Category Archives: perspectives

emDocs Wellness: A Growing Issue

Author: Jennifer Robertson, MD, MSEd (Assistant Professor of EM, Emory University) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UT Southwestern Medical Center / Parkland Memorial Hospital)

Consider the following cases:

  1. A 35-year-old male with pneumonia develops sepsis. During one physician’s emergency department (ED) shift, he goes into respiratory failure and arrests. The physician is the only one held liable by administration for this event, even though the ED was known to have inadequate staffing, equipment and training. He is reported to the medical licensing board.
  2. A 65-year-old female presents with a chief complaint of a new onset mild headache. Her head computed tomography (CT) scan is normal. Her inflammatory markers, including platelet count, erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) levels are normal.  The physician discharges her home with close primary care follow up. A week later, the patient goes blind due to temporal arteritis. She not only sues the physician for malpractice due to misdiagnosis, but she also returns to the ED and verbally accosts the responsible physician.
  3. Paramedics bring in a two-year-old female to the pediatric ED at 1am. She is barely responsive, has a large hematoma to the head, and is noted to have scattered bruises on the torso and limbs. She is intubated and sedated for airway protection. Head CT reveals a large intracranial bleed and x-rays reveal several fractures in varying stages of healing. The patient ultimately passes away due to sequelae of child abuse.

Being a physician is not an easy task. While many outsiders may believe that physicians are invincible and lead glamourous lives, these assumptions are not reality. Just like non-physicians, physicians are human and they suffer stresses and ailments that can lead to emotional burnout, mental disorders and poor physical health (1, 2). In fact, studies have shown that physicians suffer from similar rates of mood disorders actually have higher suicide rates than non-physicians (2, 3, 4). Not only do physicians have personal responsibilities and financial burdens such as student loans, but they often work long hours, are underappreciated by patients and employers, and treat complicated patients that occasionally sustain poor outcomes. Many physicians witness patients who have experienced traumatic events on a daily basis including deaths and abuse. Indeed, it has been demonstrated that heavy workloads and job difficulties are considered to be the biggest contributors to physician emotional distress, mental illness and suicide (2, 5).

While research remains ongoing, it has been suggested that poor emotional, mental and physical health in physicians may negatively impact patient care and quality of care in general (1, 6, 7). One emerging area of research is poor emotional well-being or, as others call “burnout”. In general, burnout is a syndrome of emotional exhaustion, depersonalization and reduced personal accomplishment that occurs in workers who engage with others regularly (7). Most often, burnout develops in employees who work with people who have significant psychological, social or physical problems. With burnout, workers become chronically stressed and eventually feel as though they are unable to provide any more of their own emotional resources to others. Consequently, depersonalization and negative attitudes toward clients can develop (7). Finally, lack of personal accomplishment occurs because eventually, emotional fatigue brings workers to view their work and their accomplishments negatively (7). It has been demonstrated burnout occurs more commonly in physicians than in those with other careers (8). There may be several reasons behind this, and further EMDocs articles will discuss burnout in physicians in more detail. Further articles will also discuss the etiology of burnout, how to measure it, and how to avoid it throughout your career.

Emotional burnout is also closely related to mental health, physical health and personal relationships (7,9, 10, 1l). While depression rates in physicians are similar to those of the general population, suicide risk in physicians is actually higher (2). While there are no exact numbers, it has been estimated that in the United States, doctors commit suicide at a rate of one medical school class per year (12).  Depression in physicians often goes under recognized, but it is a serious issue that must be recognized, treated and prevented.

Post-traumatic-stress disorder (PTSD) is another concerning mental illness that is seen in 5-6% of men in 10-14% of women in the United States (13). However, like depression, PTSD is often not an illness that most would consider to be an issue in physicians (14). While research remains limited in this area, PTSD does seem to occur in physicians (15). In 2005, Mills and Mills published a study on the prevalence  PTSD in emergency medicine resident. Overall, the authors found that 11.9 % of emergency residents met DSM IV criteria for the actual disorder, but 30% met one or more symptom categories of PTSD, including re-experiencing, avoidance and arousal (16).

