The (Un)Learning Process

The Gist:  Despite Harvard's medical school dean, Dr. Burwell, warning students, "Half of what we are going to teach you is wrong, and half of it is right. Our problem is that we don't know which half is which," medical education doesn't do a very good job preparing us for unlearning the wrong half.  Recent publications revealing the reversal of common medical practices demonstrate the need for this skill among clinicians [1-4]. Although unlearning is a part of the learning process, it is difficult, can feel personal, and may mirror the stages of grief [6].  Recognizing the obstacles to unlearning and arming ourselves with an enhanced awareness of ways in which we can overcome these barriers may mitigate our difficulty unlearning.

A study by Prasad et al examined studies testing the "standard of care" in publications in the NEJM and found that 40.2% of articles testing a practice that existed as "standard of care" reversed the practices, whereas 38% of articles testing the practice reaffirmed the standard [1].  The follow up commentary demonstrate that physicians should be open to unlearning and should treat studies with skepticism [2,3].  This is not to say that trainees and physicians should perform full, independent critical appraisals of each article they read but rather, beware of the barriers to scrutinizing our practice.  Through Free Open Access Medical Education (FOAM), one may keep a finger on the pulse of medical literature, through the primary literature and voyeurism into how others process the information.

The Case:  I read the Nielsen et al paper on therapeutic hypothermia (TH) in cardiac arrest in the New England Journal of Medicine with astonishment after the FOAM world exploded with chatter on the paper.  Just days before, the residency conference featured a presentation outlining the evidence behind TH, including the landmark papers by Bernard et al and by The Hypothermia After Cardiac Arrest Study Group.
This paper made me feel uncomfortable.  Medical school, Rosen's, and Tintinalli's made no mention of this aspect of medicine - how to unlearn something well ingrained. This is not to say I think we need to unlearn TH, but to re-examine the cherished practice to identify parts that create a difference in patient care. Less than one year into my residency, there have been countless interventions, diagnostic algorithms, or pathophysiologic explanations, taught to me as a medical student, that are now widely accepted as untrue or bad practice:  activated protein C in sepsis, the pathophysiology behind the hypoxic drive in COPD, the new left bundle branch block in a not so sick patient. I am not an expert, but these struggles with unlearning (or relearning) caused me to develop practices to keep my mental flexibility in check.

Stages of Unlearning and Practices to Overcome These Barriers
1.  Denial - We gravitate towards literature, dogma, experts, and practice patterns that reflect our own biases.  Thus, we may not come into contact with the information prompting a change in our practice or, alternatively, we may outright dismiss the assertion or data without a solid look.
  • Remind ourselves that publications may lead us astray if we are not careful [4,5].  
    • The first study makes the biggest splash but the second (third, fourth, etc) are the most important - don't overlook these [4].  After all, replication is the key to science, the foundation of medicine. 
    • Pay particular attention to "negative" studies, which are published far less frequently than positive studies.
    • Statistics may be easily manipulated.  This exists as data dredging, too much reliance on clinically meaningless statistics such as the p value, or misrepresentation of data or statistics in conclusions [4,5].   
  • Stay abreast of current literature which may include using others to help curate and manage the influx of evidence Examples in FOAM, such as use of Twitter, Emergency Medicine Literature of Note, Richard Lehman's Journal Scan, EM Nerd, can be found at the end of this post
2.  Anger - We tend to become defensive when our beliefs and practices come under scrutiny or are challenged - it can feel like we're being attacked.
  • Accept that we will do things that may, in hindsight, be called "wrong" even though this was not known at the time.
    • This takes a certain level of intellectual and emotional vulnerability.  Historically, this is not only an issue at the individual level, but also a barrier for institutions to unlearn a practice [6].  
  • Reassure ourselves that medical interventions do not define us as providers.  Recognize that evolution of medical practice involves a continuous state of learning and unlearning, despite our best research and efforts. Do not take individual medical interventions personally; rather, attempt to take our overall commitment to good, patient-centered medicine seriously.  
  • Beware of zealotry for a medical intervention.  If question over one of an intervention causes us unease, it may indicate that we are tied more to an idea than to patient care.  For example, I had a visceral response when prompted to re-work my thinking and use IVC ultrasound, in isolation, as a marker of fluid responsiveness.  It was scary to think how I had become so invested in a practice as a medical student.  This may be more difficult for individuals with industry ties or research embedded in one nidus of interest.
3.  Bargaining - We may engage in mental trade-offs with the evidence, using our own experiences/anecdotes or mental frameworks in an effort to trump the data driving the unlearning.  We may utter something along the lines of, "But, I saw Drug X work, in front of my very eyes," despite data demonstrating lack of efficacy.
  • Recognize the cognitive biases we have developed, our heuristics and anecdotes that may cause us to anchor in our learned practice patterns, and attempt to set these aside while we examine the data.  These cognitive short cuts and experiences certainly comprise part of one's clinical gestalt; yet, there may be times in which they act as a crutch.  Once we have a successful, miraculous clinical story of an intervention or diagnosis, we are at risk to become unconsciously attached to the steps that led us to the victorious save.  We have a similarly intense reaction when we experience a negative outcome.  Clinical experience and the best available evidence may work in concert but they also often have a tenuous relationship, filled with bargaining.
  • Similarly, recognize the familiar crutches of pathophysiology based answers or surrogate markers/endpoints.  When we dredge up complicated explanations that we were taught in medical school, with several extrapolations to fit the current thinking, this is frequently a marker that our understanding, to that point, was incomplete to begin with (and therefore, should be prime for re-examination).
4.  Depression - We may feel guilty or defeated by this unlearning process and assume that it translates into either a reflection on ourselves or demonstration of the futility of medicine, research, or evidence based medicine.
  • Recall that while we have a seemingly innate desire to intervene, sometimes even apparently harmless interventions carry risks.  
  • Reinforce that this is part of the process of practicing medicine, which is a dynamic environment teeming with uncertainty.
5.  Acceptance - Once we acquiesce to the notion that it's necessary to unlearn a practice or thought process in medicine, we are at risk of becoming complacent and failing to unlearn yet again, resulting in a vicious cycle.  Perhaps we should never be fully comfortable with the support for what we do, as that may allow us to become complacent and think that we understand when we don't. We may share in creating a dogma to replace the one we have just unlearned.
  • Given the changing landscape of medical practice, it's likely wise to regard all of our practices with a skeptical and curious eye. This may allow us the mental flexibility to alter our practice when warranted. 
  • FOAM may play a role in allowing one voyeurism into how others are adopting or processing studies so we can identify interventions that may be nearing an inflection point for reversal.
    • The use of a filter and "sounding board" for literature does have limitations:
      • Selection bias - perhaps only papers in specific areas of interest/popularity are disseminated.  Furthermore, one may only encounter those disseminated by others with similar opinions, serving only to confirm our own biases.  
      • Premature adoption - As Ioannidis and Prasad warned, medical interventions undergo reversal frequently so aggressive adoption may expose patients to harms and providers to a bruised ego [1-3].  There's an elusive "sweet spot" between changing/unlearning a practice at a dangerously early time and too late. A previous post addresses the use of FOAM and local "authority" to change practice, and the cautions regarding changing practice discussed therein are also apply here.
      • Predigested information can make staying current on literature and ramblings in the medical community easy and practical for busy clinicians but deprives one of the importance of thinking for oneself - it's in this area of work and effort that learning actually takes place.  It's also tempting to simply nod behind others with similar opinions or adopt an expert's view, although this is certainly an issue outside of FOAM as well (e.g. local experts, clinical policies, etc).
1. Prasad V, Vandross A, Toomey C, et al. A decade of reversal: an analysis of 146 contradicted medical practices. Mayo Clin Proc. 2013;88(8):790–8.
2.  Ioannidis JP a. How many contemporary medical practices are worse than doing nothing or doing less? Mayo Clin Proc. 2013;88(8):779–81.
3.  Vinay Prasad V, Ioannidis JP.  Evidence-based de-implementation for contradicted, unproven, and aspiring healthcare practices.  Implement Sci. 2014; 9: 1.
4.  Ioannidis JP a. Why most published research findings are falsePLoS Med. 2005;2(8):e124. 
5.  Nuzzo R.  Scientific method: Statistical errors Nature 506, 150–152 (13 February 2014) doi:10.1038/506150a 
6.  Rushmer R, Davies H. Unlearning in health care.  Qual Saf Health Care. 2004 December; 13(Suppl 2): ii10–ii15.

