Monday, April 7, 2014

Breadth and Length - Antibiotics in Uncomplicated Cellulitis

The Gist:  Many cases of uncomplicated, non-purulent* cellulitis can be treated with a five day course of oral antibiotics, such as cephalexin or dicloxacillin, without covering for MRSA.  The Infectious Disease Society of America (IDSA) and core emergency medicine texts support this recommendation, with provisions for extended coverage (duration and/or MRSA antibiotics) in high-risk or sicker patients [1-3]. Despite these recommendations, providers often prescribe lengthier courses with broader spectrum coverage, which may have lead to adverse effects, increased cost, or resistant microbes [4-6,8].

The Case:  A 38 year old female presents to the emergency department (ED) with right lower extremity erythema and warmth, progressing over the past four days.  She has no known trauma, no prior history of cellulitis or abscesses, and her history was remarkable for "borderline" diabetes, hypertension, and depression.  Vital signs are within normal limits and examination reveal a diffusely erythematous area of approximately 7 x 4 cm, warm to touch, with some edema but no induration or drainage.  This patient seems to be an ideal candidate for outpatient therapy.  Should the provider write for cephalexin for 5 days? 7 days? Does the patient also need TMP-SMX or clindamycin?

Despite revolutionizing medical care, antibiotics prescribed for skin and soft tissue infections are not benign as patients incur costs and may develop allergic reactions, yeast infections, antibiotic associated diarrhea, or provoke resistant pathogens.  In national survey data, antibiotics have been associated with nearly 1 in 5 ED visits for adverse drug events and more than 1 in 4 similar events in the pediatric population [5,6].  Antibiotics prescribed for skin and soft tissue infections have been associated with a large proportion of these events, at least in children [7].  As a result, there's an increasing emphasis on using appropriate antibiotics for the minimum duration needed to treat the infection.

Duration of therapy: In 2005, the IDSA issued a recommendation a 5 day course of treatment for uncomplicated cellulitis and this is offered up as an option in core EM texts [1,3,6].  However, many practitioners prescribe an initial 7-10 day course of treatment. Interestingly, the most recent iterations of both Tintinalli and Rosen's do not hazard a suggestion for antibiotic duration for any skin and soft tissue infections [2,3].

The five day recommendation** is based on study by Hepburn et al.  Outpatients presenting to the clinic or ED (n=121) with uncomplicated cellulitis were treated with levofloxacin for 5 days and then randomized (n=87), at a 5 day visit, to receive either 5 additional days of antibiotics or placebo. Patients were reevaluated at an appointment between days 10-14 and then at 28 days by telephone.  Treatment success was not different between groups, with 98% resolution in both arms [8].
  • Diabetes was not an exclusion criteria and was present in 5% (n=12) and 7% (n=16) in the treatment and placebo groups, respectively.
  • At the time of randomization (day 5), patients were allowed to have persistent erythema and warmth, as long as it had not worsened and seemed marginally improved.  This was somewhat subjective.  
  • Patients were enrolled within 24 hours of diagnosis and treatment so some patients received different antibiotics during the first 24 hours.  
  • Levofloxacin isn't routinely used for cellulitis in most populations. 
Choice of antibiotics:  Most non-purulent cellulitis is caused by streptococcus (strep), even in areas with a high prevalence of MRSA.  As such, the IDSA and core texts recommend targeting strep only for most uncomplicated, non-purulent cellulitis [1].  Literature suggests these low risk patients do no better on coverage for both strep and staph [9].  In higher risk patients or those with purulence that do require staph coverage, it is recommended that providers use anti-MRSA antibiotics in areas with high prevalence of MRSA [1-4].  Use of anti-MRSA antibiotics in high risk groups including those with history of MRSA, diabetic ulcers, systemic illness, IVDU, and other higher risk patients is less controversial and more broadly supported [1-4].

A study comparing monotherapy with cephalexin versus TMP-SMX have demonstrated that in systemically well, uncomplicated patients, cephalexin monotherapy suffices [9]. Review of the study. A trial comparing TMP-SMX, placebo, cephalexin, or combination was completed in July 2013, with no posted results at this time [11].

Of note, studies examining the microbiology of cellulitis may be skewed by selection bias, as staph and MRSA tend to cause more purulent infections which may be more likely to be cultured [12]. Furthermore, cultures are only indicated and, theoretically obtained, in the sicker patients and in those with comorbidities which may further also skew the results.