Finally, physical health may also suffer as a result of job burnout (11, 17). Physicians with proper nutrition tend to also perform better at their jobs, while those with poor nutrision perform more poorly (18). In addition, those who are more physicially active tend to better cognitive performance, lower degrees of job burnout, and less depression (19, 20). Studies have also demonstrated that psychologic stress may lead to acute or chronic inflammation, which may contribute to certain disease states (21). Job burnout has been found to be associated with cardiovascular disease, musculoskeletal disorders, sleep disturbances and even diabetes (9, 11, 17, 21).  Thus, job burnout may not only impact psychologic well-being, but it may actually lead to poor physical health.

What is wellness?

Wellness has been suggested to be the antithesis of burnout (3). While the study of wellness in medicine remains in its early stages, certain methods may deem helpful and will be discussed in future emDocs articles (8, 22). Suggested wellness measures for physicians include regular physical activity, having their own personal physicians, and adequate social support (1, 7, 19). It has been shown that mentally, emotionally and physically healthy physicians provide more empathy toward patients (22). It has also been suggested that wellness measures for physicians should be a measure of healthcare quality (6). This makes sense, since a happy and physically and emotionally healthy physician is likely going to take better care of patients. Hence, overall wellness of physicians is important and should be addressed by all hospital systems, whether community, government-run, or academic.  Further articles will discuss wellness measures as well as the growing crisis in physician burnout and mental health.

References/Further Reading

  1. Taub S, Morin K, Goldrich MS, Ray P, Benjamin R. Physician health and wellness. Occupational Medicine. 2006 Mar 1;56(2):77-82.
  2. Gold KJ, Sen A, Schwenk TL. Details on suicide among US physicians: data from the National Violent Death Reporting System. General hospital psychiatry. 2013 Feb 28;35(1):45-9.
  3. McClafferty H, Brown OW, Committee on Practice and Ambulatory Medicine. Physician health and wellness. Pediatrics. 2014 Oct 1;134(4):830-5.
  4. Center C, Davis M, Detre T, Ford DE, Hansbrough W, Hendin H, Laszlo J, Litts DA, Mann J, Mansky PA, Michels R. Confronting depression and suicide in physicians: a consensus statement. Jama. 2003 Jun 18;289(23):3161-6.
  5. Bovier PA, Arigoni F, Schneider M, Gallacchi MB. Relationships between work satisfaction, emotional exhaustion and mental health among Swiss primary care physicians. The European Journal of Public Health. 2009 Apr 29:ckp056.
  6. Wallace JE, Lemaire JB, Ghali WA. Physician wellness: a missing quality indicator. The Lancet. 2009 Nov 20;374(9702):1714-21.
  7. Maslach C, Jackson SE, Leiter MP. Maslach burnout inventory manual. Mountain View, CA: CPP. Inc., and Davies-Black. 1996.
  8. Dyrbye LN, West CP, Satele D, Boone S, Tan L, Sloan J, Shanafelt TD. Burnout among US medical students, residents, and early career physicians relative to the general US population. Academic Medicine. 2014 Mar 1;89(3):443-51.
  9. Melamed S, Shirom A, Toker S, Berliner S, Shapira I. Burnout and risk of cardiovascular disease: evidence, possible causal paths, and promising research directions. Psychological bulletin. 2006 May;132(3):327.
  10. Ahola K, Honkonen T, Kivimäki M, Virtanen M, Isometsä E, Aromaa A, Lönnqvist J. Contribution of burnout to the association between job strain and depression: the health 2000 study. Journal of occupational and environmental medicine. 2006 Oct 1;48(10):1023-30.
  11. Honkonen T, Ahola K, Pertovaara M, Isometsä E, Kalimo R, Nykyri E, Aromaa A, Lönnqvist J. The association between burnout and physical illness in the general population—results from the Finnish Health 2000 Study. Journal of psychosomatic research. 2006 Jul 31;61(1):59-66.
  12. Sargent DA, Jensen VW, Petty TA, Raskin H. Preventing physician suicide: The role of family, colleagues, and organized medicine. JAMA. 1977 Jan 10;237(2):143-5.
  13. Yehuda R. Post-traumatic stress disorder. New England journal of medicine. 2002 Jan 10;346(2):108-14.
  14. Lazarus A. Traumatized by practice: PTSD in physicians. The Journal of medical practice management: MPM. 2013 Dec;30(2):131-4.
  15. Wilberforce N, Wilberforce K, Aubrey-Bassler FK. Post-traumatic stress disorder in physicians from an underserviced area. Family practice. 2010 Jun 1;27(3):339-43.
  16. Mills LD, Mills TJ. Symptoms of post-traumatic stress disorder among emergency medicine residents. The Journal of emergency medicine. 2005 Jan 31;28(1):1-4.
  17. Peterson U, Demerouti E, Bergström G, Samuelsson M, Åsberg M, Nygren Å. Burnout and physical and mental health among Swedish healthcare workers. Journal of advanced nursing. 2008 Apr 1;62(1):84-95.
  18. Lemaire JB, Wallace JE, Dinsmore K, Lewin AM, Ghali WA, Roberts D. Physician nutrition and cognition during work hours: effect of a nutrition based intervention. BMC health services research. 2010 Aug 17;10(1):241.
  19. Toker S, Shirom A, Shapira I, Berliner S, Melamed S. The association between burnout, depression, anxiety, and inflammation biomarkers: C-reactive protein and fibrinogen in men and women. Journal of occupational health psychology. 2005 Oct;10(4):344.
  20. Hillman CH, Erickson KI, Kramer AF. Be smart, exercise your heart: exercise effects on brain and cognition. Nature reviews neuroscience. 2008 Jan 1;9(1):58-65.
  21. Black PH. The inflammatory response is an integral part of the stress response: Implications for atherosclerosis, insulin resistance, type II diabetes and metabolic syndrome X. Brain, behavior, and immunity. 2003 Oct 31;17(5):350-64.
  22. Shanafelt TD, West C, Zhao X, Novotny P, Kolars J, Habermann T, Sloan J. Relationship between increased personal well‐being and enhanced empathy among internal medicine residents. Journal of General Internal Medicine. 2005 Jul 1;20(7):559-64.