‘Roid Rage – Right Route and Dose?

The Gist:  For many indications, such as croup, asthma, and anaphylaxis, oral steroids are equally as effective and work as quickly as intravenous steroids and the effective doses are likely lower than we frequently give.   Check out this free steroid converter to prevent preposterously high doses of methylprednisolone or dexamethasone.

The case: A 13 month old presents to the ED with a harsh, barky cough.  Parents report a few days of prodromal upper respiratory symptoms but the child has good oral intake and vital signs.  The child is playful, with a snotty nose and intermittent stridor.  Given the clinical diagnosis of croup, how much dexamethasone do you give?  These bits of Free Open Access Medical education (FOAM) served as the impetus behind the development of my steroid in croup practice: EM PEM podcast, HQMedEd videoEmergency Medicine Literature of Note post

Croup (laryngotracheobronchitis)- A single dose of steroids in croup is the mainstay of treatment in mild to moderate disease as they decrease return visits (RR 0.5, 95%CI 0.3-0.7) and hospital length of stay compared with placebo [1].  The number needed to treat (NNT) is 11 in the ED population (or 5 for improvement in a clinical score).  The historically touted dose of dexamethasone is 0.6mg/kg orally as this is the most studied dose; however, lower doses have demonstrated non-inferiority and have even made it into textbook recommendations [2,3]. The 0.6mg/kg dose of dexamethasone is equivalent to ~3.75mg/kg of prednisone - overkill for this disease process?
  • Dexamethasone 0.15mg/kg PO (can give IV solution orally)
A Cochrane Review demonstrates no significant difference in return visits between "high dose dexamethasone" (0.6mg/kg) and 0.15mg/kg with a risk ratio of 1.04 (95%CI 0.62-1.75) [1]. Hospitals, particularly in Australia where the bulk of the steroid in croup literature originates, have used 0.15mg/kg routinely for the past 18 years, and observational data demonstrates a decline in admissions [3,4].

Limitations - the studies are all pretty small and are not powered to detect small differences.  Are these small differences clinically significant?  Croup also tends to be a self-limiting disease so these studies may be far underpowered to capture rare complications.  Furthermore, many of the studies only look at mild to moderate croup so selection bias may demonstrate.  Yet Fifoot et al excluded this group (Westley score <2) and still found that 0.15mg/kg was as efficacious as larger doses.  The ToPDog study is pending in Australia to demonstrate the effective dose on a larger scale.

