

                    The Gist:  Although emergency medicine has a reputation for being algorithmic, there's a good amount of variation in thinking and practice.  This is necessary (variable resources, different patient populations) and can be excellent (promoting growth, change, and innovation).  The foundation for our practice is built in the training we receive, both in text and from our local educational community.  FOAM has played a role in laying the foundation to what will become my EM practice and I think that FOAM has the ability to lead to improved patient care through discourse on evidence based medicine, updates on current practice, and insight into the thought process and practice of others (shared learning!).  

                    After spending my third year of medical school in rural Alabama and absorbing a good bit of EM FOAM, I thought I should experience the cutting edge, academic side of EM.  Realizing, through heated Twitter debates, that emergency physicians actually approach many situations rather differently, I wanted to lay a broad foundation of practice...knowing I would probably practice most similarly to wherever (and with whomever) I train.  Over the past six months, I had the privilege of training in seven excellent EDs in five states with the smartest people I've met.  Below is a smattering of bread and butter things I found...

                    Apneic oxygenation/high flow nasal cannula during intubation (NODESAT - nasal oxygen during efforts securing a tube).  One institution had adopted and implemented this by the time I rotated through, another started this after a virtual grand rounds lecture with Dr. Scott Weingart.  Pulse ox lag is real and few people talked about it in airway situations, check out this PHARM post on the subject.  

                    Use of droperidol.  Places either use it liberally or refuse to use the drug, as I discussed in this post.  At an institution that no longer uses droperidol, an attending went through the paucity of evidence behind the black box warning as well as the political/economic factors that likely played a role in the downfall of droperidol.
                    Use of ketamine.  FOAM teams with enthusiasm for ketamine (see any tweet by @embasic or @MDAware, this multi-national podcast, or one of many EMRAP episodes), but I saw this drug rarely used outside of pediatrics in all institutions, the most notable exception was to intubate asthmatic patients.  Why does this matter?  Procedural sedation can be tricky and I witness some that were executed well and others that were less than ideal.  In addition to the amnestic properties, ketamine confers some analgesia and has less respiratory depression (clinically relevant, that's uncertain).  Furthermore, one ED I rotated through had absolutely zero etomidate available.  We used whatever was available for RSI (and thus, needed to be familiar with a cornucopia of agents). 
                    Quantitative capnography (ETCO2).  Not routinely used after intubation or for procedural sedation in 5 of 7 institutions, although infrastructure was the limiting issue at one institution, which has since been rectified.  However, the FOAM community has referred to it as a 'standard of care," including Dr. Scott Weingart in his review of NAP4. 
                    Treatment of an abscess.  At nearly all institutions, antibiotics were prescribed following an I&D of an abscess, although almost all attendings mentioned that one could "probably get away without them"  A minority of cases had significant surrounding cellulitis or immunosuppressed states.  Three of six places had me pack abscesses, although this was more attending dependent than institution dependent.  The Skeptics Guide to Emergency Medicine's podcast #13 is a great review (free registration required) of the evidence base behind packing and antibiotics.  Freeemergencytalks.net also has a great talk on the subject.  
                    • Antibiotics - a review, demonstrating that most abscesses don't need antibiotics.  Antibiotics also carry harm, from resistance to Steven-Johnson and diarrhea and this recent article in Pediatrics shows that TMP-SMX adverse effects are on the rise, likely secondary to profound administration for skin and soft tissue infections.  
                      • What about MRSA abscesses?  Here are some EBM guidelines. 
                        • 90% of patients with MRSA abscesses will do just as well without antibiotics (Rajendren).
                      • What about recurrence? Less recurrence by day 10 but no change at 30 days. 
                    • Packing - The NNT summary of a small study, demonstrating no benefit to packing abscesses. Confirmed in this Kessler et al study.  During ICEM 2012, there was much tweeting on packing in an era in which some abscesses undergo primary closure (across the Atlantic).  
                    • NB:  Much of the literature on this topic is from the surgical literature, which is not exactly equivalent; however, the ED literature base on the topic is growing.  
                    Central lines.
                    • Code line of choice:  Subclavian-4, Femoral-3.  
                    • Use of ultrasound in code lines: 0.  
                    • Use of ultrasound in femoral lines: 0.  
                      • Small study: not slower than landmark approach and had better success. 
                    • Use of ultrasound in subclavian lines: 0.
                    • Use of ultrasound in the IJ: 7.
                    Ultrasound.  Each academic center used ultrasound heavily but the community hospital used ultrasound solely for FAST scans and placement of internal jugular central lines.  At the community institution, they often laughed as I dragged the single SonoSite Titan from room to room or enthusiastically discussed what I could do with a linear array probe.  When I diagnosed a SBO in <30 seconds, one of the doctors was sold.   Billing for scans and the practice of ordering confirmation scans seemed to vary the most. Also, utilization of ultrasound seemed more attending dependent than necessarily institution dependent since training and credentialing are still being worked out in many settings.  Listening to this episode may have been beneficial.

                    Observation units.  All but one place I rotated at had an observation/clinical decision unit (CDU) and the one place that did not have one, incorporated one by the time I returned a few months later.  These units provided a monitored setting where patients could have cardiac enzymes drawn for rule-out protocols, receive antibiotics, or receive rehydration, etc.  Anecdotally, these seemed to improve workflow and allow easier disposition, something supported by literature (Trzeciak, Schneider, Gordon).  In the cardiac setting, use of these seemed to buy most people either a stress test or CCTA on the spot, depending on the institution.  Although this practice is supported by the AHA, evidence seems to be mounting that this may be unnecessary and costly (See EMRAP November 2012 with Dr. Scott Weingart and SMART EM summary and podcasts on this topic).

                    Endotracheal intubation.

                    • FOAM conversations often revolve around direct laryngoscopy (DL) versus video laryngoscopy (VL) (ex: PHARM podcast 51 and post, EMRAP 9/12).  DL served as the primary means of intubation across the board and residents and attendings preferred this modality.  Each institution had at least one VL in the ED, predominantly the glidescope (although one had one in the 'resuscitation area,' a slight trek in an unpredictably difficult intubation).  Two of seven places had combined VL/DL devices available but I didn't see these used during my rotations.  
                    • Post-intubation sedation was not always ordered, but was not an institutionally dependent thing.  Attendings at one institution seemed to consistently stress ordering sedation at the time one was ordering the paralytic and induction agents versus waiting until afterward.
                    In EM, there are constants as well:
                    Emergency physicians know how to have fun

                    (EM clerkship wakeboarding and hiking days)

                    Personal thought:  FOAM levels the playing field with regard to access to information, something that can be amazing for community physicians removed from the academic setting or those in more remote locations.  Additionally, I am incredibly interested to see how FOAM can continue to evoke dialogue about these differences in practice to achieve better quality of medicine.  
                    12.14.12
                    by

                    Not Black Boxed? Droperidol as an Anti-emetic


                    The Gist:  Droperidol is a safe and effective anti-emetic at low doses (0.625-2.5 mg) (evidence based review of droperidol safety).

                    The background:  From EMCrit's podcast on chemical restraints to EM Lit of Note reviews of ondansetron, FOAM teams with support for droperidol.  My experience in the ED, however, has varied widely.  Over the past six months, I've rotated through seven emergency departments in the Eastern US.  I've discovered that people have very strong feelings about droperidol.  In some places, droperidol flowed freely yet judiciously and in others, the drug was a dirty word.  As part of a recent rotation, I gave a presentation on the use of droperidol as an anti-emetic so I figured I'd share my slide set.

                    Why do we care?  There are so many anti-emetics!
                    • Drug shortages.  Hospitals across the nation are experiencing shortages of many drugs, including anti-emetics such as ondansetron, promethazine, prochlorperazine, and metoclopramide.  Nausea and vomiting is a "bread and butter" issue in the ED and it's vital that we're equipped to take care of patients, even when we don't have our favorite drugs. 
                      • This database review found a statistically significant increase in adverse events after switching from droperidol to promethazine after the black box warning, when a shortage of prochlorperazine existed as well.  
                    • Intolerance to other medications. The charts of many patients with migraines list allergies to promethazine, prochlorperazine, and metachlopramide.  
                      • I recently had a patient with an intractable migraine who typically received relief from meperidine from his neurologist.  Unfortunately, on a long weekend, the neurologist's office was closed and the hospital didn't stock meperidine.  Opioid analgesics didn't mitigate the pain but droperidol did the trick (at 2.5 mg). 
                    • Cost.  Droperidol has been around for decades and is cheap.  Ondansetron became generic in the US a few years ago, but remains more expensive than droperidol.  
                    • Effective.  Droperidol 0.625 mg is as  effective as 4mg of ondansetron as demonstrated by Kriesler et al (this looked at post-operative nausea and vomiting).  Braude et al demonstrated that this effectiveness translates into the ED setting in a double-blind RCT comparing droperidol 1.25 mg, metoclopramide 10 mg, prochlorperazine 10 mg, and saline placebo.
                    • These drugs often end up in our "migraine cocktails" and low-dose droperidol seems to work in migraines as well, representing a cheap intervention for ill patients (1)
                    The basics:
                    • Butryophenone (like haloperidol)
                    • D2 agonist, anti-emetic effect is likely secondary to effects in the chemoreceptor trigger zone.
                    • Short-acting, works in 3-10 minutes
                    Safety

                    • Side Effects:  Drowsiness, dysphoria, dystonia, akasthisia but these effects are easily fixed with diphenhydramine and aren't the reason that hospitals and physicians are sometimes reticent to embrace droperidol...The Prolonged the QT interval
                      • Mechanism:  It's thought that droperidol blocks the rapid component of the delayed K+ and current depolarizing targets: L-type Ca2+ current, Na+-Ca2+ exchanger, and the Na+-K+ adenosine triphosphatase.  This mechanism may explain the susceptibility of individuals with Type I Long QT syndrome (2).
                    2001 Black Box Warning
                    Based on two studies (Lischke and White) and MedWatch reports.  I won't rehash all of the data here, but it's found in my slideset and in this summary.  Applies to FDA approved doses (2.5 mg and above).

                    MedWatch Reports
                    • 271 unique, spontaneous adverse cardiovascular events from 93 individuals
                    • Most cases were reported to the FDA between 1999-2001 (events dated 1970-2001)
                      • 71 cases reported on July 9, 2001 by an unknown number of sources that occurred on a variety of dates (bizarre)
                    • 10 of these cases were associated with doses of droperidol 2.5 mg or less
                      • Individuals in these cases were not your typical healthy individuals (see Table below from Habib et al) 
                      More recent evidence

                      • Charbit et al (2005) prospective, single blind study where patients (n=85) received 0.75 mg droperidol OR 4 mg ondansetron
                        • QTc prolonged before administration in 21% of subjects 
                        • Maximum Increases in QTc: Droperidol 17 +/- 9 ms, Ondansetron  20 +/- 13 ms 
                      • In 2008, Rappaport of the FDA stated that the FDA warning for droperidol did not apply to doses below 2.5 mg, as they had not evaluated that data (3).  
                      • Ondansetron has been found to prolong the QTc for up to 120 minutes and has been associated with torsades de pointes, as in this paper by Hafermann et al.  In fact, this month, the 32 mg dose of ondansetron was pulled from the market. 

                      • Treating primary headaches in the ED: can droperidol regain its role?


                      Experts' take on the droperidol black box warning
                      12.03.12
                      by

                      FOAMing Up the Wards: Glucagon in CCB Toxicity?

                      The Gist:  Although high dose insulin (HDI/hyperinsulinemia euglycemia) therapy has been embraced as a treatment modality for calcium channel blocker (CCB) toxicity, glucagon remains one of the "textbook" answers in the United States.  This is likely outdated as many experts think this should be removed or given as only a cursory measure given the other modalities available.

                      Why do we care?  CCBs are a "one pill can kill" medication in children.  Additionally, they're commonly encountered in practice and have devastating consequences.  For a case-based review of CCB toxicity, check out this toxicology conundrum and this overview by Kerns (full text) (below is not a complete review of CCB toxicity).