Contrast-Induced Nephropathy: Confounding Causation

Author: Richard Sinert, DO (Professor of Emergency Medicine / Vice Chair of Research, SUNY Downstate Medical Center) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital) and Brit Long, MD (@long_brit)

I would like to applaud the study “Risk of Acute Kidney Injury After Intravenous Contrast Media Administration” by Hinson et al[1] in the February 2017 issue of Annals of Emergency Medicine.  Before discussing the details of this study, I would like to give a historical perspective on how the study of CIN has evolved.

Since the first observation by Bartels et al[2] of the association between between contrast administration and Acute Kidney Injury (AKI), multiple studies gave further added weight to the association between intravenous contrast and AKI[3-7].

Although CIN is defined by a relatively small change in serum creatinine (SCr) (25% from baseline or an absolute increase of 0.5 mg/dl 48-72 hours post infusion), the consequences for CIN patients at least on the surface seemed dire.  Among cardiac catheterization patients, CIN increased the mortality rates[3] from 6% to 16% in one study[7] and from 0.6% to 31% in another[6].  Higher composite mortality rates and need for renal replacement (relative risk = 36) were also observed in patients who met the definition for CIN following CT-PA, after intravenous contrast in pulmonary embolism patients who developed CIN[4].

At this point an iatrogenic injury (CIN) was linked to an easily measured disease marker (timed changes in SCr) that seemed to be associated with adverse outcomes.  Not surprisingly, the medical community with the best of intentions studied the risks[5],[6] and a wide-range[7],[8],[9] of potential measures to prevent CIN.