Asthma - Glucocorticoids, given within the first hour of presentation to the ED, may reduce need for hospitalization with a NNT of 8 to prevent one hospital admission and, in pediatrics, the length of stay [8].  The literature demonstrates that IV steroids have no superiority over the oral route and the American Thoracic Society recommends oral steroids [8,9].  In fact, Rosen's strongly emphasizes the preference of the oral route, unless the patient is vomiting, in extremis, or has gastrointestinal malabsorption [7].  Prednisone can be swallowed quickly between/during albuterol treatments.
  • Pediatrics: Prednisone 1-2 mg/kg PO
    • Dexamethasone phosphate 0.6 mg/kg PO 
  • Adults:  Prednisone 40-80 mg/day PO
    • Unable to take PO? Methylprednisolone is weight based, at 1mg/kg, not the standard 125 mg given routinely in the ED, which is equivalent to approximately 156 mg of prednisone.  
COPD - no effect on hospitalizaiton rate, but steroids decrease return visits [2]. 
  • Prednisone orally, No benefit to doses higher than 60 mg[2]. 
  • 5 days equivalent to longer courses [10].  
Anaphylaxis - The treatment for anaphylaxis is intramuscular epinephrine [2,7,11].  While glucocorticoids have become part of the standard treatment in anaphylaxis, it's crucial to remember that this therapy is classified as an "adjunct," and is not a treatment for acute anaphylaxis.  Steroids may play a role in resolving the cutaneous manifestations of urticaria and may prevent biphasic or refractory anaphylaxis; however, this is not a proven treatment modality and this intervention takes hours to work.  Furthermore, we historically do not give epinephrine readily enough in anaphylaxis and emphasis on second and third-line agents may detract from actually treating anaphylaxis.

The core emergency medicine texts, Rosen's and Tintinalli's, both recommend IV methylprednisolone in anaphylaxis, followed by a short burst of prednisone for 3-5 days but these recommendations do not come with supporting citations [2,7].  A Cochrane Review turned up no evidence on this therapeutic endeavor [12].  The pathophysiologic argument for IV steroids exists in the notion that patients may have impaired absorption secondary to shunting of blood away from the GI tract.  So, what's the answer?
  • Shock/sick patients - intravenous steroids such as hydrocortisone or methylprednisolone are likely the right answer.
  • The rest of the anaphylaxis patients that are able to swallow  - oral prednisone 40-60 mg/day for 3-5 days.   
Are there downsides to giving IV medications in anaphylaxis?  Medication errors abound in anaphylaxis and an IV may create an accidental error in route of administration (although this would be needed for resuscitation, should the patient be sick) [13].

1.  Russell KF, Liang Y, O’Gorman K, Johnson DW, Klassen TP. Glucocorticoids for croup. Cochrane database Syst. Rev. 2011;(1):CD001955.
2. Tintinalli's Emergency Medicine: A Comprehensive Study Guide.  7th ed, 2011.  p509, 515, 789-790, 805
3. Geelhoed GC, Macdonald WB SOPediatr  Oral dexamethasone in the treatment of croup: 0.15 mg/kg versus 0.3 mg/kg versus 0.6 mg/kg.  Pulmonol. 1995;20(6):362.
4.  Dobrovoljac M, Geelhoed GC. 27 Years of Croup: an Update Highlighting the Effectiveness of 0.15 Mg/Kg of Dexamethasone. Emerg. Med. Australas. 2009;21(4):309–14.
7.  Rosen's Emergency Medicine.  7th ed, 2009.  p 897.
8. Bh R, Spooner C, Ducharme F, Bretzlaff J, Bota G. Corticosteroids for preventing relapse following acute exacerbations of asthma ( Review ). 2008;(4).
9.   Schatz M, Kazzi A, et al.  Joint Task Force Report: Supplemental Recommendations for the Management and Follow-up of Asthma Exacerbations.  Proc Am Thorac Soc Vol 6. pp 353–356, 2009
10.  Leuppi JD, Schuetz P, Bingisser R, Bodmer M,et al. Short-term vs conventional glucocorticoid therapy in acute exacerbations of chronic obstructive pulmonary disease: the REDUCE randomized clinical trial.  JAMA. 2013 Jun 5;309(21):2223-31. 
11.  Gaeta TJ, Clark S, Pelletier AJ, Camargo CA. National study of US emergency department visits for acute allergic reactions, 1993 to 2004.Ann Allergy Asthma Immunol. 2007 Apr;98(4):360-5.
12.  Kjl C, Fer S, Sheikh A. Glucocorticoids for the treatment of anaphylaxis ( Review ). 2012;(8).
13.  Benkelfat R, Gouin S, Larose G, Bailey B. Medication errors in the management of anaphylaxis in a pediatric emergency department. J Emerg Med. 2013 Sep;45(3):419-25. 

"Practice Changers" – Every Foundation Needs a Threshold

The Gist:  Recognizing one's threshold to change practice exists as important part of both one's education as a trainee as well as one's longitudinal practice as a health care provider but is often neglected in medical education [1].  Beware of changing practice based on a single study/role model/source of information.  Increased emphasis and comfort in having one's practice challenged and unlearning ideas/behaviors is important and these habits should be established early through encouragement from training programs, self-reflection, and judicious use of Free Open Access Medical education (FOAM) - as detailed here.

Medicine exists as a persistently changing field with a historically slow uptake and, especially in EM, there is significant practice pattern variation - between individuals, groups, and regions.  Although the majority of medical education focuses on learning the basics, learning how and when to change one's practice is an aspect that feels unnatural and is probably easier cultivated in the beginning.  Below is a variation on the curve that is typically associated with the adoption of technology but may also reflect thresholds for change in medical practice, along with characteristics associated with each group.

The adoption of medical practice based on these group reflects varied thresholds for practice change.

The Case:  A trainee read a blogpost on use of metered-dose inhalers (MDIs) versus nebulizers in asthma.  The trainee quoted "hearing" of the equal efficacy of both to an attending and was met with resistance.  As a result, a dive into the primary literature resulted in a blog on the subject.  Although the practice of MDI with a spacer is supported by texts such as Tintinalli's and several Cochrane reviews, the trainee often meets resistance from attendings using MDI+spacer in the mild to moderate population.  Some attendings encourage this practice while others renounce it, stating that the patients expect the nebulizers as part of the expectation of coming to the ED, conclude MDIs take too long, or are unaware of the recommendations for MDIs despite evidence to the contrary[2].
  • What should the trainee do in this mix of opinion?  Go along with the flow? Spark conversations that may rub some senior clinicians the wrong way?  This is a common phenomenon both in medicine and even in this particular example, as evidenced by the call for knowledge translation on this subject by Osmond et al, who identified common barriers to adoption of this treatment modality for asthma in the ED [2].  When and how do we change our practice, especially as one is simultaneously laying the foundation to one's practice?
Interpreting primary literature is important and changing practice based on a study gets a cursory nod in Rosen's [3].  A future post will delve into this; however, for junior trainees, identifying one's threshold for practice change (where on the curve does one fall/wish to fall) and noting contributors to practice patterns (peer influence, podcasts/blogs, emulation) exists as tangible aspect in the knowledge translation spectrum.  An excellent article by Diner et al details specific ways in which residencies can assist trainees with this process, exemplified by this visual representation.