                      Glucagon in CCB toxicity:
                      • Increases hemodynamic parameters in models (heart rate and blood pressure)
                      • Mechanism:  stimulates adenylate cyclase to increase cAMP which may improve cardiac contractility. 
                      • Initial dose: 2-5 mg IV over 30-60 seconds for an adult and 50 mg/kg in children and can be repeated. If the patient has a postive response, they should be started on a continuous infusion of the initial“response dose” given per hour (1).  
                      Problems with glucagon:
                      • It takes a lot of glucagon, more than many EDs generally have to offset the effects of a calcium channel blocker overdose. A one hour glucagon infusion could exhaust many hospitals glucagon supply.
                      • Vomiting.  This is precisely why glucagon is used, occasionally successfully  in patients with a food bolus.  In sick patients or those who aren't protecting their airway, this increases the risk of aspiration.
                      • Cost.  According to a consensus paper on antidote stocking in Annals of EM, an eight hour course of glucagon therapy would cost nearly $8,000 (US). 
                      • Efficacy.  The paper by Kline et al demonstrates that HDI therapy is far more efficacious than glucagon in the canine model.  
                      FOAM delivers.
                      • Duke University's Emergency Medicine grand rounds are available on iTunes and Dr. Kerns happens to cover CCB overdose in this lecture (#43).  An astounding piece of information is nestled in this talk:  Nearly all studies examining glucagon in CCB toxicity were conducted prior to the availability of recombinant glucagon and used Eli Lilly's standard glucagon preparations instead.  What are the repercussions of this?  
                        • The standard preparation of glucagon, made from mammalian pancreatic extract, contained insulin (also from pancreatic cells) until recombinant glucagon was available in 1998.  Some vials of glucagon, when analyzed by this study group at Carolinas Medical Center, contained 100 units of insulin.  This was demonstrated in the study on HIE therapy in verapamil poisoning Kline et al.  Thus, benefit seen with glucagon may be partially a result of the insulin in the preparation.  I couldn't find any published studies of this.   
                      • EMCrit podcast #27 features the renowned Dr. Leon Gussow of The Poison Review and supports the notion that glucagon probably does nothing for CCB toxicity, whereas the published clinical experience supports HDI. 
                      But does this FOAM appear on the wards?  Yes!
                      I had the fortune to learn from Dr. Kerns at Carolinas Medical Center on a recent toxicology rotation.  The voice from the Duke EM podcast above sounded familiar and I had the opportunity to ask him about CCBs in detail.   He suggested the following algorithm in the case of known CCB toxicity, with emphasis on moving quickly through some of the earlier steps:
                      • Activated charcoal if appropriate, especially if a sustained release preparation.
                        • All CCBs are not equal.  Verapamil seems to be the worst, with diltiazem next, and the dihydropyrines behind diltiazem.  
                      • IV fluids -careful with heart failure. Will likely have minimal response, just fill the tank.
                      • Calcium - Often doesn't work.  If one gives enough calcium, may be able to overcome competitive inhibition in some individuals. Push the calcium to 15-20 mg/dL.  Effect is short lived (15-20 minutes) so repeat boluses and begin infusion if patient responds.
                        • Calcium gluconate - peripherally start with at least 3 amps
                        • Calcium chloride - central administration. 
                      • Glucagon - can give it but move past this step quickly because it has limited utility.
                      • Vasopressors - use bedside ultrasound to look at cardiac contractility
                        • Insulin will increase cardiac contractility so if there's already decent contractility, try pressors (norepinephrine) and escalate the dose every 5 minutes.  If contractility is Ionotrope depressed, move on to HDI
                      • High dose insulin (HDI) - Move fairly quickly through above interventions to this point in the sick, hypotensive, bradycardic patients.   
                        • Improves the utiliziation of glucose by the myocardium.  In the stressed state, the heart switches from predominantly using free fatty acids to using carbohydrates as a substrate.
                        • CCBs induce a state of relative insulin resistance and deficiency by preventing insulin release by the pancreas and organ/cellular uptake.
                        • Give a bolus initially to saturate the insulin receptors since it takes ~20-45 minutes for the metabolic response to insulin to really become apparent at a dose of 1-10 units/kg, followed by a infusion at the bolus response rate (per hour) (2).
                        • Requires q30 minute glucose checks and frequent potassium monitoring (insulin drives potassium intracellularly so levels appear low while body stores are normal) (2)
                        • Is there a downside?  Nickson (of LITFL fame) and Little articulate them well in this article.  Essentially, HDI therapy is cumbersome and toxicologic patients are not well-suited for RCTs (due to number of patients and the very individual nature of the circumstances) so data are limited. Also, due to the infrequent nature of these toxicities are all providers knowledgeable about the beneficial role of early HDI?
                      I also had the privilege of training with South Carolina's toxicologist who added in two additional pearls:
                      • Lipid emulsion - experiential and published case reports demonstrates improved morbidity and mortality, including a marked decrease in norepinephrine requirements (Ozcan and Weinberg and Cave et al).
                      • ECMO - case reports suggest that ECMO may work in some patients but published data is limited and a bias toward publishing positive results may exist (Koltz et al, De Rita et al) 

                      References:
                      1. Zaologa GP, Malcolm D, Holladay J, Chernow B. Glucagon Reverses the Hypotension and Bradycardia of Verapamil overdose in rats. Crit Care Med 1985;13:273
                      2. Kerns, W.  Management of b-Adrenergic Blocker and Calcium Channel Antagonist Toxicity.  Emerg Med Clin N Am 25 (2007) 309–331

                        11.20.12
                        by

                        Reserved For Grilling? – Activated Charcoal

                        The Gist:  Use of activated charcoal (AC) for toxic ingestion is controversial and has been a polarizing topic at times, but most people agree that it's individual and situation dependent.  The research and evidence base in toxicology is different than much of medicine due to the variable, unpredictable nature of exposures and the reporting bias of these cases.  Weigh the benefits (toxicity of the substance, time of ingestion..the sooner the better, availability of an antidote) with the risks (mentation, airway status) in each situation.  If in doubt, ask a toxicologist/call the poison center.

                        I just completed a toxicology rotation and sometimes it felt like I was cheating as a result of my prior interactions with toxicology via FOAM.  A bread and butter topic that arose frequently at the poison center and hospital was the use of activated charcoal and many practitioners calling in weren't sure of the role of charcoal.  I realized I, too, needed a review on the topic.  I found good reviews in the Freeemergencytalks.net talk 'Is Charcoal Obsolete?' and a debate, "Activated Charcoal is Obsolete" and the excellent toxicologists and reading filled in the rest.  The AACT position statement on activated charcoal summarizes the data on specific drug recommendations and continues to recommend individual consideration of whether charcoal would benefit a patient when given within an hour of ingestion.

                        Review of AC 
                        Predominantly from Goldfrank's Toxicologic Emergencies 
                         "Antidotes in Depth - Activated Charcoal" by Hammond
                        Composition - the process generates an absorptive material due to massive surface area
                        • Carbonaceous materials heated to decomposition and treated with oxidizing agents at high temperatures to create pores.  
                          • Size of these pores dictates the surface area of the material (which affects toxin adsorption)
                        Adsorption - binding of the xenobiotic to the charcoal.  This may reduce blood levels of drugs between 24-47%, depending on the time frame of administration but does not necessarily translate into a clinically significant outcome.
                        • Various forces at play.  Typically adsorbed in dissolved, non-ionized form
                        • Adsorptive capacity directly related to surface area (higher surface area = greater adsorptive capacity)
                        • pH dependent
                          • Weak bases adsorbed better at higher pH, weak acids at lower pH
                        • May desorb
                          • pH dependent process (weak acids may desorb from AC as the complex passes from the acidic stomach to the small intestine, freeing up toxins later)
                        Adverse effects
                        • Aspiration - incidence has varied from 4-25%, some association with altered mental status.  
                          • Debatable about how much this matters.  Some claim that we all aspirate but charcoal is the “bad guy” because it’s very clearly noticeable in the endotracheal tube but may not be clinically relevant. For example, this article by Moll et al demonstrates a low incidence of new infiltrate after AC administration.  There are reported cases of long term sequelae from charcoal aspiration such as this one in Pediatrics, but in this case the problem actual resulted from accidental placement of the nasogastric tube into the trachea (thus directly filling the lungs with charcoal).
                        • Peritonitis (if perforated GI tract)
                        • GI:  Emesis, Constipation, Diarrhea
                        • Corneal abrasions 
                        Administration - recommendations are on an individual basis with attention to risk versus benefit
                        • In favor of administration
                          • Xenobiotic available for adsorption in the GI tract
                            • Early presentation after ingestion
                          • Substance is toxic (removal from system very beneficial to patient) and no antidote available
                        • Opposing administration
                          • Tenuous airway status/high aspiration risk
                          • Suspected or known GI perforation or need for endoscopy (caustic ingestions)
                          • Abnormal GI exam, impaired motility
                        • Co-therapies
                          • Not recommended in conjunction with whole bowel irrigation or cathartics
                        • Not very palatable
                          • Tip from PharmD at the poison center - administer in chocolate syrup
                        Home and Prehospital
                        • Studies demonstrate variable success in administration and airway/mental status is a concern.  According to a 2007 report in the Journal of Medical Toxicology, prehospital administration is often not in accordance with the AACT position statement (ie charcoal was administered at greater than one hour after ingestion). This paper did not delve into clinical significance of these deviations.  Also, many efforts in toxicology are "last ditch" efforts due to the often severe, novel nature of these exposures.
                        Dosing
                        • 1 g/kg of body weight
                        • Attempt at a 10:1 ratio of AC to xenobiotic to tie up the toxin
                        • Usually ~ 50-100 g in an adult (10-25 g in children <1 year old, 25-50 in children 1-10 years old)
                        Multiple-dose AC (MDAC) - Mostly out of favor.
                        • Consider In:
                          • Delayed/prolonged release (bezoars, enteric coating, extended release formulations)
                          • Prevent reabsorption (activated metabolites/xenobiotics)
                          • Drugs that undergo enterohepatic circulation (dapsone, quinine, theophylline). 
                          • Drugs with toxicokinetics similar to hemodialysis: low volume of distribution, low protein binding.
                        • Dosing - depends on the individual and the specifics of the ingestion
                          • Load with standard dose of AC
                          • Repeat at 0.25-0.5 g/kg body weight every 1-6 hours.
                          11.08.12
                          by

                          (Don’t) Mind The Gap

                          The Gist:  Despite our best intentions and with regard to the combined literature, research, and clinical experience, we practice medicine in the past.  Information disseminates and is adopted by individuals instantaneously in many other aspects of life.  Public discourse resulting from this information sharing, applied in medicine (Knowledge Translation) has the potential to improve health care...and FOAM (Free Open Access Meducation) is a promising means to tackle this problem.

                          What's the problem?  In an epidemiology class for my Master of Public Health, I was shocked when my professor declared that it often took a decade, if not more, before evidence was practiced by clinicians.  But we're so educated!
                          • Gaps between knowledge/information/experience and clinical practice (1).  Medical and health care research is booming.  Things change quickly and it's difficult to stay up to date, especially if your specialty involves every organ system and environment imaginable.  What is this worth if we can't integrate it in clinical practice to benefit our present patients?
                          • Physicians practice despite guidelines or evidence favoring a different outcome (2).  We have collections and evaluations of the best evidence from the Cochrane Library and BestBets
                          Knowledge translation (KT): “Knowledge translation is defined as the exchange, synthesis and ethically sound application of knowledge—within a complex system of interactions among researchers and users—to accelerate the capture of the benefits of research… through improved health, more effective services and products, and a strengthened health care system.”  (1)

                          KT tutorials:


                          Goals of KT:
                          • Changing behavior
                          • Changing health outcomes
                          • Achieving both of the above outcomes in an ethical, non-coercive way.
                          How can FOAM improve KT?
                          • Can precede national guidelines.