Do we prescribe antibiotics appropriately? Not commonly.
Hurley et al conducted a retrospective cohort study in Denver of ED patients and outpatients in 2010-2011 that measured the frequency of "avoidable antibiotic exposure." The authors defined "avoidable" antibiotics with a broad spectrum of gram-negative activity (beta-lactam/beta-lactamase inhibitor combinations, second, third, or fourth-generation cephalosporins, fluoroquinolones, carbapenems, or aminoglycosides); combination therapy (2 antibiotics or more); or treatment for more than 10 days.
    • n=364 of whom 155 had cellulitis
    • Only 7% (n=8) of patients with cellulitis received 5 days of antibiotics and 47% (n=54) received 10 or more days of antibiotics
    • 61% of patients with cellulitis received MRSA coverage [9]
Also, there's no benefit to a single dose of IV antibiotics in the ED and blood cultures aren't helpful in these patients.  On a more controversial note, a recent retrospective chart review by Paolo et al found that blood cultures may not significantly alter management in cases of complicated cellulitis as the contaminant rate (3%) was roughly equivalent to our true positive rate (4%).

*Complicated - varies by reference, but typically includes immunocompromised, those with signs of systemic illness, extremes of age, or diabetes.
Purulent - drainage or signs of abscess. History of abscess and eschar are also associated with staphylococcus (staph).  
**It's difficult to determine what, precisely, the 7 and 10 day historical attachments are based on other than history and familiarity.
References:
1.  Stevens DL, Bisno AL, Chambers HF, et al. Practice guidelines for the diagnosis and management of skin and soft-tissue infections. Clin Infect Dis. 2005;41(10):1373–406. 
2.  Kelly EW, Magilner D.  "Soft Tissue Infections."  Tintinalli's Emergency Medicine: A Comprehensive Study Guide.  7th ed. p 1017-1018.
3 .Marx JA, Hockberger RS, Walls RM.  Rosen's Emergency Medicine , Eighth Edition. Chapter 137, 1851-1863.e1
4. Meislin HW, Giusto G.  Rosen's Emergency Medicine , Seventh Edition. Chapter 135, 1836-1838. 
5.  Shehab N1, Patel PR, Srinivasan A, Budnitz DS. Emergency department visits for antibiotic-associated adverse eventsClin Infect Dis. 2008 Sep 15;47(6):735-43. 
6.  Bourgois FT, Mandl KD, Valim C et al.  Pediatric Adverse Drug Events in the Outpatient Setting: An 11-Year National AnalysisPediatrics. Oct 2009; 124(4): e744–e750.
7. Goldman JL, Jackson MA, Herigon JC et al.  Trends in Adverse Reactions to Trimethoprim-Sulfamethoxazole.  Pediatrics. Jan 2013; 131(1): e103–e108.
8. Hepburn MJ, et al. Comparison of short-course (5 days) and standard (10 days) treatment for uncomplicated cellulitis.  Arch Intern med 2004; 164, 1669-1674
9. Hurley HJ, Knepper BC, Price CS, et al. Avoidable antibiotic exposure for uncomplicated skin and soft tissue infections in the ambulatory care setting. Am J Med. 2013;126(12):1099–106. 
10. Pallin DJ, Binder WD, Allen MB et al.  Clinical Trial: Comparative Effectiveness of Cephalexin Plus Trimethoprim-Sulfamethoxazole Versus Cephalexin Alone for Treatment of Uncomplicated Cellulitis: A Randomized Controlled Trial.  Clin Infect Dis. (2013) 56 (12): 1754-1762.
11.  ClinicalTrials.gov: A Service of the U.S. National Institutes of Health (NCT00729937). 
12.  Ray GT1, Suaya JA, Baxter R. Microbiology of skin and soft tissue infections in the age of community-acquired methicillin-resistant Staphylococcus aureus. Diagn Microbiol Infect Dis. 2013 May;76(1):24-30.

Saturday, March 15, 2014

We Don't Know What We Don't Know

The Gist:  Overestimation of our level of mastery is common and is referred to as the Dunning-Kruger effect [1-3].  This effect persists in medicine and may have deleterious effects both at the bedside and in the training process [4-6].  Use of practice testing or simulation, metacognition, and the push of information to an individual may mitigate the dangers of unconscious incompetence by identifying areas of weakness and keeping the practitioner skilled.