What residencies and clinical educators can do:
  • Empower residents to order/engage in different interventions or practices.  Experienced clinicians can act as safety and feasibility stops, but giving residents the support, encouragement, access to interventions (or omission of), and ability to think on their own or apply evidence is valuable.
  • Recognize individual thresholds to changing practice and communicate these thresholds with residents [1].  Expert clinicians have practices rooted in habit and experiential outcomes in addition to data, contesting these practices may be difficult, particularly for junior trainees.  Structuring discussions with faculty using examples of practitioners' thresholds for practice change could be valuable. 
  • Use journal club to discuss items beyond methodological rigor, but also as practice identifying what might be needed to change practice - within one's own settings or others: Research? Health care structure? Funds? Education?
  • Ask, "Why?" of the trainees, particularly the most junior trainees when going forth with routine plans in the ED.  Oftentimes the answer may be, "an attending told me to do it this way," or "that's what I thought we did here," or "I don't know." However, these all offer opportunities to demonstrate critical thinking apropos to the patient's clinical scenario.  Understanding the information upon which one builds the foundation of their practice may change one's threshold for change (Is it based on dogma? Irrelevant literature from the 1940's? Mandates?)
What is beholden upon the trainee:
  • Ask, "Why?" This may not always be the most appropriate way to frame the question (change the semantics to suit the situation), but inquire from supervising physicians about what makes them employ diagnostic or therapeutic modalities.  It's a way of engaging in balanced, non-aggressive dialogue about things one might do differently and offers a way to introduce and think about integrating a new practice or literature at the bedside (for either trainee or attending).  
  • Seek information that challenges one's own beliefs.  The alternative information may not always be accurate, but one does a disservice to oneself by neglecting the opposing viewpoint and selectively looking at information that supports our own biases.  This is part of what creates the "laggards" in the above graph.
  • Recognize hero idolatry.  We inevitably develop heroes and role models but despite deep respect and eagerness to please, it's important to maintain a skeptical eye towards what they preach and practice because they, too, are human.  For example, one can use innovative podcasters as a barometer for change, but read and think carefully about these ideas/interventions before adopting them or blindly quoting them.  The latter can also make a conversation about practice changing go awry - so use the best available evidence as a guide.
Something for everyone:
  • Develop a system for keeping up with new thoughts in medical practice - a method that allows one to filter the signal from the noise.  Information overload and the onerous task of attempting to "keep up" with evolving literature and ideas exist as a barrier to knowledge translation [1].
  • Understand aspects of practice influenced by external factors such as industry (pharmaceutical companies), administrators (how does the intervention affect the system?), personal incentives (RVUs), and mandates from supervisory agencies (ex: blood cultures in pneumonia).  For example, use of a nebulizer in an ED visit can increase the level charge for the visit making it an easy way to increase reimbursement for the visit.
  • Recognize one's own biases.  This requires introspection. For example, we often practice in a reactionary fashion - if we see an intervention "work" at the bedside, we may be more prone to neglect evidence to the contrary or safety data based on our experience.  This is more likely to gather momentum as the breadth of our experience increases throughout training and practice.
  • Understand the limitations of groupthink.  Most graduates of EM residency programs practice in the community setting and, in addition to resource barriers, there may be less flux or diversity of thought without monthly journal clubs and group debates.  Practitioners generally practice what they learn during training, which offers a single institution's perspective. Recognizing this as a limitation and seeking and expanded, diverse viewpoints is important.  
1.  Diner BM, Carpenter CR, O’Connell T, et al. Graduate medical education and knowledge translation: role models, information pipelines, and practice change thresholds. Acad.Emerg.Med.2007;14(11):1008–14.
2.  Osmond MH, Gazarian M, Henry RL, Clifford TJ, Tetzlaff J. Barriers to metered-dose inhaler/spacer use in Canadian pediatric emergency departments: a national survey. Acad.Emerg.Med.2007;14(11):1106–13. 
3.  Young KD, Lewis RJ.  "Medical Literature and Evidence-Based Medicine."  Rosen's Emergency Medicine. 7th ed. p2517.

Small Bowel Obstruction – A Likely Story?

The gist:  Small bowel obstruction (SBO) often presents with murky historical and physical features but quick bedside ultrasound exists as a modality that may expedite a patient's workup, with limited training and good sensitivity.  Uptake of US for SBO in US EDs has not been quick, despite nearly 20 years of literature, but perhaps Free Open Access Medical education (FOAM) such as this stellar tutorial on ultrasound (US) diagnosis will reduced the knowledge translation gap [1].

The case:  A 62 y/o male presented to the Janus General ED with a one day history of abdominal pain, mostly located in his right upper quadrant. He reported no fevers, or chill but did have nausea, poor appetite, and a few episodes of non-bloody, non-bilious emesis containing food/clear.  He reported a "normal" bowel movement last night and had a soft abdomen with normoactive bowel sounds.  As the chief complaint was "RUQ pain," a bedside ultrasound was placed on the patient's abdomen during the initial H&P.  Merely touching the probe the the patient's abdomen yielded the following image
Having watched the Ultrasound Podcast's episode on SBO merely weeks prior, the diagnosis of SBO was made expediently.  The workup at this point changed - the patient was admitted to the surgery service, who ordered a CT to localize the cause of the obstruction.