                          • Easily accessible from nearly anywhere. 
                            • TheNNT has a host of evidence-based reviews on frequently encountered topics.  These are frequently revised.
                            • MDCalc allows one to easily calculate a score like PESI or CHADS2-VASC score in seconds.
                            • Many apps for smart phones and tablets have these built in calculators as well (Medscape under "calculators" and other ones that are paid apps).
                          • Asynchronous updates in literature and research at no charge to the consumer.  Continuing Medical Education (CME) can be expensive and time consuming but blogs, podcasts, and various RSS feeds allow one to access information when, where, and in the quantity one desires (I prefer mine at the gym, in the car, or during anything that involves waiting).
                            • SMARTEM is a podcast that takes deep dives through the literature to assess and interpret the evidence behind various clinical practices.
                            • The Skeptics Guide to Emergency Medicine (The SGEM) has a free podcast in which they address specific articles or 
                          • Bridging academic and community settings, "flattening the world" (to borrow Thomas Friedman's analogy for technology and knowledge/goods dissemination).  Knowledge and experience varies across the regions (ex: see the Prehospital and Retrieval Medicine multinational podcast on procedural sedation).
                            • A group of FOAM masters recently began a "Rural Masterclass," to extend and involve rural physicians in a relevant and current continuing learning endeavor.
                          • Dialogue.   Individuals in the medicine field frequently debate and discuss guidelines, criteria, and "standards of care" on Twitter, blogs, and podcasts.  This frequently engenders further examination of preconceptions, understandings, and barriers to implementation of interventions/therapies.
                            • At times it seems there's peer pressure to conform to how others are doing things, even if it's not necessarily the most appropriate intervention (example: prescribing antibiotics for acute sinusitis in otherwise healthy patients or failing to prescribe steroids in acute asthma exacerbations).  Discourse between professionals can function as a support system and allow individuals to troubleshoot and benefit from each others experiences in implementation.
                          Is there a downside to KT?
                          • Medicine is not a unilateral encounter but a dialogue and decision making process with a patient. Some individuals worry that emphasis on evidence and guidelines have the potential to overshadow the individual nature of clinical encounters (4).  Properly understood, however, KT is not a trendy guise for CMS guidelines or core measures (which are designed to be coercive).  The essence of KT is to produce better health outcomes based on all available evidence.
                          • Implementation is not homogenous for each system or practice.  KT involves the attitudes, knowledge base, and infrastructure of complex systems.  In fact, there's an entire journal dedicated to implementing evidence (Implementation Science).
                          • Creating and disseminating guidelines do not necessarily result influence practice at the bedside.  Effective KT is the product of integration into a clinician's cognitive approach of each situation, which is not an insignificant endeavor (5). 

                          References
                          1.  Davis D et atl. The case for knowledge translation: shortening the journey from evidence to effect BMJ 2003; 327 http://www.bmj.com/content/327/7405/33?ijkey=3d8eebc236964c68d0cfafade252097a5374503c&keytype2=tf_ipsecsha
                          2.  Lang E, Wyer P, Haynes R. Knowledge translation: closing the evidence-to-practice gap Ann Emerg Med. 2007 Mar;49(3):355-63. Epub 2006 Nov 3. (full text)
                          3.   Straus S, Tetroe J, Graham I.  Defining Knowledge Translation. CMAJ August 4, 2009 vol. 181 no. 3-4 Full Text

                           
                        • Wieringa S.  
                          • Is it time to drop the ‘knowledge translation’ metaphor? A critical literature review 
                          J R Soc Med vol. 104 no. 12501-5095.  Green L and Siefert C.  Translation of Research Into Practice: Why We Can’t “Just Do It” J Am Board Fam Medvol. 18 no. 6541-545

                          11.01.12
                          by

                          Double Gloving It – Hands-on Defibrillation

                          The Gist:  In the pursuit of minimally interruptive, excellent CPR, there has an increasing interest in hands-on defibrillation.  Mounting literature suggests that external, biphasic defibrillation, with a gloved individual providing chest compressions, is safe (but wear double gloves).  The literature isn't conclusive in either direction and this practice hasn't been endorsed by the American Heart Association,  allowing providers to make their own conclusions and practices.  

                          The recent paper: Sullivan J, Chapman F.  Will medical examination gloves protect rescuers from defibrillation voltages during hands-on defibrillation? Resuscitation. 2012 Aug 25.
                          • Simulated (lab) study evaluated the voltage needed to cause current flow and breakdown in various exam gloves (latex, nitrile, etc).
                          • Exam gloves performed differently based on composition (and variably within the composition group).  Double nitrile, vinyl, and latex performed best.
                          • Some single gloves broke down in the biphasic defibrillator range.
                          • Double gloves leak within the biphasic defibrillator range but only broke down when the voltage exceeded this range.
                          • The leakage of current in these gloves often occurred at levels below 'the level of sensation.' I.e. a provider may not detect current when, in fact, it is passing through the glove.
                            • Clinical significance of this is unknown but the authors make interesting points in their discussion regarding the duration of shock, amplitude of the voltage, likelihood of the current's path including the heart, and intrinsic health characteristics of the health care provider. 
                          • There are limitations: these gloves weren't soaked in ultrasound jelly/patient sweat/condensation from cooling packs, weren't stretched out because there were no appropriate sized gloves available in the room, and were likely evaluated for rents.  
                          The impetus:  About a week ago, the following video appeared, accompanied with lively discussion, on my Twitter feed. 

                          I thought this was neat because last year, I heard about hands-on defibrillation on this ERCAST episode.  I gasped, as this opposed the "all clear" dogma I lapped up in BLS and ACLS.  I found the following articles and a good LITFL post.

                          Convinced, I was nervously excited to try it.  It took many charming smiles, print outs of references, and attempts with various attendings but I got my chance.  And, well, I really didn't feel anything.  Granted, I was wearing a couple sets of gloves and I ensured I wasn't touching any metal, but I felt good about it.  I've repeated my attempts in the various institutions I've rotated through recently, to no avail.  After evaluating the paper above, I'll still try (perhaps with triple gloves).  We argue that interventions for our patients must be "clinically significant and, in a fit, healthy individual, I think that any current leakage to me is going to be insignificant.

                          Why does this matter?
                          • "Good quality CPR" depends on constant, consistent, adequate compressions as well as early defibrillation.  Guidelines, training programs, and leaders emphasize no interruptions while recommending defibrillation (a necessary interruption) - a somewhat contradictory set up.  
                            • One of my favorite FOAM professors, Dr. Amal Mattu, brought the following to my attention in the following UMEM pearl: "For every 10 seconds of hands-off time during cardiac arrest, the patient's chances of successful return of spontaneous circulation decreases by 50% due to reductions in cerebral perfusion." (Edelson et al in Resuscitation 2010)
                          • Chest compression interruptions during CPR are more common than we think.  This month's Resuscitation also ran a study by McInnis et al evaluating code leaders perception of error.  The most commonly unidentified error?  Interruptions in chest compressions (>10 sec), which occurred in 32/40 cases (pulse check and defibrillation were the most often cited reasons although, I think sometimes a lack of awareness/fatigue is more likely the culprit)
                            • Hands-on defibrillation could aid us in achieving interruption-less CPR!
                          10.27.12
                          by

                          FOAM: Fighting Oligoanalgesia And Meanness

                          The Gist:  Analgesia in the sick emergency department  (ED) patients is inadequate and sick patients seem to suffer the most, which is just plain mean.  Dr. Scott Weingart articulates it best in "Pain and Terror as Effective Pressors."  Adopt a protocol or algorithm to consider analgesia early on and with every patient.  If you have access to EBMedicine, check out their August 2012 summary on the trauma patient (subscription required).

                          Like most trainees I have a fear of patients taking advantage of my naiveity and started off wary of liberal analgesia.  For example,  early on in third year when I was hanging out in the ED, an attending told me, "2 mg of morphine? Do you want to piss on them or treat their pain."  I was pretty mean.   Over the past few months, however, I've noticed that I'm actually advocating for more analgesia from residents and attendings.  This is a result of influence by FOAM (EMCrit podcasts, an Annals audio summary, etc), and I first noticed a change in my practice when I saw something along the lines of:
                          •  A rugby player presented with his right hip flexed and internally rotated after a tackle went awry over an hour before.  It appeared shortened and the patient refused to move the leg.  Both extremities were neurovascularly intact and a quick AP of the hip and pelvis demonstrated a posteriorly dislocated hip.  The patient moaned in pain.  Procedural sedation with propofol was planned and the physician did not want to give opioids prior to the hopefully quick reduction due to hemodynamic and respiratory concerns (no ETCO2 used).  Eventually, the patient was given 4mg of morphine IV for analgesia after advocating for the patient.  The hip was reduced with significant effort under propofol, with respiratory depression requiring bagging. (An amazing piece on procedural sedation from St. Emlyn's)
                          Is this actually a problem?  Yes! Multiple studies corroborate this assertion, with good literature in trauma patients in the ED.  It's plausible that the run of the mill abdominal pain patient may experience oligoanalgesia in the ED, but the really sick and damaged patients?
                          • Neighbor et al study was a retrospective chart review of all Level 1 tier trauma patients over the course of one year. 
                            • n = 540 (excluded patients who received opioids solely within 10 minutes of chest tube placement or fracture manipulation) 
                            • 258 patients (47.8%, 95% CI 43.5-52.1) got IV opioids within 3 hours of arrival to ED (average time to administration = 40.1minutes  (+/- 41.1 min), 5 had prehospital IV opioids
                            • The sickest patients (with the lowest Revised Trauma Scores) were less likely to receive analgesia.
                          • It's bad for patients.
                          Why don't we give adequate pain medications? There's a review in the Journal of Pain Research (free full text) that address many factors associated with oligoanalgesia in the ED.  Below are some I've encountered first hand.


                          We forget.  Emergency physicians are great under pressure, seamlessly MacGyvering difficult airways, obtaining hemostasis, and managing the chaos associated with 5-25 people in a cramped trauma bay.  Clearly, securing an airway and resuscitating a patient are crucial, but pain has physiological (and psychological) repercussions that can be deleterious as well. 
                          • I include it as part of my algorithm in patient assessment (and reassessments).  It takes little physician time and a protocol may help, as seen in this study.  A study by Chao et al in the Journal of Trauma demonstrated a mean time to administration of analgesia of 57 minutes.  There's probably time in there for some analgesia.
                          • From a purely (limited) anecdotal experience, I see patients undergo initial resuscitation and, after their whisked away to the CT scanner and some of the thrill has dissipated, never receive analgesia once they return to the ED.
                          The patient doesn't complain of any pain.
                          • Intubated and paralyzed patients.


                            • The Neighbor et al study referenced above demonstrated that only 23.5% of intubated patients received opioids.  Probability = 0.40 (95% CI 0.30-0.53).  
                            • A study looking specifically at post-intubation analgesia showed that 53% of intubated patients (95% CI 44-62) received no analgesia after intubation (Bonomo et al).
                          • "Shell shocked" - a mother involved in a car accident in which her children are also under treatment may be too emotionally wrecked to initially complain of pain.
                          The patient is "too out of it" to feel pain.  The Neighbor study showed an association between low GCS and lack of IV analgesia.  Thirty patients with a CGS 9–13  received analgesia and of those with GCS 3–8, 13.5% received IV analgesia.
                          • In many of these cases, especially if there's some sort of head injury, an analgesic such as fentanyl may be somewhat protective against the catecholamine surge of intubation.  Check out Brian Lin's talk on intubation in head injury.
                          The patient is hypotensive. Hypotension in sick patients is bad (although "permissive hypotension" in trauma is another store, well explained on trauma.org here). There are some ways to work around and with this. 
                          • Per the EM/Critical Care guru, Dr. Weingart - start a pressor if you have to, but treat the patient's pain.  He advocates for a pain first algorithm in the post-intubation period on Podcast #21, preferentially, a fentanyl drip or an appropriate amount of morphine.
                          • Ketamine has analgesic properties, doesn't depress hemodynamic parameters, and is even fine in the head injured patient! Here's a good discussion of ketamine in the ED.   
                          • Consider nerve blocks in patients with isolated limb injuries, if time permits (ex: hip fractures from the Emergency Ultrasound podcast). 
                          If I show up to the ED, please give me adequate analgesia (do unto others...) 
                          10.20.12
                          by

                          Don’t You Know That You’re Toxic?