"Ignorance more frequently begets confidence than does knowledge" - Charles Darwin [6]

The Case:  A 48 year old female with hypertension presented to Janus General with the sensation of the room spinning and feeling off balance for the past day.  The resident performed a head impulse, nystagmus type, test of skew (HINTS) exam, which demonstrated the presence of a saccade during the head impulse component. and determined that the patient likely had a central cause.  The patient was admitted to the hospital for questionable TIA/CVA workup, which was negative.
  • The problem: a saccade during the head impulse component is suggestive of a peripheral cause of vertigo.  While use of the HINTS exam by emergency providers has not been validated and is outside the bounds of this discussion, this example demonstrates the overconfidence of the resident in their skills and interpretation and the potential for perpetuation of this misunderstanding.  
The Dunning-Kruger Effect - These researchers demonstrated a large discrepancy between the way incompetent people actually perform and the way they perceive their own performance level.  This discrepancy appears smaller for highly skilled individuals, who may underestimate their mastery. The studies demonstrating this effect often result in a graph akin to the one below.


The Danger in Medicine - A little knowledge is a dangerous thing.  In medicine, a balance exists between the confidence to commit and act and the insight to see that we have uncertainty or lack the appropriate skill set.  In emergency medicine this line may be particularly difficult to walk as patients often require immediate intervention at times when data is limited, clouding certainty.
  • Diagnostic Error -  Overconfidence may result in premature closure, confirmation bias, or failure to use clinical aids such as practice guidelines or decision aids.  It turns out that compared with tempered attendings and insecure medical students, residents may be most susceptible to diagnostic overconfidence [8]. 
  • Unsafe Procedures - An attending once told me, "Procedures in emergency medicine exist to keep us humble."  After a novice learner's first string of successful intubations, it's tempting to believe we've become "good" at intubations.  However, this hubris may cause us to expose patients to harm if we take short cuts in preparation or fail to continue to maintain contingency plans.  Furthermore, in emergency medicine, we must be able to cue up live saving procedures at any moment that we may only see or perform once in a career.  Without accurate awareness of our competence, we may we fail to recognize that our skillsets are weak or a procedure/tools/kits have changed leading to suboptimal outcomes.  
“Real knowledge is to know the extent of one's ignorance” – Confucius

Mitigating the Effect
  • Practice Testing (or retrieval practice) - While the quality of the evidence is poor, Davis et al write that physicians are particularly not keen at assessing themselves [6].  As a result, we are unlikely to identify our areas of incompetence ourselves.  Assessment through practice testing, however, may identify weak areas in our knowledge base or skill set that we may otherwise not identify. In this way, we may decrease the discrepancy between what we think we know and what we actually know.
  • Simulation - Practice and rehearsal can identify weak areas in procedures or situations we may not often encounter or, conversely, give us the confidence in our ability to act when needed.  This doesn't require mannequins and computers - simply rehearsing procedures and scenarios in our minds works quite well.  Dr. Cliff Reid eloquently stated, “We have the most powerful, 3D, high-fidelity simulator in the known universe," reference the mental simulator.
  • Information Push - Most of us only review topics we believe we have previously mastered when we discover a weak spot in our understanding or make a mistake.  However, when information is pushed to the us, we encounter a wider array of information.  
    • Free Open Access Medical education (FOAM) serves as a prime example of the concept of information push, as topics collated in RSS aggregators such as Feedly and delivered by subscriptions to podcasts or twitter feeds cover information not intentionally sought by the learner.  So, while some find FOAM overwhelming, it can be used in an interesting way to strengthen the areas that we don’t know that we don’t know.
  • Metacognition - Awareness of weak points in our reasoning or systemic traps may help us overcome overconfidence, particularly with regard to diagnostics.  The post, Metacognition For the Pragmatist, discusses ways in which we can overcome our cognitive biases.  
  • Remain skeptical of the feeling of complete ease and mastery, which may cause to stop working and striving to improve.  In his talk “The Path to Insanity” at SMACC 2013, Dr. Scott Weingart advises that we "never assume your own excellence" [9]. 
What's the underpinning of the Dunning-Kruger effect?
  • It's difficult to estimate the quality of one's performance.
  • Self-enhancement bias - We tend to think we're better than we actually are.  For example, very few bad drivers actually recognize the fact that they, in fact, are the poor drivers.
  • Regression to the mean - This explanation exists as one of the primary criticisms of the Dunning-Kruger Effect and argues that the effect may be, in part, statistical artifact.  When people are asked to evaluate themselves, incompetent people may simply regress toward the mean when asked to evaluate their own performance. On the other hand, people who have extremely high levels of performance, those who have mastery in a given area, are also less likely to underestimate their skills to the degree that those who are incompetent.
“I know that I know nothing” – Socrates
References:
1. Dunning D, Heath C, Suls JM. Flawed Self-Assessment: Implications for Health, Education, and the Workplace. Psychol Sci Public Interes. 2004;5(3):69–106. doi:10.1111/j.1529-1006.2004.00018.x.
2. Kruger J, Dunning D. Unskilled and unaware of it: how difficulties in recognizing one’s own incompetence lead to inflated self-assessments. J Pers Soc Psychol. 1999;77(6):1121–34. 
3. Dunning D, Johnson K, Ehrlinger J, Kruger J. Why people fail to recognize their own incompetence. Curr Dir Psychol Sci. 2003;12(3):83–87. doi:10.1111/1467-8721.01235.
4. Edwards RK, Kellner KR, Sistrom CL, Magyari EJ. Medical student self-assessment of performance on an obstetrics and gynecology clerkship. Am J Obstet Gynecol. 2003;188(4):1078–1082. 
5. Hodges B, Regehr G, Martin D. Difficulties in recognizing one’s own incompetence: novice physicians who are unskilled and unaware of it. Acad Med. 2001;76(10 Suppl):S87–9.
6.  Davis DA, Mazmanian PE, Fordis M, Harrison R Van, Thorpe KE, Perrier L. CLINICIAN ’ S CORNER Accuracy of Physician Self-assessment Compared A Systematic Review. 2006;296(9).
7. Darwin C. 1871. The Descent of Man, and Selection in Relation to Sex, 1st edition. London: John Murray.
8. Berner ES, Graber ML. Overconfidence as a cause of diagnostic error in medicine. Am J Med. 2008 May;121(5 Suppl):S2-23. doi: 10.1016/j.amjmed.2008.01.001.
9. Weingart S.  EMCrit.  Podcast 105.  August 20, 2013.  Available at: emcrit.org/podcasts/path-to-insanity/