Recently, I've seen cases of SBO blending into the barrage of gastroenteritides fluxing into the ED, prompting me to review the literature.  I found a Taylor et al review of the likelihood ratios (LR - a concept FOAM helped me understand) of various diagnostic modalities helpful.
  • LR+ >5-10: Significantly increases likelihood of the disease
  • LR+  0.2 -5 (esp if close to 1): Does not modify the likelihood of the disease
  • LR+ below 0.1-0.2: Significantly decreases the likelihood of the disease
History and Physical - Sparse ED literature exists on diagnosis of SBO, particularly with regard to history and physical where the literature is minimal and consists of 2 studies.  The theme of these findings seem to be that if these clues are present, it increases the likelihood, but the absence of these findings doesn't really alter the likelihood of SBO.

Patients often endorse vague abdominal complaints, typically comprising intermittent pain, nausea, vomiting, constipation, and have a history of prior abdominal surgery [2,3]. Unfortunately these are non-specific and variably present.  While insensitive, the following demonstrated the most useful LRs:
  • Constipation  +LR = 8.8 and –LR = 0.59 
    • Sensitivity 37-44%
  • History of abdominal surgery  +LR = 3.86 and –LR = 0.19 
    • Sensitivity 69-85% [4]
The physical exam can play a role in determining the patient's degree of illness (ex: peritonitis, fever, etc) but physical signs are not consistent.  Impressive distention and "tinkling" bowel sounds are board answers and impressive for SBO, but these are not sensitive.
  • Abdominal distention +LR between 5.64-16.8 and –LR of 0.34 to 0.43 depending on the study 
  • Abnormal bowel sounds had a +LR of 6.33 and a –LR of 0.27 [4]
X-ray - the historical initial screening test of choice, yet has poor sensitivity, especially for partial SBO (PSBO) and rarely yields a diagnosis/changes management [5].  While x-ray is cheap with minimal radiation, results may falsely reassure providers and this may re
  • Sensitivities range between 59-93% [5].
  • +LR 1.55 (95% CI = 1.10-2.19) and -LR 0.59 (95% CI = 0.43-0.82) (*after the removal of a study with significant heterogeneity) [4]
Bedside Ultrasound in the ED- this modality is gaining momentum as it can provide a very rapid rule in/rule out, but it is still not recommended in core EM texts or become commonplace in many EDs [1,2,3].  The Eastern Association for the Surgery of Trauma (EAST) guidelines give US a cursory nod, in the event the surgery service questions the ability of US to diagnose SBO [6].
  • Sensitivity: 97% (95% CI= 92–99); Specificity 90% (95% CI=84–95) [4] 
  • +LR 9.5 and -LR 0.04 [4]
  • Good interrater reliability compared with formal US- Kappa of 0.8 [4]
The quick run down: place a curvilinear or phase array probe on the abdomen and search for dilated loops of bowel >2.5 cm.  Decreased peristalsis is a later finding also present in SBO, with lower sensitivity [7].

Advantages: Quick, cheap, easy, able to identify other etiologies, may expedite work-up.  In the Jang et al study, the residents had, in addition to their prior training, a 10 minute course and 5 SBO scans prior to enrolling patients - a minimal time investment.
Disadvantages: Images may not be available to inpatient/admitting team, does not demonstrate the cause of the obstruction.  Furthermore, no literature demonstrates that ED bedside US demarcates transition points well, but future studies may elucidate utility in this area.  Ileus and SBO may appear similarly on US, so providers should entertain this in the differential.

Note bene: The bedside ED literature in this realm is small in numbers (2 prospective studies), uses CT or surgical/1 month follow up as the gold standard, and some of the confidence intervals in studies are fairly wide and have sensitivities down to 74.5% when solely looking for dilated bowel.

CT - EAST gives a level I recommendation to CT scans in all patients with SBO to determine etiology and grading [6].  Often, these patient's get CT scans to evaluate for other pathology; however, CT scans can take time, contributing to issues with flow.  CT may be needed for the admitting service, but there's often no need for this to occur prior to getting the admission process started.  With regard to diagnosis, in the two relevant studies that used thin slices, CT demonstrates excellent sensitivity.
  • Sensitivities: 96% (95% CI = 80% to 100%) and 93% (95% CI = 87% to 97%)
  • Specificity of 100% (95% CI = 69% to 100%) and 93% (95% CI = 88% to 96%) [4]
There's also no need for the time consuming oral contrast.
Labs - may help in risk stratifying patient based on degree of illness but add little to the diagnosis.
  • Lactate - if elevated, may indicate ischemia or sepsis
  • WBC >20,000 cited as concerning for ischemia, abscess, or peritonitis [2,3]
  • Elevated BUN or creatinine may indicate volume depletion
How the literature/FOAM has shaped my practice:
  • Do the history and physical, but don't be entirely reassured. Absence of distention or a vomiting patient with diarrhea in the midst of several gastroenteritis patients may cause me to engage in premature closure without recognizing the limitations of these historical and physical factors.
  • Bring the ultrasound into the room of abdominal pain patients while doing the H&P and have a low threshold for taking a quick look when SBO is a consideration.
1.  Carpenter CR, Pines JM. The end of X-rays for suspected small bowel obstruction? Using evidence-based diagnostics to inform best practices in emergency medicine. Acad. Emerg. Med. 2013;20(6):618–20.
2.  Vicario SJ, Price TG.  "Bowel Obstruction and Volvulus." Tintinalli's Emergency Medicine: A Comprehensive Study Guide.  7th ed. pp 581-583.
3.  Torrey SP, Henneman PL.  "Disorders of the Small Intestine."  Rosen's Emergency Medicine. pp 1184-86.
4.  Taylor MR, Lalani N. Adult small bowel obstruction. Acad. Emerg. Med. 2013;20(6):528–44.
5. Böhner H, Yang Q, Franke C, Verreet PR, Ohmann C. Simple data from history and physical examination help to exclude bowel obstruction and to avoid radiographic studies in patients with acute abdominal pain. Eur. J. Surg. 1998;164(10):777–84. 
6.  Maung AA, Johnson DC, Piper GL et al. Evaluation and Management of Small-Bowel Obstruction.  J Trauma. 73(5):S362-S369, November 2012
7. Jang TB, Schindler D, Kaji AH.  Bedside ultrasonography for the detection of small bowel obstruction in the emergency departmentEmerg Med J. 2011 Aug;28(8):676-8.