                          The Gist:  Many medications have narrow therapeutic indices and additive adverse effects, making patients susceptible to inadvertent toxicity.  These effects may be identified less frequently in individuals with mental illness due to difficulty teasing out differences from the patient's baseline and assumptions that a patient's complaints are a result of the underlying mental illness.

                          A case of lithium toxicity from my prior career in the social work field drove me toward medicine and another served as my first patient of clinical clerkships.  A recent case in the ED, coupled with FOAM tweets from a toxicology conference, induced nostalgia regarding medications and mental illness (a surprise given my gratefulness when I see a dedicated mental health "pod").  The nostalgia seemed rather fitting for residency application season and I figured I'd share since each case I've been involved in has had a seemingly preventable delay in diagnosis.

                          The case that drove me into medical school:

                          Part 1.  A 34 year old male presents in early autumn with a few day history of increasingly slurred speech, staggering "wobbly" gait, and confusion (usually psychotic but oriented and "with it").
                          • HPI: Patient complains of nothing (murky due to his cognitive and mental health issues).  Support staff at the patient's residence denied any changes in routine and stated he had normal oral intake, including his fondness for Coca-cola.
                          • PMH: severe schizophrenia, autism spectrum disorder, hypothyroidism, and urinary incontinence 
                          • SH:  Works on a supervised landscaping crew, lives in a group home, no alcohol, drugs, or tobacco. 
                          • Medications: ziprasidone, levothyroxine, benztropine, oxybutynin, lithium, and risperidone (and perhaps a few others I don't recall).    
                          I called the patient's psychiatrist and primary care doctor (PCP) with the concern that there was something seriously wrong with my client.  Both physicians perceived the situation to be a product of the patient's mental health issues and suggested arranging appointments for the following week.  Still concerned by the reports from my staff, I ventured to see my client in person.  When I saw him, I immediately decided we were going to the ED.  He was so ataxic that I physically helped him walk to my car and drove him to a nearby ED.  His lithium level was ~4 mEq/L.
                          • Treatment:  IV fluids, observation, held lithium.  The emergency physicians wanted to perform dialysis on the patient but wavered since they felt the patient lacked decision making capacity.  He spent 5 days in the hospital and was released (and later restarted on lithium).
                          What's the big deal?  This case was likely preventable.  
                          • Adequate hydration may reduce risk of lithium toxicity.  Another case as a third year medical student involved a patient who wouldn't eat and was obtunded but was still receiving medications via NG tube, including lithium).  
                          • Monitoring lithium level.  In the three cases of lithium toxicity I've seen, another provider has seen the patient prior to me, without checking a lithium level despite the patient's list (or actually prescribing that medication to the patient).
                          • Not assuming that the patient's symptoms are the result of mental illness.  
                          A little on lithium toxicity:
                          Acute/Acute on Chronic:  LITFL's clinical cases has a great Q&A case on lithium overdose and the basics of lithium toxicity, which usually presents with gastrointestinal symptoms of nausea, vomiting, and diarrhea, CNS (sluggishness, ataxia, confusion), cardiac (arrhythmias, prolonged QT interval - but these appear less common) (2)
                          • Serum levels don't correlate with toxicity (2)
                          • Often due to intentional ingestion.
                          Chronic: Neurologic symptoms of sluggishness, ataxia, confusion, tremors, and seizures predominate in chronic toxicity.  These are often gradual in onset.
                          • Often occurs when there is impaired excretion of lithium, generally in the setting of decreased renal function (1)
                            • Dehydration (hot weather, decreased oral intake)
                            • NSAIDs
                            • ACE-inhibitors
                          • Serum levels more likely to correlate with toxicity
                          Treatment:
                          • Hydrate (twice maintenance for 2-3 liters)
                          • Labs: lithium level every 6-12 hours, electrolytes, creatinine, TSH (hypo/hyperthyroidism reported), ECG
                          • Dialysis in some cases.  The data on initiation of dialysis appear fuzzy but suggested indications include:  >4 mEq/L, >2.5 with neurologic sequelae or renal failure (2).  Treat the patient, not the lithium level.
                          • Disposition:  admit.  Monitor patient until at baseline and has a serum level <1.5 mEq/L (levels may rebound after dialysis due to tissue equilibration).  
                          • Stop the lithium.
                          References:
                          1.  Oakley P, Whyte IM and Carter GL. Lithium toxicity: an iatrogenic problem in susceptible individuals. Australian & New Zealand Journal of Psychiatry 2001; 35:833-840.
                          2.  Perrone J and Chatterjee P.  Lithium Poisoning.  UpToDate.  August 12, 2012.
                          10.16.12
                          by

                          One Way to Get a Fat Lip -Crickey!

                          The Gist:  ACE-inhibitor (ACE-I) induced angioedema (ACE-I AE) is a serious and common adverse effect that may be under-called.  ACE-I AE requires careful attention to the patient's airway.  If you're not scared of ACE-I AE, listen to this PHARM podcast.  Obtain a patient's current medication history (don't rely on just the patient's memory or the most recent EHR list) and communicate instances of ACE-I AE with the patient's primary doctor.

                          The Case:  A 34 year old male presented to the ED complaining of a bee sting to his lower lip.  The patient stated he was outside cleaning his pool when he noticed his lip swelling.  He did not see a stinging insect, but states he must have been stung as there are often bees and wasps in the yard.  He had no pain or dyspnea.
                          • No known environmental or medical allergies.
                          • Past Medical History:  Hypertension, high cholesterol, sleep apnea, and borderline "sugar problems." Didn't know medications but after running through options with the patient, we found that one ends in -astatin, and another ends in -pril.
                          • Vital signs are stable and within normal limits.  
                          • Physical exam significant for a massively edematous lower lip, more predominant on the right than the left.  No notable area of puncture or sting. Oropharynx without notable edema, patient is a Mallampati 3.  
                          We observed the patient and saw the swelling subside. We stopped his ACE-I, called his primary physician and counseled the patient on ACE-I AE and he did just fine.

                          On Sunday, I tallied the number of cases of ACE-I AE I've seen recently.  I've seen an average of one case per week since mid-May at institutions from Massachusetts to Florida, something I discovered when a recent case prompted me to do the math.  I've collected quite the case series, perhaps because I look for it (availability bias?).  

                          Hold up, is ACE-I angioedema really that common?
                          • This week the Archives of Internal Medicine published (online) a database study on the incidence of ACE-I angioedema between 2001-2010 capturing cases that presented to a provider.
                            • ACE-I AE Incidence of 1.79 (1.73-1.85) per 1000 people with a Hazard Ratio 4.38 per 1000 person years
                            • Of the Angiotensin Receptor Blockers (ARBs, end with -artan), losartan carried the highest risk (first to become generic)
                            • Greatest risk within 90 days of initiation (66% of reported events)
                          • Yes, according to an article published in Emergency Medicine News in July.  Apparently between two Philadelphia hospitals (at 82,000 visits/year) had 91 cases in one year, of which 60 patients were admitted.
                          • After the article in Emergency Medicine News came out in July, there was some Twitter discussion regarding whether ACE-I AE is really the silent epidemic that the article claimed.  Given my anecdotal experience, I naturally fell on the side of "yes, it really is."  
                            • One common thing I've noticed from the patients presenting to the ED (or in a few cases to the family practice clinic) is that they give pretty convincing stories for alternative exposures, as evidenced by the "bee sting" above.  Another patient came in with a "shellfish reaction."  She ate crab the day before and woke up with a massive lip.  She left her medications at home, but after having her daughter raid the medicine cabinet, we discovered the offending lisinopril. 
                          A quick ACE-I AE refresher:

                          • Can occur at any point during ACE-I therapy (1st dose or 600th dose) and sometimes with ARBS.  AE is due to the ACE-I interference with the degradation of bradykinin.
                          • Typically features edema of the mucosal and subcutaneous tissues of the face, lips, and upper airway but can extend to subglottic tissue (1).  ACE-I may also cause uvulitis, which can cause a patient to feel as if they're choking.
                          • Most cases resolve spontaneously within 2 days (peak swelling within minutes to hours) (1).
                            • Note:  this isn't always the case.  I had a patient remain nasal intubated in the ICU for over a week without improvement in her massive tongue swelling.
                          • Mainstay of treatment:  monitor airway and STOP the ACE-I
                          • May cause intra-abdominal pathology.  The Poison Review reviews an article on visceral angioedema.  More than 50% occur within first few days of ACE-I therapy (1)
                          • Has been associated with penile angioedema 
                          Why is ACE-I a big deal?
                          • Airway, airway, airway!  Listen to this podcast from the PHARM featuring Dr. Jordan Schooler's frightening experience with a surgical airway on an ACE-I AE patient as an intern.  The tongue and soft tissue of the airway can become so edematous that the patient's airway may become completely compromised (and this progression isn't necessarily predictable).  Case presentation from the PHARM by Dr. Peter Sherren details another ACE-I AE airway experience.
                          • These reactions are not amenable to the standard allergic reaction/anaphylaxis cocktail of histamine blockaders, glucocorticoids, and epinephrine.  See University of Maryland's pearl on treatment.  Most pharmaceutical interventions have minimal evidence, mostly derived from hereditary angioedema and from case reports.
                            • Fresh frozen plasma (FFP)
                            • Icantibant, a bradykinin receptor antagonist (case series).  Apparently this is thrombogenic

                            • Ecallantide (inhibits plasma kallikrien to prevent conversion to bradykinin)
                            • C-1 inhibitor.    

                          • Patients are susceptible to recurrence if an ACE-I is not resume these medications if there is inadequate communication between the treating physician, the patient, and the patient's primary care physician.  
                            • Call the patient's primary physician know that they were treated at the ED for ACE-I AE.  Many ED notes aren't able to be accessed by PCPs and patients may assume that their PCP knows precisely why they were seen in the ED.  Take guess work out of the equation by contacting the PCP's office.
                            • Tell the patient to list ACE-I as an allergy.  
                            • If possible, make sure they don't go home with their ACE-I.
                          • The incidence and severity of ACE-I AE has caused physicians to petition the FDA for a black box warning.  This was denied after a petition in 2002 (notably, a decade has passed since then and, as an idiosyncratic reaction, many more cases have presented).  ACE-I are a core measure for diabetics and in heart failure, is this a double edged sword? 
                          References:
                          1.  Guyer A, Banerji A. ACE inhibitor-induced angioedema.  UpToDate.  Updated June 2012.

                          10.11.12
                          by

                          Sweating Bullets and Killing ‘em With Kindness – Calling a Consult

                          The Gist:  Although it's not an exciting or popular topic, communicating with consultants is vital in the emergency department (ED).  Trainees are often less than stellar at communicating with consultants (as evidenced by the Henn paper below), but there are resources available to combat this problem, distilled in this free EM:RAP EE podcast.

                          Before my third year of medical school, I would have balked at the idea of receiving training for telephone consultations and it wasn't a part of our curriculum.  In fact, I recall skimming through an EM: RAP Educators Edition podcast on communicating with consultants during a road trip after I had exhausted my other podcasts.  Could it really be that difficult?

                          Over the past several months, rotating at several different institutions in the United States, noticing that the relationships between emergency physicians and consultants varies widely.  In some institutions, I watch residents sweat profusely at the prospect of calling surgery, postpone the consult as long as possible, or have an inpatient team balk when asked to admit a patient with a concerning story for ACS and an unequivocally positive delta troponin (that was 11 only a couple of hours later).  When I experienced my first difficult consult from the ED, my solid presentation transformed into a fragmented stutter.  I realized that I needed help.  I listened to my attendings and other residents discuss patients with the consultants and began modeling my calls after what I overheard.  Then, I read an article that made me realize I was not alone (and motivated me to find other resources to improve myself).