Monday, February 17, 2014

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.
Action:
  • 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.
Action:
  • 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.
Action:
  • 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.
Action:
  • 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.
Action:  
  • 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).
References:
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.

Tuesday, January 21, 2014

'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].

References:
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. 

Tuesday, January 7, 2014

"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.  
References:
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.

Sunday, December 29, 2013

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]
Imaging
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.
References:
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.

Wednesday, December 11, 2013

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.

Age?
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].

Comorbidities
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.

Limitations:
  • 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.

References:
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. 

Saturday, October 26, 2013

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.

References:
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.

Thursday, October 17, 2013

A System for the System - System Errors in the ED

The Gist: In addition to cognitive biases, systems errors are ubiquitous in the emergency department (ED).  Free Open Access Medical education (FOAM) has inspired me to realize that one may mitigate some of these errors to improve patient care/outcomes by vigilance.

As a fan of metacognition, I attempt to mitigate my cognitive errors through simple practices. A few months into residency, I occasionally find myself frustrated by systems-based errors.  Finally, something to blame other than myself!  As that attitude is not terribly productive, I've adopted steps to attempt to overcome these errors, something I foresee as an evolving and expanding process.

Systems-based errors: reflect flaws or problems with process that are part and parcel of the health care delivery system.  These errors are often rooted in inefficiencies, issues with coordination of care, and communication [1].
Case #1:  A 54 y/o male presented to Janus General with fever to 38.8C, malaise, and weakness over the past 2 days. BP 126/82, HR 90. Patient had a PICC line to the right arm that appeared clean, status-post left hip wash out for septic arthritis 3 weeks prior.  I ordered labs and fluid, with plans for antibiotics.  Despite repeatedly checking for the lab results, they didn't appear.  Eventually, I called the lab - who reported receiving the specimens just minutes earlier as the hospital's tube delivery system had malfunctioned.  This resulted in another blood draw from the patient for a repeat lactate (which turned out to be 6), as the specimen was too old, a delay in more aggressive care, and a silly/guilty feeling doctor.  Studies demonstrate that delays in antibiotic administration impact mortality, so while the patient didn't appear to be in the sickest group of patients this still could have resulted in a bad outcome [2].  But, it's the system's fault, right?

Things I try to do to mitigate systems errors:
Communicate with nursing and support staff.  Oftentimes, they can help get things done more expeditiously or identify barriers to the proposed treatment plan.

Call the lab, radiology, pharmacy, etc.  Many steps exist between placing an order for a diagnostic evaluation or intervention and the completion of the order and an error can occur at any point. Furthermore, it's anecdotal, but I've been impressed with how face-to-face or verbal discussion of the "why" or need for urgency can expedite care.

Establish a consistent method to reassess patients/labs.  Time can fly in the ED and often our attention is divided by unexpected sick patients.  For example, we can handle a mostly stable GI bleeder, a septic patient, and a chest pain patient.  However, the minute one begins to crash or a code rolls in, our attention becomes divided and non-critical patients may be placed on the back-burner.  As a trainee, it's easy to think that a stable patient will remain stable but this isn't always the case.  Furthermore, interruptions are rampant in the ED and this forced shift in attention may lead to delays in reassessment [3].
  • Some keep running list of things in their pocket/workstation that need follow up.  A unique solution offered by Dr. Jeremy Faust - use Siri [4].  "Siri, remind me to re-examine room 4 in 30 minutes." 
Beware of alarm fatigue.  Alarms constantly ring in the ED and pop up in the EMR - but on occasion, they actually mean something.  It's important to catch it when it does.