Yet all these studies documenting CIN incidence, risks, outcomes, and prophylactic strategies suffer a bias common to many observational studies— confounding bias[10],[11].   Confounding bias occurs when an exposure is inappropriately causally linked to an outcome, when a separate exposure (confounding variable) other than the one of interest better explains the observed outcome.  Since the definition of CIN requires a second timed measurement of SCr, these studies must select for a relatively ill group of hospitalized patients undergoing repeated laboratory testing; selection bias must be considered.  Decrements in kidney function signaled by a rise of SCr could have occurred from the incident disease before or after contrast administration.  In addition, intercurrent hemodynamic instability (eg., sepsis, hemorrhage, diuresis) and a multitude of nephrotoxins (eg., NSAID’s, ACE-Inhibitors, antibiotics) are common complications during hospitalization, which may also explain an increased SCr and associated higher mortality rates.  Newhouse et al[12] found that among 32,161 hospitalized patients not exposed to contrast, 19% of patients had a 25% increase in SCr, which would have fulfilled diagnostic criteria for CIN had they been exposed to IV contrast.

Lipsitch et al[13] stated that non-causal associations between outcomes and exposures are the result of either mismeasurement (recall bias), confounding bias, or selection bias.  To prevent confounding, Lipsitch et al[13] suggests designing a negative control experiment where the observation is repeated under conditions that are not expected to produce the outcome of interest.  If the outcome is encountered without the exposure, then a confounding bias may exist. This form of negative control experiment in which the incidence of AKI is compared across patients exposed and unexposed to contrast has been studied by multiple investigators[14], [15], [16], [17] , all failed to find a statistically significant difference in AKI rate (using CIN definition) between those exposed to contrast and controls.

These studies[18-21] that compared the incidence of CIN between contrast- exposed and unexposed groups also posed methodological issues related to the differences in the baseline risks of AKI between the two study groups.  It is not surprising that the patients hospitalized after requiring a contrast-enhanced CT may be inherently different that those not requiring a similar study.  To account for this potential selection bias, multiple studies have compared the incidence of AKI between contrast exposed and unexposed patients utilized propensity-scoring matching.  Propensity-score matching is a methodology that balances the baseline outcome risks between the study groups[18].  Even utilizing propensity-score matching for AKI, multiple studies[19], [20], [21], [22], [23] again failed to find a statistically higher incidence of AKI in the contrast- exposed compared to unexposed group of hospitalized patients.  In addition, the increases in risks of higher mortality rate in the CIN patients were not found when propensity-scoring matching accounted for the baseline risk of mortality of the contrast-exposed and non-contrast exposed patients.

The most recent CIN study by Hinson et al[1] in this recent issue of Annals of Emergency Medicine represents the latest in the line of investigations into the causal relationship between contrast and AKI.  Hinson et al[1] conducted a retrospective study over a 5-year period comparing the incidence of AKI among three groups, including contrast-enhanced CT (n=7,201), non-contrast enhanced CT (n=5,499), and those in whom CT was not performed (n=5,234).  These three groups were propensity-scoring matched for AKI risks.  AKI was defined both using the common CIN definition and definitions of AKI as reported in the Acute Kidney Injury Network/Kidney Disease Improving Global Outcomes (KDIGO) guidelines[24].   Applying the traditional definition of CIN, AKI was found in 10.6%, 10.2%, and 10.9% in contrast-enhanced CT, non-contrast CT, and non-CT groups, respectively.  Utilizing the KDIGO AKI definitions, AKI occurred in 6.7%, 8.9%, and 8.1% in contrast-enhanced CT, non-contrast CT, and non-CT groups, respectively.

Compared to previous propensity-scoring matched studies mentioned above, Hinson et al[1] went a step further by conducting a multiple logistic regression analysis, including in their model known predictors of AKI and contrast administration. From the multiple logistic regression model, contrast administration produced a non-significant odds-ratio for AKI as defined by both the CIN (0.96 [95% CI, 0.85-1.08]) and KDIGO criteria (1.00 [95% CI, 0.87-1.1.6]).  Moreover, the authors found no differences among the three study groups for the development of chronic kidney disease, need for dialysis, or renal transplantation in the following 6 months post-contrast exposure.