                          The paper:  Henn et al A metric-based analysis of structure and content of telephone consultations of final-year medical students in a high-fidelity emergency medicine simulation BMJ Open 2:e001298 

                          • 113 final year medical students completing an emergency medicine clerkship conducted simulated phone calls to consultants after receiving education on telephone calls throughout their medical school curriculum.  They were told how to introduce themselves and told they would be evaluated on communication skills.  61% of phone conversations included in study (n=69)
                          • 72% (n=50) did not identify expectations from their supervisor
                          • 97% did not write down and repeat the recommendations of the consultant 
                            • This is failing to "close-the-loop" and may lead to differences in expectation, errors, or frustration
                          • 29% did not identify their role and 31% did not give full name and title
                            • Some doctors demand to talk to attendings or superiors, so it may be tempting to skip this step; however, it's an absolutely necessary component.
                          So, perhaps many of the issues I faced in calling a consultant revolved around my own lack of clarity.  

                          Once again, I turned to FOAM to improve my skills and was not disappointed by a closer listen to the free EM: RAP podcast.

                          Life In The Fast Lane (LITFL) does a superb job summarizing key points for communicating with consultants.

                          • Be nice 
                          • Anticipate the preferences and personalities of the consultants.
                          • Again, be nice but hold your ground on the actual issues.  

                          Emergency Physicians Monthly ran an article by Dr. Chad Kessler on learning to call consultants.  In the article, Dr. Kessler cites the "5 C" model that he and others coined and developed, published in an article in the Journal of Emergency Medicine:
                          • Contact - Say precisely who you are and ask with whom you are speaking.
                          • Communicate - Be very clear, very nice.
                          • Core Question - Ask a specific question and say precisely what you want.
                          • Collaborate - Allow consultant to respond and be flexible with what they want.
                          • Close the Loop - Repeat your understanding of the consultants recommendations to ensure all parties are on the same page.
                          freeemergencytalks.net has some great talks on the subject.

                          Give Dr. Kessler's talk a listen:
                          • Ensure you have a purpose and a very specific question.  What do you want?
                          • Prepare.  Gather your information so you're ready to go.
                          • Kill them with kindness without cutting corners on the issues.
                            • Respect their view.
                          • Use a standardized framework -the 5 C's.  
                          • Record the conversation.  Write down the name of the individual you spoke with, the time, and the recommendations.
                          • Practice calling consults (just don't actually dial them with fake consults on a slow night shift)
                          Dr. Peter Rosen shares his perspective on difficult consultants in the first portion of this talk:
                          • Sometimes you have to be unpopular.  If someone's sick - hold your ground!
                          • Treat them the way they want to be treated (the platinum rule).
                          • Recognize the consultant's situation.  
                            • At 0300 or in the midst of a child's violin recital, it may be necessary/prudent to adapt your communication (less jokes, more forgiving for grumpiness)
                            • Sometimes people do admit patient's because it's the easier option.  Do what's right for the patient.
                          • Make decisions and commit to them (if you don't want to - go into another specialty).
                          The SBAR format is another popular format for presentations and hand-offs that may improve performance with consults when presenting the patient to the consultant (1).  The Southampton Emergency Medicine Education Project blog has a great review of SBAR in this role. 
                          Situation - Who (you and your patient), Why (you're calling)
                          Background - What (is going on with the patient), where (they are and where they've been...CTs/labs, pertinent history)
                          Assessment - Assessment of the patient
                          Recommendations - How (you want to proceed) and what you expect out of the consultant

                          References:
                          1.  Matthew C. Tews, J. Marc Liu, and Robert Treat (2012) Situation-Background-Assessment-Recommendation (SBAR) and Emergency Medicine Residents' Learning of Case Presentation Skills. Journal of Graduate Medical Education: September 2012, Vol. 4, No. 3, pp. 370-373.

                          10.01.12
                          by

                          Are There Pros to Procalcitonin?

                          The Gist:  Procalcitonin (PCT) is gaining popularity in identification of serious bacterial infections and in attempts to curtail antibiotic usage; however, it has many limitations and has not been proven to conclusively and consistently alter patient oriented outcomes.  An elevated PCT probably indicates infection, but this goes out the window in trauma or surgery.  The data seem to support using PCT over other biomarkers to help inform length of antibiotic use, especially in respiratory infections (i.e. if it falls to <0.5 mcg/L then it's likely safe to cease antibiotics).  This benefit is derived after the decision to initiate antibiotics has been made.  

                          As part of my clerkship, I recently attended a lecture on the use of PCT in the ED and ICU for sepsis identification and management.  The lecture was overwhelmingly promising - a better biomarker to aid in an attempt to sort out bacterial infections and stratify sick from less-sick patients in clinically murky situation?  Sounds awesome, but the lecture was industry sponsored and FOAM has taught me to ask a few questions about any diagnostic method I employ.  What does the test actually indicate (if positive or negative)?  How good is it, really?  How will it change my management of this patient?  Is it costly?  Timely?  Thus, I decided to investigate the test for myself.  Naturally, I went to my trusty FOAM sources to aid in this endeavor.

                          • I started with PulmCCM.org, where I recalled reading several things on procalcitonin.  They have an fantastic review on use of procalcitonin and pneumonia, which also answers some of the more general questions about procalcitonin.  They also have a summary of some recent literature reviews. 
                          • Then however, it was time to go to the pool, so I found a free talk by Dr. Talan on procalcitonin in the ED.  
                          • In typical FOAM fashion, two days later, a brand new podcast on PCT (episode 194) by the Society of Critical Care Medicine started playing while I was at the gym.  It's a good review of some recent literature and some projections for the future of PCT.

                          Basics of Procalcitonin
                          • More specific for bacterial etiology compared with other markers such as WBC and c-reactive protein (CRP) due to interferon-gamma from host response to virus (1)
                          • Short half-life so theoretically easily trended and reflects patient's current situation (1)
                          • Not as altered by inflammatory states, glucocorticoids, or other known drugs as WBC and CRP; however, it does rise immediately after major trauma and surgery in the absence of bacterial pathogens (1)
                          • Costs ~$25 per test in the US (charge is ~$38)

                          Below is essentially a run-down of the primary sources referenced in the above reviews (it's covered by the FOAM sources above, but I'm trying to get better at going through the primary literature).  Note:  most of these studies looked at PCT use in patients with respiratory symptoms and some of them use various cut-off points for interventions.


                          Identification of Serious Bacterial Infections (SBI) - not ready for prime time.
                          • 2010 pediatric study randomized febrile kids to either have a PCT value available to the provider or not.  Used a cut off of 0.5 mcg/dL.  Sensitivity of PCT for SBI 77%, Specificity 64%
                          • June 2011 study by Bafadhel et al evaluated PCT and CRP values in Community Acquired Pneumonia (CAP) versus COPD/asthma.  For identifying pneumonia, CRP >48 mg/L had a sensitivity of   91% (95% CI, 80%-97%), specificity 93% .  A PCT of 0.8 mcg/L had a sensitivity of 89% (95% CI, 78%-95%) and specificity of 78% (95% CI, 72%-82%). 
                          • This study by El-Solh et al in Critical Care Medicine 2011 did not differentiate between aspiration pneumonitis and bacterial aspiration pneumonia.
                          • Muller et al published an analysis of the ProHosp data and found that patients with PCT levels <0.25 mcg/L were extremely unlikely to have positive blood cultures (<1%) 
                          • Reynolds et al found that shock elevates PCT levels regardless of bacterial infection in a study of medical ill and post-operative patients.  Higher PCT levels were assosciated with infection, but this data support the notion that general inflammation does affect PCT levels regardless of the presence of bacterial pathogens. 
                          Clinically meaningful outcomes for patients
                          Morbidity/Mortality - probably no difference in mortality using PCT guided algorithms, questionable change in length of stay
                          • In the ProHOSP RCT by Schuetz et al in 2009, utilization of PCT did not reduce the incidence of adverse effects (primary outcome of the study), although the authors conclude that the incidence was "similar." 
                          • Another 2011 systematic review by Schuetz et al (who published many of the PCT trials) showed no mortality difference in patients with PCT guided therapy versus standard care groups despite reduced antibiotic usage in the PCT guided cohort
                          Length of Stay (LOS) - unlikely that PCT has any effect. Would you discharge someone based solely on a lab value?  I'm pretty sure everyone uses the clinical picture in this setting.
                          • In Agarwal and Schwartz's systematic review, only 2 studies demonstrated decreased LOS.
                          • Jensen et al's 2011 study in Critical Care Medicine investigate the effect of using an algorithm based on PCT values to escalate antimicrobial therapy (escalated at 1 mcg/L, a higher cut-off level than the 0.5 mcg/L used in most other studies).  The study, reviewed here by EM Lit of Note, demonstrates that there's actually an increase antibiotic usage, LOS, and ventilator dependent days.  
                          Antibiotic Usage - studies pretty consistently demonstrate that trending  PCT can reduce the length of antibiotic usage in respiratory infections but should not be used to initiate antibiotics.
                          • June 2011 study by Bafadhel et al  Derivation of PCT values to guide therapy: PCT value of > 0.25 ng/mL would have incredibly reduced antibiotic usage in patients with asthma or COPD exacerbations while slightly reducing the antibiotic usage in the pneumonia cohort.  Counterpoint:  A CRP value of >48 mg/L also resulted in very similar reductions
                            • Asthma - from 57% to 4% (reduction in antibiotic usage of 93%; 95% CI, 88%-98%)
                            • COPD - from 76% to 7% in patients with exacerbation of COPD (reduction of 91%; 95% CI, 87%-95%)
                            • Pneumonia - from 100% to 73% (reduction of 27%; 95% CI 17%-40%).
                          • Antibiotic duration in PCT group 5.7 days vs 8.7 days in standard care group in the ProHosp trial 
                          • A 2011 systematic review by Agarwal and Schwartz (including only RCTs) concluded that use of PCT to inform antibiotic length decreases usage of antimicrobials.
                          • The primary outcome of the  2010 pediatric study was antibiotic usage, which was the same in the group who had PCT available and those that did not.  If antibiotics were given to all kids with a PCT >0.5 mcg/L, more antibiotics would have been utilized (24% 95% CI, 15-33), not less.  Additionally, there's an argument that an even lower cutoff value should be employed (0.25 mcg/L has been proposed)
                          • Schuetz et al's systematic review  concluded that PCT reduced antibiotic duration and prescriptions in the outpatient, ED, and ICU settings for patients with respiratory infections (note: included more trials than the Agarwal and Schwartz trial). 
                          • Not all studies demonstrating a statistically significant reduction in the exposure to antibiotics, including the 2009 Schuetz RCT, used this as a primary endpoint in the study.  In this cohort for lower respiratory tract infections, the mean length of antibiotic exposure was 5.7 days in the PCT group compared with 8.7 in the standard care group. 
                          • Limiting initiation of antibiotic therapy is probably not effective at a cut-off of 0.5mcg/L (so use your clinical judgment) (2)
                          Risk Stratification 
                          • EPs are good at determining who is extremely ill and those who aren't that sick but in situations where the patient can seem to go either way, lab tests may help. Harbarth et al found that patients on the SIRS/sepsis spectrum had poorer prognoses if their PCT levels didn't fall (3).
                            •  High risk:  PCT levels >2 mcg/L.  
                            • Low risk: < 0.25 mcg/L  
                            • The cut-off of 0.5mcg/L seems to be the most referenced
                          Economics - the test is presently more expensive than the vague counterparts, the WBC count and CRP.  However, some argue that there are cost savings in LOS reduction, antibiotic usage, blood cultures (using PCT as a surrogate - see Muller et al Table 5), and reduced ICU days.  Presently, most of these arguments are projection of data based on derivation and internal, retrospective validation of certain PCT cut off and theoretical algorithms.  

                          PCT is gaining steam in the US.  The test llooks better than WBC and CRP so far, but studies are beginning to show that the test has some confounding issues.  Exercise caution when ordering PCT and recognize the soft lines drawn for the "cut-off" levels of the test.