The Breaking Point – Rib Fracture Risk Stratification

The Gist:  Rib fractures are common and may be associated with significant injury and sequelae.  While rib fractures, even in elderly, don't necessitate transfer to Level I trauma centers, have a low threshold for ICU admission for aggressive pulmonary treatment and analgesia, especially in those with multiple injuries, older patients, some patients with 3+ rib fractures, inadequate pain control/pulmonary toilet, or patients with poor baseline health status (note: based on analyses of largely observational studies without controlled data on outcome differences in). Engage in shared decision making according to the patient's individual situation and check out this podcast by EAST for a Free Open Access Medical Education (FOAM) summary.

The Case: A 62 y/o male with a 50 pack year history of smoking presents as a trauma transfer to Janus General's Level I trauma center after a fall off of a horse, no loss of consciousness, GCS 15 with chest pain. BP 132/68, HR 78, O2 97% RA. He has exquisite tenderness over his right lateral chest wall, some pain and discomfort at rest, exacerbated by deep breathing and movement, and is accompanied by a chest CT scan demonstrating a mildly displaced fracture of the lateral 5th rib, non-displaced fractures of ribs 6-7th posteriorly and a tiny collection of fluid in the right base.
  • Where should I send this patient?  Home-he seems to be ok presently without significant other traumatic stigmata? The floor-his saturations are good, his pain seems to be controllable and he's not that old?  The ICU?
This case represents a common scenario encountered on my trauma surgery rotation and in the ED, and probably similar to other systems as rates of rib fractures in trauma patients reported at 10%[1].  The disposition varied based on the attendings involved and the outcomes, as I followed along for the month, were often surprising.  The initial "sick or not sick" impression didn't necessarily cut it with regards to assessment.  How might I better stratify these patients in the ED to advocate for appropriate disposition?

Risk Stratification - Why It May Matter
Rib fractures are associated with significant morbidity (30-50%) and mortality (~10%) [3,8,9].  It is clear that rib fractures can herald badness as they may signal underlying injury - pulmonary contusion, hemothorax, pneumothorax, or intra-abdominal injury [3].  Additionally, these patients are prone to develop pneumonia (on their own or after mechanical ventilation), which is associated with morbidity and mortality.  For example, a review of the literature demonstrated OR for mortality of 5.24 (95%CI 3.51–7.82) in rib fracture patients with pneumonia versus those without [4].

So, these patients present across a broad spectrum of injury severity (isolated rib fractures vs multiple traumas) and have a decent chance of not doing well, may require significant analgesia, and, depending on who you talk to can go home, to the floor, the ICU, or the OR.  As much of the morbidity/mortality is not evident immediately, risk stratifying, in the absence of a crystal ball, is important.

The breadth of literature suggests that older age is associated a worse prognosis in patients with rib fractures.  For example, this systematic review and meta-analysis found an OR of 1.98 (95%CI 1.86–2.11) for mortality in blunt chest trauma patients >65 y/o compared with younger cohorts  [4].  This makes sense as older patient often have:
  • weaker muscles of respiration
  • decreased physiologic reserve
  • less elasticity of lungs (decrease in volumes, inspiratory/expiratory forces)
  • decreased mucociliary clearance [5] 
These factors often create a great setup for pneumonia, which is associated with the aforementioned badness.   Additionally, older patients may have comorbidities that may predispose them to complications which, result in additional morbidity/mortality [6,7].

Battle et al analyzed data from a retrospective cohort of blunt chest trauma patients and found that the following co-morbidities are associated with complications from rib fractures:
  • Chronic lung disease 3.3 (95% CI 1.6–6.8) - already compromised lungs with set-up for pneumonia
  • Pre-injury anticoagulant use 2.3 (95% CI 1.1–4.8) - signifying underlying disease or propensity to develop hemothorax
  • Oxygen sat < 90% 5.0 (95% CI 1.0–25.7) - sicker patient [7]
Congestive heart failure has also been shown to be associated with an OR of 2.62 (95%CI 1.93–3.55) for mortality [4].

In addition, patients with other traumatic injuries fare worse if they also have rib fractures as they may be predisposed to thrombosis, decreased pulmonary reserve, compromised hemostasis, head injury, and foci of infection [3,4].

How about the number of rib fractures? 3? 6?
Mortality has been quoted as 19% for each rib fracture, but note that this statistic comes from a retrospective review where the OR for mortality was calculated as 1.19 for each rib fracture, with no confidence intervals reported [2].  According to EM texts, elderly patients with 6+ rib fractures should be admitted to the ICU [8,9]. A review of the literature, however, demonstrates that there's no clear answer but somewhere between 3-6 rib fractures is associated with more badness.
  • Lee et al wrote a paper proclaiming that 3+ rib fractures exists as an indication for transfer to a trauma facility.  In this data review, patients with >3 rib fractures had higher injury severity scores - a subgroup of patients with 3+ rib fractures who may benefit from trauma center care due to their potential underlying injuries and complications [10].  
    • Limitations: no outcome data. 
  • A review of the National Trauma Data Bank data demonstrated that mortality does increase with rib fractures but noted that the tipping point for mortality peaked at 6+ ribs with mortalities of 11.41% (n=1771) for 6 rib fractures, 15.03% (n=1114) for 7 rib fractures, and 34.42% (n=1994) for 8 rib fractures [3].
This paper asserts that patient's with more rib fractures are more likely to have underlying traumatic injuries, which is used as justification for a necessary Level 1 trauma center transfer.  One can assume that trauma professionals who treat a copious quantity of rib fractures may provide more targeted care to the patients, including employment of modalities such as epidural analgesia, NIV, and surgical fixation, outcome data for this is missing.  It's not clear that the patients couldn't receive intense pulmonary therapy and analgesia at other centers.