Although patients with elevated SCr (> 4.0 mg/dl) were excluded from their primary analysis, multiple logistic regression analysis of patients with elevated baseline SCr found no independent risk of AKI for contrast administration.

In conclusion, comparing the methodological rigor of more recent CIN studies to those in the past, it seems clear that earlier studies purporting a causal relationship between AKI and contrast administration were only identifying an association but not a true clinical entity. Older CIN studies were biased by confounding variables (e.g., hemodynamic instability, nephrotoxins), with well-established links to AKI providing a sufficient cause for AKI without implicating contrast as an additional AKI risk.

The history of the study of CIN is just another example of evidence-based medicine successfully applied to the debunking of a common belief in a clinical syndrome.  As ED physicians are faced with the challenge of rapidly diagnosing life-threatening conditions (i.e. aortic dissection/aneurysmal rupture, pulmonary embolism, occlusion or aneurysmal rupture of cerebral vessels, traumatic vascular injury), we should not delay emergent contrast-enhanced CT scans waiting for SCr.


References / Further Reading

[1] Hinson JS, Ehmann MR, Fine DM, et al. Risk of Acute Kidney Injury After Intravenous Contrast Media Administration. Ann Emerg Med 2017.

[2] Bartels ED, Brun GC, Gammeltoft A, Gjorup PA. Acute anuria following intravenous pyelography in a patient with myelomatosis. Acta Med Scand 1954;150:297-302.

[3] Pickering JW, Blunt IR, Than MP. Acute Kidney Injury and mortality prognosis in Acute Coronary Syndrome patients: A meta-analysis. Nephrology (Carlton, Vic) 2016.

[4] Mitchell AM, Jones AE, Tumlin JA, Kline JA. Prospective study of the incidence of contrast-induced nephropathy among patients evaluated for pulmonary embolism by contrast-enhanced computed tomography. Acad Emerg Med 2012;19:618-25.

[5] Mehran R, Aymong ED, Nikolsky E, et al. A simple risk score for prediction of contrast-induced nephropathy after percutaneous coronary intervention: development and initial validation. J Am Coll Cardiol 2004;44:1393-9.

[6] Lin KY, Zheng WP, Bei WJ, et al. A novel risk score model for prediction of contrast-induced nephropathy after emergent percutaneous coronary intervention. International journal of cardiology 2017;230:402-12.

[7] Li H, Wang C, Liu C, Li R, Zou M, Cheng G. Efficacy of Short-Term Statin Treatment for the Prevention of Contrast-Induced Acute Kidney Injury in Patients Undergoing Coronary Angiography/Percutaneous Coronary Intervention: A Meta-Analysis of 21 Randomized Controlled Trials. American journal of cardiovascular drugs: drugs, devices, and other interventions 2016;16:201-19.

[8] Wang N, Qian P, Kumar S, Yan TD, Phan K. The effect of N-acetylcysteine on the incidence of contrast-induced kidney injury: A systematic review and trial sequential analysis. International journal of cardiology 2016;209:319-27.

[9] Subramaniam RM, Suarez-Cuervo C, Wilson RF, et al. Effectiveness of Prevention Strategies for Contrast-Induced Nephropathy: A Systematic Review and Meta-analysis. Ann Intern Med 2016;164:406-16.

[10] Grimes DA, Schulz KF. Bias and causal associations in observational research. Lancet 2002;359:248-52.

[11] McNamee R. Confounding and confounders. Occup Environ Med 2003;60:227-34; quiz 164, 234.

[12] Newhouse JH, Kho D, Rao QA, Starren J. Frequency of serum creatinine changes in the absence of iodinated contrast material: implications for studies of contrast nephrotoxicity. AJR Am J Roentgenol 2008;191:376-82.

[13] Lipsitch M, Tchetgen Tchetgen E, Cohen T. Negative controls: a tool for detecting confounding and bias in observational studies. Epidemiology 2010;21:383-8.

[14] Cramer BC, Parfrey PS, Hutchinson TA, et al. Renal function following infusion of radiologic contrast material. A prospective controlled study. Arch Intern Med 1985;145:87-9

[15] Heller CA, Knapp J, Halliday J, O’Connell D, Heller RF. Failure to demonstrate contrast nephrotoxicity. Med J Aust 1991;155:329-32.