                          References:

                          1.  Jin M et al Procalcitonin: Uses in the Clinical Laboratory for the Diagnosis of Sepsis Lab Medicine 2010 41, 173-177 


                          2.  Agarwal and Schwartz.  Procalcitonin to Guide Duration of Antimicrobial Therapy in Intensive Care Units: A Systematic Review Clin Infect Dis.53 (4):379-387.
                          3. Harbarth et al.  Diagnostic Value of Procalcitonin, Interleukin-6, and Interleukin-8 in Critically Ill Patients Admitted with Suspected Sepsis Am. J. Respir. Crit. Care Med.vol. 164no. 3 396-402
                          09.25.12
                          by

                          Overestimates, underestimates, and things unseen – Sifting through pharmaceutical studies

                          The Gist:  Initial literature regarding a drug generally overestimates the benefit of the pharmaceutical while underestimating the risk of the intervention.  Listen to Dr. David Newman's excellent discussion on this topic on EM: RAP's June 2012 episode, using heparin as an example (note: paid subscription required).  The Cochrane reviews on major topics are excellent for analyzing the benefit of , although these are subject to problems as well (not as good for harms as benefit since they generally don't include comprehensive post-marketing data).

                          It's intuitive that early data on interventions demonstrate the most benefit.
                          • Publication bias.  Journals tend to publish positive and statistically significant results (even if not clinically significant).  A Cochrane analysis demonstrated that only 63% of results from abstracts are published in full and demonstrated an increased odds that a paper would be published if it demonstrate a positive outcome (1).  It is well known that much trial data remains unpublished and is thus not available to clinicians and individuals compiling meta-analysis.  In fact, many groups and individuals are fighting for access to this data citing moral and ethical issues.
                            • This BMJ study demonstrates that the conclusions of a meta-analysis is, in fact, altered by the inclusion of unpublished data (2).
                            •  Mark Crislip of "Gobbets O' Pus" and "Persiflager's Puscast" fame frequently states the following analogy (rephrased) with regard to meta-analysis "if you put together a bunch of cowpies, you don't get gold, you still just have a load of poo."  This serves as a reminder that even systemic reviews and meta-analyses are fallible. 
                          • Submission bias.  Studies that are not submitted for publishing are far less likely (ever?) published.  Would a drug company submit results for publishing that reflected poorly on their drug?  Additionally, when studies are submitted, the data may be "interpreted" or presented in such a way that a positive outcome, even if it's not a primary outcome, is reported.
                          • Industry funded data.  Following the above point, when an industry funds a study, they typically only publish data that supports the efficacy of their medication.  This paper showed that many of the efficacy trials referenced in applications to the FDA for new drugs are not published after five years or published without reference to primary outcomes (3).  Dr. Ryan Radecki has written about this (here) and also frequently sorts through some of this on his excellent blog.
                          • Excitement. Physicians, patients, and innovators want drugs and interventions to work.  We want patients to do well, fight illness, and be able to maximize their quality of life.  This can lead to bias among the studied individuals and those studying the the drug.  Also, there's a component of expectation bias, as we expect that expensive and novel agents will perform, especially if approved by governing authorities. 
                          It also make sense that later data often demonstrate more harm than initially recognized.
                          • Longer follow up times capture longitudinal risks.  Some risks or adverse effects may not show up in shorter time frames initially investigated.
                          • Data subjected to real-world use of intervention.  Initial studies investigate the pharmaceutical in demarcated, controlled groups of individuals.  When these products reach the market, physicians utilize these drugs in a broader population base and oftentimes in non-approved settings.  Similarly, patients take these medications with their other medications, highlighting interactions between drugs.  When medications reach the market, problems with patient compliance also become evident (missing doses, doubling up on medications, issues with reversal, etc), as these are not typically not accounted for in the well-controlled studies.
                          • FDA withdrawals often demonstrate the ways in longitudinal data exposes harms of medications.  
                          The recent example  Rivaroxaban in Patients with a Recent Acute Coronary Syndrome.  In this paper, published in the NEJM in January 2012, the authors concluded that the increased bleeding in the rivaroxaban group is acceptable because the cardiovascular mortality was reduced in the cohort and there wasn't an increase in fatal bleeds.  

                           Safety Results:
                          • Pre-defined safety endpoint:  TIMI major bleeding not related to CABG
                            • Rivaroxaban arm 2.1% versus 0.6% in the placebo group
                          • TIMI minor bleeding (1.3% vs. 0.5%, P=0.003)
                          • TIMI bleeding requiring medical attention (14.5% vs. 7.5%, P=<0.001)
                          • intracranial hemorrhage (0.6% vs. 0.2%, P=0.009)
                          • No difference in fatal bleeds
                          So, there actually is an increase in clinically important bleeding.  Do the benefits actually outweigh this morbidity?  I asked this question of the material and, while sorting through this, had my question answered.

                          The Archives of Internal Medicine recently published several papers on Novel Oral Anticoagulants (NOACs), the Factor Xa inhibitors such as rivaroxaban and the direct thrombin inhibitors such as dabigatran, following acute coronary syndromes.  This systematic review and meta-analysis demonstrates that the NOACs have a net negative clinical impact, when accounting for the bleeding risk (see above) and the minimal reduction in ischemic events.  The authors of this paper also highlight the importance of absolute measures to contextualize relative effects (for more on this, check out this post).  They state that the reduction of ischemic outcome is reported as a risk reduction of 14% but the absolute reduction is only -1.3%.

                          This was a great reminder for me to exercise caution and encourage inquisition when looking at data or becoming excited about interventions.

                          References:
                          1.  Scherer RW, Langenberg P, von Elm E (2007) Full publication of results initially presented in abstracts. Cochrane Database of Systematic Reviews 2007, Issue 2.
                          2.Hart B, et al.  Effect of reporting bias on meta-analyses of drug trials: reanalysis of meta-analyses BMJ 2012;344:d7202
                          3.  Rising K, Bacchetti P, Bero L (2008) Reporting Bias in Drug Trials Submitted to the Food and Drug Administration: Review of Publication and Presentation. PLoS Med 5(11): e217. 
                          09.19.12
                          by

                          I’ve Been Framed! My #twitterstatslesson

                          The Gist:  The way in which one frames a drug or intervention may severely alter the way in which one perceives the most objective information.  Patients and physicians are similarly affected by framing bias (a cognitive bias, perhaps amenable to metacognition).  The use of absolute risks and terms rather than relative terms helps mitigate this bias.  Number needed to treat (NNT) and number needed to harm (NNH) are probably better ways of evaluating interventions and testing, even though these have limitations as well.  Bookmark theNNT.com !.

                          I have no statistics background except a biostatistics class that's part of my MPH curriculum, and attempts to keep up with SMART EM and Dr. David Newman on EM:RAP's mini JC section.  I realized we're often not formally taught to interpret and integrate bits of statistics, although the USMLE Step 2 is now beginning to attempt testing this aspect.  Thus, this stuff is important both to trainees and clinicians.  As I've begun to learn to sort through evidence and literature, I've found that FOAM delivers.  One evening, I found following conversation regarding absolute versus relative risk among some world-renowned physicians dominated my Twitter feed (only parts are listed below):


                          So, I began to think about my own shortcomings in understanding these statistical dilemmas and figures. Amazingly, I stumbled upon a paper on framing the following day via Emergency Medicine Abstracts.  Apparently, I had good reason to worry...

                          We frame things constantly, providing a context for information and a means of understanding the information.  Like most things, this has both positive and negative implications.  For example, when one is trying to admit a patient to a particular service, one might phrase things rather differently than when one tells a patient why you plan on discharging them.  Oftentimes we use paternalism or the legitimate best interest of the patient to justify these 'frames.'

                          However, pharmaceutical companies do this as well through well-crafted consumer (and provider) advertising.  For example, this advertisement states that Pradaxa (dabigatran) reduced stroke risk 35% more than warfarin.  Thus, individuals may believe that the drug will reduce their stroke risk by a similar amount.  However, the 35% reduction in stroke risk only existed for a subset of patients.  Patients and populations are heterogeneous so these numbers don't necessarily apply any given patient.  As a pretty well educated bunch, health care providers should be really good at detecting framing differences and less susceptible to this bias, right?  Wrong!

                          The Paper:  Perneger T,  Agoritsas T.  Doctors and Patients' Susceptibility to Framing Bias: A Randomized Trial.  J Gen Intern Med 26(12):1411-7
                          • Sent questionnaires to physicians and patients recently discharged from the hospital asking the respondent to judge the efficacy of a new drug based on the information provided
                          • Information on the new and old drug was identical but presented in only one of the following ways:  
                            • Absolute mortality:  with the new drug, 4% were died by the end of the study versus 6% for those who received the old drug
                            • Absolute survival: with the new drug, 96% lived versus 94% who lived with the old drug.   Least favorable reviews of the drug by both groups (Physicians 51.8%, patients 51.7%, p=0.98 between groups)
                            • Relative mortality reduction:  of those who received the old drugthose that got the new drug had their mortality reduced by 1/3.  Both patients and physicians presented with relative mortality reduction perceived the drug most favorably (Physicians 93.8%, patients 89.3% p=0.11 between groups).  The odds ratio (OR) of a respondent perceiving the drug more favorably with the information presented in this format compared with other formats was 4.40 (95% CI 3.05 - 6.34, p<0.001)
                            • All three presentations of risk.  with the new drug, 96% lived, 4% died versus 94% lived, 6% died  with the old drug, so those that got the new drug had their mortality reduced by 1/3
                            • Physicians were also tested on the NNT (50) and the relative survival extension.
                          • Doctors responded to the presentations with no statistical difference from the patients. OR of Doctor (versus patient) = 1.06 (95% CI 0.87 - 1.29, p = 0.55)
                          • The notion that information presented in relative terms rather than absolute terms is more favorably received is not new (1).
                          There is so much to learn from the ever-relevant FOAM world.

                          References:
                          1.  Malenka DJ, Baron JA, Johansen S, Wahrenberger JW, Ross JM. The framing effect of relative and absolute risk. Journal of general internal medicine. 1993;8(10):543-8.
                          09.09.12
                          by

                          FOAM Party! (The Future of Medical Education)

                          The Gist:  Free Open Access Meducation (FOAM, #FOAMed) is essentially a personalized, continually expanding medical curriculum that embraces an individual's attention deficits, evolves as one learns, encourages active learning, and pushes the bounds of one 'ought' to know.  Here's a good summary of FOAM.  Life in the Fast Lane has an extensive list of FOAM resources and there's a new FOAM search engine. 

                          What is FOAM?  Dr. Mike Cadogan and those at Life in the Fast Lane founded the FOAM initiative and continue to build, encourage, and curate FOAM on the web.

                          Each day, I try to spread FOAM among the other rotating medical students, residents, paramedics, and attendings.  I talk about blogs and podcasts, refer people to Dr. Mike Cadogan's video on FOAM, and, if at all possible, try to have the individual set up GoogleReader or an iPhone/Android/iPad app while I'm there.  Although this may occasionally make me appear nerdy (which is clearly not the case) or overzealous, the rewards are excellent and manifest when an individual returns with, "So, what other blogs should I follow?" or "I used _____ on shift yesterday that I heard on one of the podcasts."  It's amazing how quickly people get hooked!

                          Some individuals are skeptical or ambivalent towards FOAM, perhaps unaware of how this broad collection of resources can translate into real world clinical knowledge or wary of the time investment  (note: it actually increases efficiency!).  I can't comprehend why anyone would not partake in this amazing medical education outlet if they actually comprehended the intellectual benefit, personalization, and efficiency of FOAM.

                          I can't articulate the concept of FOAM adequately in the rare minute of downtime in the ED (hence the reason for this blog entry).  In the hopes that others buy into  the FOAM concept, I am compelled to share how the ways that FOAM is transforming me into a better future physician.