Limitation: Not all rib fractures are created equal and the number doesn't reflect the nature of the fracture, displacement, or presence of hemo/pneumothorax.
    Is it a clear algorithm?
    Just because some patients do poorly, this doesn't mean that all patients are high risk. Some patient can certainly be discharged or admitted to low acuity settings, provided they have good follow up and analgesia.  Afterall, hospitalization and medical interventions have associated complications and costs.

    Chauny et al demonstrated that in their cohort of patient with rib fractures felt well enough to be discharged from the ED, pneumonia within the first two weeks was relatively uncommon at 0.6% of study population (n=6) [11]. So, it appears that discharge is safe in some patients, even those with 3 rib fractures but this is where clinical assessment comes into play.

    • Of note, very few in cohort (n=86; 8%) had 3+ confirmed rib fractures
    • Patients followed up by emergency physicians and research physicians at 1, 2 weeks, with AP chest x-rays, and by telephone at 4, 12 weeks.  This follow up certainly is not guaranteed in a good deal of our patient population and could have led to over-calling of pneumonia or overall more aggressive care.
    • Very few patients had outcome of interest.
    Consider using an incentive spirometer to gauge inspiratory effort/volume at the bedside as part of assessing how the rib fractures may be contributing to the patient's overall status.

    1. Ziegler DW, Agarwal NN. The morbidity and mortality of rib fractures. J. Trauma. 1994;37(6):975–9.
    2.  Bulger EM, Arneson M a, Mock CN, Jurkovich GJ. Rib fractures in the elderly. J. Trauma. 2000;48(6):1040–6
    3.  Flagel BT, Luchette F a, Reed RL, et al. Half-a-dozen ribs: the breakpoint for mortality. Surgery. 2005;138(4):717–23; discussion 723–5.
    4.  Battle CE, Hutchings H, Evans P. Risk factors that predict mortality in patients with blunt chest wall trauma: a systematic review and meta-analysis. Injury. 2012;43(1):8–17.
    5.  Callaway DW, Wolfe R.  Geriatric Trauma.  Emerg Med Clin N Am 25 (2007) 837–860
    6.  Harrington DT, Machan PB, Zacharias N. Factors associated with survival following blunt chest trauma in older patients: results from a large regional trauma cooperative.Arch Surg. 2010 May;145(5):432-7.
    7. Battle CE, Hutchings H, James K, Evans PA. The risk factors for the development of complications during the recovery phase following blunt chest wall trauma: a retrospective study. Injury. 2013;44(9):1171–6.
    8.  Eckstein M, Henderson S.  "Thoracic Trauma." Rosen's Emergency Medicine 7th ed. p. 387-388.
    9.  Brunett P, Yarris L, Cevik A.  "Pulmonary Trauma." Tintinalli's Emergency Medicine.  7th ed. p1756-1757.
    10 . Lee RB, Bass SM, Morris JA, MacKenzie EJ. Three or more rib fractures as an indicator for transfer to a Level I trauma center: a population-based study. J. Trauma. 1990;30(6):689–94.
    11.  Chauny J-M, Émond M, Plourde M, et al. Patients with rib fractures do not develop delayed pneumonia: a prospective, multicenter cohort study of minor thoracic injury. Ann. Emerg. Med. 2012;60(6):726–31. 

    Voodoo or EBM – Discharging the Asthmatic

    The Gist:  When discharging adult patients home from the Emergency Department (ED) following an acute asthma exacerbation, give a short burst of corticosteroids and an albuterol metered dose inhaler (MDI) with spacer [1].  Consider prescribing a short course of inhaled corticosteroids (ICS), although this is less strongly supported by the evidence [2-5].

    The "art of medicine" (i.e. voodoo) sneaks into the prescriptions given at discharge from the Emergency Department (ED) with acute asthma exacerbations.  Which oral steroid, what dose, and what duration?  What about an ICS?  Free Open Access Medical Education (FOAM) has educated me well on handling the asthmatic in extremis (ex: EMCrit, LITFL), but after generating and hearing questions about discharge medications from colleagues - I realized I should examine the rationale behind my practice.

    The Case:  A 21 year old female with a history of asthma never requiring intubation presents to the ED with gradually increasing shortness of breath over the past day.  She has a history of 2 days of preceding upper respiratory symptoms. The patient states she "used up" her remaining albuterol inhaler but continued to get worse. She states she moved to the area 2 months ago and her prescription for her daily inhaler ran out and she hasn't established a local physician.  EMS found the patient working to breath and administered albuterol via nebulizer with some relief.  In the department, she receives 15 mg nebulized albuterol, 6 puffs via MDI with spacer, and 60 mg of oral prednisone. Afterward, the patient has good air movement, is comfortably chatting with her visitor, has a sparse, occasional expiratory wheeze and would like to go home. What prescriptions should I write?

    Beta-agonist MDI + spacer
    Prescribing a beta-agonist inhaler at discharge is standard practice.  As a medical student, I wrote about this here, emphasizing the importance of the spacer and training. Ensure patients have a spacer and can adequately use an inhaler [1].