Approach sign out with caution.  This area of emergency medicine has garnered much attention as it may lead to a hotbed of cognitive errors and the nature of sign-out can vary within the institution. Most of the literature revolves around the inpatient experience, but I think that the vulnerability of this process translates into the ED [5]. Physicians and hospitals approach sign out differently, but there's a call for increased standardization [6].  Consider standardizing your own approach.
  • Re-examine the patient, their vital signs, and crucial diagnostic/interventional endeavors.  
  • Tip from Dr. Jeremy Faust - start sign-out saying something along the lines of: I'm intentionally going to be a bit annoying, don't take it personally.  Then, aggressively go through the case. Two heads are better than one. 
Reexamine information received from outside physicians/transferring facilities.  Information often gets left out or lost in the series of communications surrounding transfers in care or partial work ups - minimize this by utilizing the patient's data.
  • Take a gander at a patient's EKG or diagnostics for yourself.  The "sinus bradycardia" for suspected accidental beta-blocker overdose may actually be a high degree AV block or a radiograph may be revealing.  
Establish a consistent method of follow up.  A myth exists that emergency physicians do not or should not follow up their patients.  As a result of the discontinuity of care, we will not typically see our mistakes unless we look for them. Check out the EM Res podcast on this topic.
  • In the EMR, I keep a list, by month, of patients I see in the ED so I can easily check up on patients.  This takes 1 extra click per patient but saves time attempting to recollect the name and has created the expectation within myself that I will follow up on some of those patients.
  • Consider a "bounceback" program.  This provides larger buy-in, but provides an invaluable educational opportunity.  At my institution, if a patient returns within 7 days, we receive a notification.  Oftentimes these are unpreventable (the daily drunk patient) or an indication that we provided good discharge instructions; however, more often than not there's a pearl for the future.
Use the EMR or family members to get to know the patient.  In the ED we don't know (most of) our patients, which can create fragmented care and an incomplete picture of our patient.  Valuable information can be found in the EMR (ex: the patient does, in fact, have baseline confusion and left sided weakness) or from family members who may be able to explicitly detail how the patient is different from baseline.

Case #2 (months later): A 51 y/o female presented to Janus General with cough, tachypnea, decreased oral intake.  Temperature 37.6C, BP 106/78, HR 136. Physical exam significant for tachypnea, rhonci in bilateral lung fields, and dry mucosa.  I discussed the plan with the nurse, emphasizing the patient's need for fluids and aggressive care.  The patient had no access and prior unsuccessful attempts, so the nurse quickly identified the need for ultrasound guidance.  Siri reminded me to check on the antibiotics and reassess the vital signs while suturing another patient.  The patient's vital signs, lactate, and clinical appearance normalized in the ED after several liters of fluid and the patient went on to do well.

Are there problems with attempted fixes for systems errors?
  • Improvements will fade as time passes secondary to decreased awareness, other foci of improvement, and lessened enthusiasm [1]
  • Fixes may produce opportunities for more errors
References:
1. Graber M, Gordon R, Franklin N. Reducing diagnostic errors in medicine: what’s the goal? Acad. Med. 2002;77(10):981–92. Available at: http://www.ncbi.nlm.nih.gov/pubmed/12377672.2.
2.  Gaieski DF, Mikkelsen ME, Band RA,et al.  Impact of time to antibiotics on survival in patients with severe sepsis or septic shock in whom early goal-directed therapy was initiated in the emergency departmentCrit Care Med. 2010 Apr;38(4):1045-53.
3. Elson, Ordell. Emergency Department Workplace Interruptions: Are Emergency Physicians “‘Interrupt-driven’” and “‘Multitasking’”? Academic Emergency Medicine 2000;7(11):1239–1243.
4.  Faust, JS. "The 'Sultan of Signout'" ACEP News. August 2013. p 12-13.
5. Arora V, Johnson J, Lovinger D et al. Communication failures in patient sign-out and suggestions for improvement: a critical incident analysisQual Saf Health Care. 2005 December; 14(6): 401–407.
6.  Dhingra KR, Elms A, Hobgood C. Reducing error in the emergency department: a call for standardization of the sign-out process. Ann Emerg Med. 2010 Dec;56(6):637-42.