                          How does FOAM work for me?
                          Twitter - I used to scoff at this form of social media, but I became a convert a few months ago.  Since that time, this venue has proven to be incredibly useful.
                          • Virtually attend conferences.  I've "attended" EM conferences around the world, including Society of Academic Emergency Medicine (SAEM), International Conference of Emergency Medicine (ICEM), and multiple locally based EM conferences (NY, CA, Australia, etc).
                          Celebrating ICEM 2012, held in Dublin, from the United States
                          • Discover new content.  I used to think I had an extensive blogroll, but Twitter continuously expands my list.  Individuals often tweet links to journal articles, videos, and blogs and following.  This allows one to "read" more extensively than one would otherwise.  It's impossible to keep up with the copious amount of medical literature published, but Twitter helps with this as it's a portal into what others are reading and their take on the article/issue (intellectual voyeurism made incredibly simple)
                          • Active learning.  
                            • Distilling an idea or message into 140 characters is tough, but definitely forces one to be mindful of the core content.
                            • Twitter allows one to engage in conversations with individuals across the globe.  This engenders collective problem solving, brainstorming, and debate.  One can learn to think critically about clinical practice and literature.  Recently, a Google Hangout journal club-esque event was organized and publicized via Twitter with EM/CC heavyweights.
                            • Virtual pimping.  Several people tweet "Question of the Day," including @Radiopaedia - on imaging, @jvrbntz - based on Academic Life in EM's Paucis Verbis cards, and @EMEducation.  These are useful to test knowledge, but also often spark debates and conversations.
                          • Diversify.  Medicine and EM exist outside of the confine of one's nation.  Learn what's going on across the world and track global trends and thought in medicine.  
                          • Build professional relationships across the globe.
                          Podcasts - These are truly gems of FOAM, allowing one to listen to lectures and conversations from world renowned physicians and speakers at one's leisure. Learn more about them in this post, dedicated to podcasts.  

                          Blogs - FOAM blogs are the personalized, up-to-date textbooks of this century.  They deliver information and insight with one's own interest and goals as a filter.  Choose what you interests you, and see how quickly your interests are broadened.  A comprehensive repository from LITFL.  All about FOAM blogs.  

                          Videos - There's a plethora of 10-15 minute videos, packed with incredible medical education, on the web. Many of these are tweeted out and EMCHATTER also has a searchable database with summaries.
                          Questions - The Global Medical Education Project (GMEP) - is an evolving question bank that is interactive and fun.  
                          It seems that whenever I encounter a topic on a podcast or blog that seems esoteric or uninteresting, I invariably encounter the scenario in the clinical setting. I feel compelled to share a few examples of recent intersections between my clinical experiences and the #FOAMed world.  Just a few examples:
                          Pimping made easy:
                          •  On 8/26/12, I skimmed over the blog "Mushrooms in the Valley" from the St. Emyln's blog.  The post was on Morel-Lavallee lesions, something I barely filed away in my brain as esoteric knowledge.  On 8/28/12, my second day of a new rotation, my attending pimped me on Morel-Lavallee lesions and I was able to answer without pause.  Can FOAM predict the future?  I'm pretty convinced.
                          A self-built curriculum:
                          • On 8/27/12 and 8/29/12, I wrote on metacognition and cognitive bias.  Days later, Dr. Michelle Johnston of LITFL posted an outstanding case based blog on cognitive error.  The FOAM world supplemented my curriculum on cognitive error and clinical decision making in real time!  Then, Dr.  Javier Benítez posted a piece on Academic Life in EM on diagnostic tests and asking the right questions.  Ask and ye shall receive (or, an example of availability bias).
                          Improved clinical skills resulting in tangible outcomes (a few examples as I can no longer quantify what FOAM brings to the table):
                          • The Cunningham technique from ERcast to successfully reduce a shoulder dislocation without pain medication
                          • A solid ocular ultrasound curriculum from the Ultrasound Podcast and SonoSpot allowed me to confidently diagnosis my first retinal detachment (and as a mac-off detachment, at that).
                          • Countless discussions with patients on risks and benefits of diagnostic imaging in which I can talk to patients and physicians in terms that each understands (thanks to SMART EM and Duke's Emergency Medicine talks on iTunes).
                          Improved clinical skills that I use on a daily basis:
                          • EMBasic's podcasts on various chief complaints have allowed me to assess patient's quickly and confidently present a solid differential with an accompanying plan.  I no longer get nervous/try to avoid the charts with a chief complaint of "dizzy."  
                          • Employing evidence based medicine in everything from strep throat treatment to resuscitation (credit to innumerable pieces of FOAM).
                          Improved "book" knowledge.  I've used FOAM since just prior to entering medical school to supplement my education.  As a clinically based learner, many FOAM sources make it easy for me to absorb the pathophysiology behind disease processes.  Although I'm a trial of n=1, podcasts, blogs, and Twitter have allowed me to study at the gym, in the car, or while walking/waiting in lines.  This has allowed me to maintain a "life" outside of studying.
                          My FOAM journey
                          09.09.12
                          by

                          FOAM Party! (The Future of Medical Education)

                          The Gist:  Free Open Access Meducation (FOAM, #FOAMed) is essentially a personalized, continually expanding medical curriculum that embraces an individual's attention deficits, evolves as one learns, encourages active learning, and pushes the bounds of one 'ought' to know.  Here's a good summary of FOAM.  Life in the Fast Lane has an extensive list of FOAM resources and there's a new FOAM search engine. 

                          What is FOAM?  Dr. Mike Cadogan and those at Life in the Fast Lane founded the FOAM initiative and continue to build, encourage, and curate FOAM on the web.

                          Each day, I try to spread FOAM among the other rotating medical students, residents, paramedics, and attendings.  I talk about blogs and podcasts, refer people to Mike Cadogan's video on FOAM, and, if at all possible, try to have the individual set up GoogleReader or an iPhone/Android/iPad app while I'm there.  Although this may occasionally make me appear nerdy (which is clearly not the case) or overzealous, the rewards are excellent and manifest when an individual returns with, "So, what other blogs should I follow?" or "I used _____ on shift yesterday that I heard on one of the podcasts."  It's amazing how quickly people get hooked!

                          Some individuals are skeptical or ambivalent towards FOAM, perhaps unaware of how this broad collection of resources can translate into real world clinical knowledge or wary of the time investment  (note: it actually increases efficiency!).  I can't comprehend why anyone would not partake in this amazing medical education outlet if they actually comprehended the intellectual benefit, personalization, and efficiency of FOAM.

                          I can't articulate the concept of FOAM adequately in the rare minute of downtime in the ED (hence the reason for this blog entry).  In the hopes that others buy into  the FOAM concept, I am compelled to share how the ways that FOAM is transforming me into a better future physician.

                          How does FOAM work for me?
                          Twitter - I used to scoff at this form of social media, but I became a convert a few months ago.  Since that time, this venue has proven to be incredibly useful.
                          • Virtually attending conferences.  I've "attended" EM conferences around the world, including Society of Academic Emergency Medicine (SAEM), International Conference of Emergency Medicine (ICEM), and multiple locally based EM conferences (NY, CA, Australia, etc).
                          Celebrating ICEM 2012, held in Dublin, from the United States
                          • Discover new content.  I used to think I had an extensive blogroll, but Twitter continuously expands my list.  Individuals often tweet links to journal articles, videos, and blogs and following.  This allows one to "read" more extensively than one would otherwise.  It's impossible to keep up with the copious amount of medical literature published, but Twitter helps with this as it's a portal into what others are reading and their take on the article/issue (intellectual voyeurism made incredibly simple)
                          • Active learning.  
                            • Distilling an idea or message into 140 characters is tough, but definitely forces one to be mindful of the core content.
                            • Twitter allows one to engage in conversations with individuals across the globe.  This engenders collective problem solving, brainstorming, and debate.  One can learn to think critically about clinical practice and literature.  Recently, a Google Hangout journal club-esque event was organized and publicized via Twitter with EM/CC heavyweights.
                            • Virtual pimping.  Several people tweet "Question of the Day," including @Radiopaedia - on imaging, @jvrbntz - based on Academic Life in EM's Paucis Verbis cards, and @EMEducation.  These are useful to test knowledge, but also often spark debates and conversations.
                          • Diversify.  Medicine and EM exist outside of the confine of one's nation.  Learn what's going on across the world and track global trends and thought in medicine.  
                          Podcasts - These are truly gems of FOAM, allowing one to listen to lectures and conversations from world renowned physicians and speakers at one's leisure. Learn more about them in this post, dedicated to podcasts.  

                          Blogs - FOAM blogs are the personalized, up-to-date textbooks of this century.  They deliver information and insight with one's own interest and goals as a filter.  Choose what you interests you, and see how quickly your interests are broadened.  A comprehensive repository from LITFL.  All about FOAM blogs.  

                          Videos - There's a plethora of 10-15 minute videos, packed with incredible medical education, on the web. Many of these are tweeted out and EMCHATTER also has a searchable database with summaries.
                          It seems that whenever I encounter a topic on a podcast or blog that seems esoteric or uninteresting, I invariably encounter the scenario in the clinical setting.  Recently, however, there have been an incredible number of intersections between my clinical experiences and the #FOAMed world.  Just a few examples:
                          Excelling at pimping:
                          •  On 8/26/12, I skimmed over the blog "Mushrooms in the Valley" from the St. Emyln's blog.  The post was on Morel-Lavallee lesions, something I barely filed away in my brain as esoteric knowledge.  On 8/28/12, my second day of a new rotation, my attending pimped me on Morel-Lavallee lesions and I was able to answer without pause.  Can FOAM predict the future?  I'm pretty convinced.
                          A self-built curriculum:
                          • On 8/27/12 and 8/29/12, I wrote on metacognition and cognitive bias.  Days later, Dr. Michelle Johnston of LITFL posted an outstanding case based blog on cognitive error.  The FOAM world supplemented my curriculum on cognitive error and clinical decision making in real time!  Then, Dr.  Javier Benítez posted a piece on Academic Life in EM on diagnostic tests and asking the right questions.  Ask and ye shall receive (or, an example of availability bias).
                          Improved clinical skills resulting in tangible outcomes (a few examples as I can no longer quantify what FOAM brings to the table):
                          • The Cunningham technique to successfully reduce a shoulder dislocation without pain medication
                          • A solid ocular ultrasound curriculum from the Ultrasound Podcast and SonoSpot allowed me to confidently diagnosis my first retinal detachment (and as a mac-off detachment, at that).
                          • Countless discussions on risks and benefits of diagnostic imaging  (thanks to SMART EM and Duke's Emergency Medicine talks on iTunes).
                          Improved clinical skills that I use on a daily basis:
                          • EMBasic's podcasts on various chief complaints.  I no longer get nervous/try to avoid the charts with a chief complaint of "dizzy."  
                          • Employing evidence based medicine in everything from strep throat treatment to resuscitation (credit to nearly every piece of FOAM).
                          09.09.12
                          by

                          FOAM Party! (The Future of Medical Education)

                          The Gist:  Free Open Access Meducation (FOAM, #FOAMed) is essentially a personalized, continually expanding medical curriculum that embraces an individual's attention deficits, evolves as one learns, encourages active learning, and pushes the bounds of one 'ought' to know.  Here's a good summary of FOAM.  Life in the Fast Lane has an extensive list of FOAM resources and there's a new FOAM search engine. 

                          What is FOAM?  Dr. Mike Cadogan and those at Life in the Fast Lane founded the FOAM initiative and continue to build, encourage, and curate FOAM on the web.

                          Each day, I try to spread FOAM among the other rotating medical students, residents, paramedics, and attendings.  I talk about blogs and podcasts, refer people to Dr. Mike Cadogan's video on FOAM, and, if at all possible, try to have the individual set up GoogleReader or an iPhone/Android/iPad app while I'm there.  Although this may occasionally make me appear nerdy (which is clearly not the case) or overzealous, the rewards are excellent and manifest when an individual returns with, "So, what other blogs should I follow?" or "I used _____ on shift yesterday that I heard on one of the podcasts."  It's amazing how quickly people get hooked!

                          Some individuals are skeptical or ambivalent towards FOAM, perhaps unaware of how this broad collection of resources can translate into real world clinical knowledge or wary of the time investment  (note: it actually increases efficiency!).  I can't comprehend why anyone would not partake in this amazing medical education outlet if they actually comprehended the intellectual benefit, personalization, and efficiency of FOAM.

                          I can't articulate the concept of FOAM adequately in the rare minute of downtime in the ED (hence the reason for this blog entry).  In the hopes that others buy into  the FOAM concept, I am compelled to share how the ways that FOAM is transforming me into a better future physician.