    Steroids to go. Steroids prevent relapses and hospitalizations [6,7].  Most practitioners and guidelines recommend a short burst of prednisone 40-60 mg for 5 days, although there is limited literature directly comparing dosage/duration of steroids in the dischargeable emergency department patient.
    • Little literature directly comparing doses.  Despite a 55-fold variation in steroid dosing, there's no added benefit from higher doses of steroids [6,7].
      • In medicine, it's becoming more apparent that more doesn't necessarily translate into better patient outcomes (ex: duration of antibiotics in uncomplicated UTI, steroids in croup) and this is likely the case with steroids in asthma.
    • Two dose dexamethasone (16mg)- a prospective RCT in adults (n=257) found that this regimen was non-inferior to a five day of prednisone (60 mg) with regard to asthma symptoms and relapse [8].  Note: This is probably an unnecessarily large dose of dexamethasone (60mg prednisone = 8 mg dexamethasone), but it appears that two doses of dexamethasone may be a good alternative to patients where compliance may be an issue - perhaps more in the future? More on this from EM Lit of Note
    ICS at discharge - Isn't this a primary care physician's (PCP) role?
    This is the most controversial point of discharging an asthmatic - many say it's not an EP's role to prescribe these medications, yet core emergency medicine texts recommend at least considering this at discharge and it's more common practice in other countries [3,7].

    In 2012, a Cochrane review covered the topic of ICS in addition to oral corticosteroids at discharge, including three RCTs with a total n=909 [4].
    • Asthma relapse at 7-10 days = OR 0.72 (95% CI 0.48-1.10) and 20-24 days OR 0.68 (95% CI 0.46-1.02).There were no statistically significant differences in the number of people experiencing an asthma relapse between patients treated with ICS and those on placebo (in addition to oral steroids).  There was a trend towards benefit.
    • Hospital admission was very low, at 2%, with no difference between groups so there's not sufficient power to determine a difference.
    • Asthma symptoms - subjective endpoint, difficult to quantify and extrapolate, and studies have yielded conflicting results.
    • One consideration with these studies is that patients were typically contacted for information at various intervals during the follow up period, serving as a reminder for compliance with various interventions (not quite real world).
    Non-evidence based thoughts on ICS:  
    • Access to PCP. While it's easy for us to write "follow up with your PCP within X days," this is less readily translated into reality. Patients may not have a local physician, there may be a paucity of appointment slots, or the patient may not have the time, means, or desire to follow through.  Furthermore, of those who do follow up with a PCP, many do not receive a prescription for an ICS as controller therapy according to a single center retrospective review [2].  
    • Cost-effectiveness.  Researchers at MUSC performed a cost-effectiveness analysis in pediatric patients presenting with asthma and found that routine ICS prescription at discharge showed cost-savings over recommending that a patient follow up with their PCP [9].  This model is limited in that it is merely a model and based on many assumptions, but is interesting.
    • The "teachable moment." ICS, in patients with asthma, prevent relapses and have thusly earned the role of "controller medication."  Experts who recommend ICS at discharge cite this as one reason 10].
    • Not all patients need ICS long-term, such as those patients with mild intermittent asthma. Many providers assert that as emergency providers, it's not our role to determine the long-term management of a patient's asthma.  Yet, patients visiting the emergency department with asthma exacerbations are cited as being the patients who typically benefit from ICS therapy. The side effects of ICS are minimal and local, especially considering a short term
      • Personally, I evaluate the individual patient, their access to care and compliance, their history and make a decision based on those components - knowing that a prescription for a beta-agonist MDI + spacer and a burst of systemic steroids will benefit the patient the most.  If a patient has been on an ICS in the past, I'm more likely to prescribe this at least a bridge until they see their PCP.
    Note bene:  Dr. Rowe is an author on many of these papers and has the following conflict of interest: received research support and speakers fees from GlaxoSmithKline (once: $1000) and AstraZeneca (multiple: ~$3000/year) in the past 3 years; he is not a paid consultant or employee of either.

    1. Cates CJ, Crilly JA, Rowe BH. Holding chambers (spacers) versus nebulisers for beta-agonist treatment of acute asthma (Review). Cochrane Database Syst Rev. 2006 Apr 19;(2):CD000052.
    2. Cydulka RK, Tamayo-Sarver JH, Wolf C, Herrick E, Gress S. Inadequate Follow-up Controller Medications Among Patients With Asthma Who Visit the Emergency Department. Ann. Emerg. Med. 2005;46(4):316–322.
    3. Cydulka R.  "Acute Asthma in Adults."  Tintinalli's Emergency Medicine. 7th ed. p 507-510.
    4. Edmonds ML, Milan SJ, Brenner BE, Camargo CA Jr, Rowe BH. Inhaled steroids for acute asthma following emergency department discharge.  Cochrane Database Syst Rev. 2012 Dec 12;12:CD002316 
    5. Waxman MA, Barrett TW, Schriger DL. A tale of two steroids: answers to the September 2011 journal club questions.  Ann Emerg Med. 2012 Feb;59(2):147-55. 
    6. Krishnan JA, Davis SQ, Naureckas ET, et al. An umbrella review: Corticosteroid therapy for adults with acute asthma.  Am J Med. 2009 November; 122(11): 977–991.
    7.  Rowe BH, Spooner CH, Ducharme FM, et al. Corticosteroids for preventing relapse following acute exacerbations of asthma.  Cochrane Database Syst Rev. 2007 Jul 18;(3):CD000195.  
    8. Kravitz J, Dominici P, Ufberg J, Fisher J, Giraldo P. Two days of dexamethasone versus 5 days of prednisone in the treatment of acute asthma: a randomized controlled trial.  Ann Emerg Med. 2011 Aug;58(2):200-4. 
    9.  Andrews AL, Teufel RJ , Basco WT , Simpson KN. A cost-effectiveness analysis of inhaled corticosteroid delivery for children with asthma in the emergency department. J Pediatr. 2012 Nov;161(5):903-7. 
    10.  Rowe RH, Bota GW, Clark S, et al. Comparison of Canadian versus American emergency department visits for acute asthma. Can Respir J. 2007 September; 14(6): 331–337.