[16] Bruce RJ, Djamali A, Shinki K, Michel SJ, Fine JP, Pozniak MA. Background fluctuation of kidney function versus contrast-induced nephrotoxicity. AJR Am J Roentgenol 2009;192:711-8.

[17] Sinert R, Brandler E, Subramanian RA, Miller AC. Does the current definition of contrast-induced acute kidney injury reflect a true clinical entity? Acad Emerg Med 2012;19:1261-7.

[18] Haukoos JS, Lewis RJ. The Propensity Score. JAMA 2015;314:1637-8.

[19] Davenport MS, Khalatbari S, Dillman JR, Cohan RH, Caoili EM, Ellis JH. Contrast material-induced nephrotoxicity and intravenous low-osmolality iodinated contrast material. Radiology 2013;267:94-105.

[20] McDonald RJ, McDonald JS, Carter RE, et al. Intravenous contrast material exposure is not an independent risk factor for dialysis or mortality. Radiology 2014;273:714-25.

[21] Hsieh MS, Chiu CS, How CK, et al. Contrast Medium Exposure During Computed Tomography and Risk of Development of End-Stage Renal Disease in Patients With Chronic Kidney Disease: A Nationwide Population-Based, Propensity Score-Matched, Longitudinal Follow-Up Study. Medicine 2016;95:e3388.

[22] Tremblay LN, Tien H, Hamilton P, et al. Risk and benefit of intravenous contrast in trauma patients with an elevated serum creatinine. J Trauma 2005;59:1162-6; discussion 6-7.

[23] Cely CM, Schein RM, Quartin AA. Risk of contrast induced nephropathy in the critically ill: a prospective, case matched study. Critical care (London, England) 2012;16:R67.

[24] Kidney Disease: Improving Global Outcomes (KDIGO) Acute Kidney Injury Work Group. KDIGO clinical practice guideline for acute kidney injury. Kidney Int Suppl. 2012;2:1-138.

The Pros and Cons of Emergency Medicine as a specialty

Today we host some thoughts on the positives and negatives of practicing Emergency Medicine from Dr. Broders. This post contains pearls on what you should consider in EM. For more, check out this EM Mindset piece by Dr. Broders:

Author: A. Compton Broders, MD, MMM, FACEP (Professor, UT Southwestern) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital) and Brit Long, MD (@long_brit)


  1. Exciting and varied
  2. Time Control
  3. Pay ok
  4. Learning specialty
  5. Worthwhile work
  6. Center of healthcare
  7. Great prep for healthcare leadership


  1. Grossly abnormal time schedule.
  2. Night and holiday work
  3. Sometimes lack of system support
  4. Sometimes chaotic
  5. Frequent difficult patients


  1. No long term patient relationships
  2. No continuity of care
  3. Varied pace of work
  4. All patients cared for without regard to ability to pay
  5. Work with a wide variety of professionals

Historical perspective:

When EM started it was disrespected; not now

Reasons people leave

  1. Night work
  2. Frustration with emergency patients

Personal traits of physicians with a long emergency career

  1. Large sense of humor
  2. Sense of whimsy about human frailties
  3. Tolerance
  4. Some degree of insensitivity to human suffering
  5. Biologic clock in center of day
  6. Intellectual curiosity
  7. Strong outside interests
  8. Good Support systems
  9. Some comfort with work messiness

Thanks for reading! Please post any thoughts you have below.

#EMConf: Live Tweeting?