                          How does FOAM work for me?
                          Twitter - I used to scoff at this form of social media, but I became a convert a few months ago.  Since that time, this venue has proven to be incredibly useful.
                          • Virtually attend conferences.  I've "attended" EM conferences around the world, including Society of Academic Emergency Medicine (SAEM), International Conference of Emergency Medicine (ICEM), and multiple locally based EM conferences (NY, CA, Australia, etc).
                          Celebrating ICEM 2012, held in Dublin, from the United States
                          • Discover new content.  I used to think I had an extensive blogroll, but Twitter continuously expands my list.  Individuals often tweet links to journal articles, videos, and blogs and following.  This allows one to "read" more extensively than one would otherwise.  It's impossible to keep up with the copious amount of medical literature published, but Twitter helps with this as it's a portal into what others are reading and their take on the article/issue (intellectual voyeurism made incredibly simple)
                          • Active learning.  
                            • Distilling an idea or message into 140 characters is tough, but definitely forces one to be mindful of the core content.
                            • Twitter allows one to engage in conversations with individuals across the globe.  This engenders collective problem solving, brainstorming, and debate.  One can learn to think critically about clinical practice and literature.  Recently, a Google Hangout journal club-esque event was organized and publicized via Twitter with EM/CC heavyweights.
                            • Virtual pimping.  Several people tweet "Question of the Day," including @Radiopaedia - on imaging, @jvrbntz - based on Academic Life in EM's Paucis Verbis cards, and @EMEducation.  These are useful to test knowledge, but also often spark debates and conversations.
                          • Diversify.  Medicine and EM exist outside of the confine of one's nation.  Learn what's going on across the world and track global trends and thought in medicine.  
                          • Build professional relationships across the globe.
                          Podcasts - These are truly gems of FOAM, allowing one to listen to lectures and conversations from world renowned physicians and speakers at one's leisure. Learn more about them in this post, dedicated to podcasts.  

                          Blogs - FOAM blogs are the personalized, up-to-date textbooks of this century.  They deliver information and insight with one's own interest and goals as a filter.  Choose what you interests you, and see how quickly your interests are broadened.  A comprehensive repository from LITFL.  All about FOAM blogs.  

                          Videos - There's a plethora of 10-15 minute videos, packed with incredible medical education, on the web. Many of these are tweeted out and EMCHATTER also has a searchable database with summaries.
                          Questions - The Global Medical Education Project (GMEP) - is an evolving question bank that is interactive and fun.  
                          It seems that whenever I encounter a topic on a podcast or blog that seems esoteric or uninteresting, I invariably encounter the scenario in the clinical setting. I feel compelled to share a few examples of recent intersections between my clinical experiences and the #FOAMed world.  Just a few examples:
                          Pimping made easy:
                          •  On 8/26/12, I skimmed over the blog "Mushrooms in the Valley" from the St. Emyln's blog.  The post was on Morel-Lavallee lesions, something I barely filed away in my brain as esoteric knowledge.  On 8/28/12, my second day of a new rotation, my attending pimped me on Morel-Lavallee lesions and I was able to answer without pause.  Can FOAM predict the future?  I'm pretty convinced.
                          A self-built curriculum:
                          • On 8/27/12 and 8/29/12, I wrote on metacognition and cognitive bias.  Days later, Dr. Michelle Johnston of LITFL posted an outstanding case based blog on cognitive error.  The FOAM world supplemented my curriculum on cognitive error and clinical decision making in real time!  Then, Dr.  Javier Benítez posted a piece on Academic Life in EM on diagnostic tests and asking the right questions.  Ask and ye shall receive (or, an example of availability bias).
                          Improved clinical skills resulting in tangible outcomes (a few examples as I can no longer quantify what FOAM brings to the table):
                          • The Cunningham technique from ERcast to successfully reduce a shoulder dislocation without pain medication
                          • A solid ocular ultrasound curriculum from the Ultrasound Podcast and SonoSpot allowed me to confidently diagnosis my first retinal detachment (and as a mac-off detachment, at that).
                          • Countless discussions with patients on risks and benefits of diagnostic imaging in which I can talk to patients and physicians in terms that each understands (thanks to SMART EM and Duke's Emergency Medicine talks on iTunes).
                          Improved clinical skills that I use on a daily basis:
                          • EMBasic's podcasts on various chief complaints have allowed me to assess patient's quickly and confidently present a solid differential with an accompanying plan.  I no longer get nervous/try to avoid the charts with a chief complaint of "dizzy."  
                          • Employing evidence based medicine in everything from strep throat treatment to resuscitation (credit to innumerable pieces of FOAM).
                          Improved "book" knowledge.  I've used FOAM since just prior to entering medical school to supplement my education.  As a clinically based learner, many FOAM sources make it easy for me to absorb the pathophysiology behind disease processes.  Although I'm a trial of n=1, podcasts, blogs, and Twitter have allowed me to study at the gym, in the car, or while walking/waiting in lines.  This has allowed me to maintain a "life" outside of studying.
                          My FOAM journey
                          09.06.12
                          by

                          Never Trust Your Patient(‘s Med List)

                          The Gist:  In addition to physician-borne cognitive errors, patients and the system may contribute to medical errors/misdiagnosis in the ED due to unreliable and incomplete medication histories.  The ED patient may be more likely to experience these errors because:  trauma patients generally don't update their medication lists and ensure it's readily accessible prior to getting into a motor vehicle accident or stabbing, critically ill patients often can't communicate well, access to patient information across multiple databases is insufficient (the ED attracts patients who are away from home or at hours when pharmacies/physician offices are closed), etc.  Second guess medication lists.  Take a better medication history, even if there's one listed on the chart, and assume the patient is on medications that you don't know about (I have no evidence for the latter statement other than the fact that omission errors in medication lists are the most common).  There's a great, free full text article by FitzGerald in the British Journal of Clinical Pharmacology that summarizes this problem nicely.  

                          The case:  A 52 year old female presented with syncope.  She had an episode of syncope and several episodes of near syncope over the prior day.  Overall, she complained of not feeling well.  The patient's vital signs were significant for a blood pressure of 82/50 and a pulse of 58.  Her symptoms worsened when she stood or moved abruptly, which she hasn't been doing much of because she feels terrible.  No other positives on history or physical.  She had a PMH of hypertension (on 3 medications per medical record/history) and diabetes (glucose 125 on metformin).  Patient's IVC had <30% respiratory variation on ultrasound and ECG showed sinus bradycardia and no other changes.

                          Diagnosis:  Iatrogenic hypotension and bradycardia secondary to anti-hypertensives.  

                          Outcome:  Patient's blood pressure was stablized and her medications were reviewed and decreased to two anti-hypertensives at relatively small doses.  She was seen for follow-up by her PCP 4 days after hospital discharge, still feeling "weak."  Her blood pressure and pulse were both still low, 90/64 and 58 beats per minute.  In addition to the medications the patient was supposed to be on: metformin, losartan/hydrochlorothiazide, and atenolol, the patient's medication bag contained the following (all blood pressure pills, three of which were beta-blockers):
                          Apparently, when doses were changed, she filled the new script and added it to what she had at home.  The patient didn't have great medical literacy, a learning point for when we give verbal or written instructions (hence the bottles labeled "STOP" that were then covered with tape).  

                          The paper:  This month's American Journal of Emergency Medicine has an article, How reliable are patient-completed medication reconciliation forms compared with pharmacy lists?, describing how inaccurate medication reconciliation forms are in the ED setting.  This is not the first study demonstrating the incredible error rates in patient medication lists.
                          • Prospective study using a convenience sample
                          • Patient completed medication reconciliation forms and a research assistant tracked down information from patient pharmacies that covered the preceding 3 months
                          • 484 eligible, n=315 with complete data sets opted to enroll.
                          • 33 % (n=104) had errors of omission, 12.7% (n=40) had errors of addition, and 18.1% (n=57) had both types of errors
                          The scope of the problem:  
                          • In one study, 78% (n=637) of ED medication histories were inaccurate.  This has been corroborated by multiple other studies, summarized in this systematic review (full text).   
                          • Most susceptible populations:  individuals with extensive medication lists, minimal health literacy, and limited communication capacity
                          Ways theses errors cause problems:
                          • Hypersensitivity/Allergic Reactions
                          • Cause of patient's ailment
                            • Directly due to drug.  ex:  NSAIDs/ASA/anti-platelet agents/warfarin - bleeding; diuretics - acute kidney insufficiency
                            • Polypharmacy.  ex: anticholinergic toxicity from multiple medications which could be detected via a complete medication list
                            • Narrow therapeutic index.  ex:  phenytoin, lithium, digoxin
                          • Masking signs or symptoms of illness
                            • Ex:  Beta-blockers or anti-pyretics
                          • As the case above demonstrated, it's not only important to know a patient's medication list, but precisely how the patient is actually taking the medications.  
                            Solutions  Note: Most papers are targeted at the inpatient services, but a few have targeted the ED to improve medication history accuracy.
                            • Review patient's medications verbally.  This is still largely inaccurate as demonstrated by the aforementioned study, although apparently better than reading from a patient's list.  
                            • Assume that the patient is on medications that are not reflected in their medication list/history.  
                              • When I see a large, swollen lip I presume the patient is on an ACE-I until proven otherwise.  If they have no idea, my assumption doesn't change initial management (airway, airway, airway, and the anaphylaxis cocktail) but it will cause me to pursue whether or not the patient is on an ACE-I and whether or not I get in touch with their PCP.  All too often, the patient eventually remembers being on a pill for years for blood pressure that ends in "-pril" or a family member brings in the offending bottle of pills.
                            • Careful attention to the ways we obtain medication lists. A RCT by DeWinter et al (n=260) showed that having EPs ask specific medication history questions can significantly reduce ommision errors, which seem to be the most common in the ED.  In this study, the intervention reduced errors from 1.1 per patient to 0.6 per patient (still pretty high) (2). 
                            • Systems-level changes.  These are likely more expensive, time consuming, and difficult to implement than individual changes but certainly an area for future improvement.  In fact, this is likely the area that will need to change the most to truly address the problem.
                              • Changes in ED medication reconciliation process that utilizes "waiting" time and are driven by the patient have been proposed.  This BMJ article proposes that patients could organize medications in the waiting room and be provided with a "toolkit" to assemble their medication lists (numbers to reach physician offices, pharmacies, instructions to call home), if needed.  This would be used in line with electronic medical records reconciliations and confirmation by the nurse when the patient is taken to a treatment room (3).  Looks promising but would take some effort to implement (and benefits are not yet proven).
                              • Use of pharmacists or technicians within the ED to obtain and confirm medication lists has demonstrated improved accuracy in a few studies, including a small Canadian study that achieved excellent results in obtaining accurate medication histories.  Pharmacists and technicians spent about 8-10 minutes per encounter on the phone with the patient's pharmacy in addition to obtaining medication histories from the patients and electronic medical records (4).  This is a pretty expensive option but if you have them, utilize this resource.
                            • Electronic Medical Records.  These have short-comings as well, as patients don't always take the medications as prescribed and often receive medications from multiple providers that may or may not be reflected in the system.  This is certainly one piece to the puzzle, and a benefit in patients who may not be able to communicate (due to trauma, sickness, or baseline deficit). 
                            References:
                            1.  Mueller SK, Sponsler KC, Kripalani S, Schnipper JL.Hospital based medication reconciliation practices: A systematic Review Arch Intern Med. 2012 Jul 23;172(14):1057-69.
                            2.  De Winter S, et al.  A simple tool to improve medication reconciliation in the emergency department. Eur J Int Med.  2011 Aug;22(4):382-5. 
                            3.  Hummel J, et al  Qual Saf Health Care.   Medication reconciliation in the emergency department: opportunities for workflow redesign.2010 Dec;19(6):531-5.
                            4.  Johnston R, et al.  Best possible medication history in the emergency department: comparing pharmacy technicians and pharmacists.  Can J Hosp Pharm. 2010 Sep-Oct; 63(5): 359-365