Author: Vidya Eswaran, MD (EM Resident Physician, Northwestern University Feinberg School of Medicine) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital) and Brit Long, MD (@long_brit)

It’s no secret that the #FOAMed movement is strong on Twitter. Blogs, articles, and opinions are shared on a nearly 24/7 basis. Within minutes, clinical questions can be answered, connections can be made, and knowledge can be shared among physicians from around the world. Increasingly, Twitter use at conferences has also grown. An analysis of tweets sent from an Australian Emergency Medicine Conference from 2011 to 2014 showed a 920% increase in the number of tweets from 460 to 4694, and an increase in number of tweet generators from 54 to 572.[1] This phenomenon is not limited to Emergency Medicine, and specialties such as Family Medicine,[2] Urology, Oncology,[3] and Surgery[4] have all participated in this trend. It has even been posited that “Global twitter conferences could be a cost-effective and low-carbon complement to traditional conferences”.[5]  Beyond tweets from large-scale meetings, residency programs are increasingly tweeting ‘pearls’ from their weekly educational conferences using the hashtag #EMConf.[6] From Dec 28, 2016 to Jan 6, 2017, 277 tweets were sent with the hashtag #EMConf by 145 users, reaching an audience of 135,835. I myself have sent numerous tweets from national conferences as well as from my own residency program’s weekly conference and have found myself asking the questions: Are my tweets serving any purpose, or am I merely adding to the background noise on the Twitter-sphere? Could my tweets serve more harm than good?

The Case for Live-Tweeting

Attending conferences is expensive – the flight, hotel, and food expenses can add up, especially for residents on a limited income. The core behind the entire FOAMed movement is to break down barriers to accessing medical education, and tweeting conferences is another means to this end. By attending conferences-by-proxy via Twitter, physicians can learn what is on the forefront of clinical innovation as well as review the fundamentals. This makes us better physicians, and thereby can improve the care we give our patients – our ultimate goal.

One thing I’ve learned in my, albeit short, time as an EM physician, is that practice variation abounds – regionally, hospital-wide, and even amongst providers in the same department. By sharing information from conferences we encourage engagement and discourse from physicians around the world. From this there is the possibility to learn how different physicians practice, and with careful consideration, physicians could apply a new practice pattern to their patient care through further education on the topic.

One might question the percentage of conference tweets which actually hold educational value. One study, at least, seems to show the majority does. The authors analyzed data from 2014 European Public Health Conference held in Glasgow. 1066 tweets were retrieved, of which 60% had session-related content while social/logistic-related tweets were only 16%.[7]

While providing free access to educational content to emergency physicians is a very benevolent task, I would be remiss to say that live-tweeting a conference is without any personal benefit. The conference attendee who sends out tweets has the potential to expand his or her personal network on social media. For some an increase in the number of followers is in itself an achievement, and as the case with networking of any kind, can lead to increased opportunities in the future. Benefits also exist for the speaker whose lecture is being tweeted. Live-tweets of your presentation can serve as free publicity of your research or of your presentation skills and could lead to opportunities to speak at other institutions or conferences. Finally, conferences themselves benefit from live-tweeting of their events. By raising awareness of their conference, Twitter serves as a free source of advertising and branding, and might encourage those not in attendance to register in the future. Additionally residency programs which tweet their conferences may find their tweets to be a source of advertising to residency applicants.

The Case against Live-Tweeting

A common criticism of FOAMed in general is that the content published is not as rigorously assessed for accuracy as more traditional sources of education. FOAMed proponents have responded by emphasizing that peer-review does in fact occur both prior-to and after publication of FOAMed pieces. Live-tweeting magnifies this issue. Tweets are often sent rapidly, as the tweet writer sits in the conference – opening potential for mistakes not only from the conference speaker but from the transcriber as well. One study analyzed tweets sent from an emergency medicine conference where speakers were asked to assess the level to which tweets from their talk accurately represented what they intended to convey. The investigators found that speakers believed that 43.2% tweets represented, 43.2% partly represented, and 8.1% misrepresented what they intended to convey.[8] While likely a genuine mistake on the part of the tweet generator, the implications could be grave if wrong information were applied in a clinical situation. Along these lines, it is possible that comments made by the speaker may be taken out of context leading to sensationalization and misrepresentation, which can be harmful not only in terms of the veracity of the tweet but may have negative repercussions for the speaker him/herself.

FOAMed is often criticized because its content is not broad. One study found that topics such as airway techniques, ECG interpretation, resuscitation, ultrasonography, and analysis of literature were overrepresented while cutaneous, hematologic, obstetric and gynecologic, and non-traumatic musculoskeletal disorders were rarely covered.[9] A similar case could be made for tweets from conferences. Just as we will never know if an unattended tree in the forest makes a noise as it hits the ground, we cannot glean information from a talk at which nobody tweets. A larger number of tweet generators may attend talks at conferences about popular or exciting topics, and other, perhaps more mundane, but equally important topics may not be broadcasted.

We can all remember a lecture in which we have found our minds wandering, or had the experience of being in a thoroughly engaging presentation, only to forget what was taught the next day. Those who tweet during conferences have two tasks: they must both pay attention to the content being delivered as well as expend mental energy to summarize important points into 140 character ‘pearls’. It seems inevitable that some content will be missed in the process. Not only is the tweet generator missing out on educational content, but their Twitter followers are also not gleaning the entirety of the presentation. Of all the critiques regarding live-tweeting, I think this to the most dangerous and in need of the most investigation. The primary goal for any learner, whether it be in a residency program setting or at a national conference, is to fill his or her own personal educational needs. Only then can one focus on spreading that knowledge to others. If live-tweeting prevents active engagement in the course, then it can be argued that the ‘risks’ of tweeting outweigh the benefits. On the other hand, others may find tweeting to be in line with their personal learning style by encouraging them to listen, synthesize, and summarize the main points of a lecture in real-time. Additionally, the act of typing may in itself serve as further ‘active learning’ to cement key topics.

To Tweet or Not to Tweet?

There are many questions yet to be answered – can learning from tweets be quantified, is there a way to ensure the greatest degree of accuracy in live-tweets, can we ensure that learners aren’t distracted from lecture content while tweeting? At this point in time I think I will continue to live-tweet. I enjoy being a part of the FOAMed community both as a generator of tweets as well as an enthusiastic reader of others’. As I ride the bus into shifts on Thursday mornings I find myself skimming through tweets from residency programs around the country, saving the ones I find interesting for further investigation. As with most things on the internet, however, I approach everything I read with a healthy dose of skepticism. It is on me to trust, but verify, what others tweet before implementing it into my clinical practice.

To those of you considering live-tweeting your next conference, I encourage you to pay close attention to how tweeting affects your learning. If you feel it is a distraction, perhaps take notes during the lecture and then tweet afterwards, when you have more time summarize and synthesize the material. If you wonder about the veracity of a statement or if you are unclear about whether you are representing the speaker’s point, perhaps wait to send the tweet until you can confirm your doubts with the speaker him/herself.

Will Twitter completely obviate the need to attend conferences? I doubt it. There are many benefits, both tangible and intangible to being physically present: from engaging in discourse, to asking the speaker questions directly, networking with other conference participants and having fun with friends, new and old, in different locales.  But for those who cannot attend, with a bit of caution, Twitter can offer an invaluable avenue to be a part of the clinical dialogue.

For more on Twitter use at conferences, see these great sites:

References/Further Reading:

[1] Udovicich C, Barberi A, Perera K. Tweeting the meeting: A comparative analysis of an Australian emergency medicine conference over four years. J Emerg Trauma Shock 2016;9:28-31.

[2] Mishori R, Levy B, Donvan B. Twitter use at a family medicine conference: analyzing #STFM13. Fam Med. 2014 Sep;46(8):608-14.

[3] Wilkinson S, Bastro M, Perovic G, Lawrentschuk N, Murphy D. The social media revolution is changing the conference experience: analytics and trends from eight international meetings. BJU International 2015: 115(5):839-846.

[4] Logghe H, Maa J, Schwartz J. Twitter usage at Clinical Congress rises markedly over two years. Bull Am Coll Surg. 2013 Feb;98(2):22-4.

[5] S Avery Gromm, S Hammer, G Humphries. The age of the Twitter conference. Science 2016: 352(6292): 1404.

[6] MR Haas et al. #EMConf: utilizing Twitter to increase dissemination of conference content. Medical Education 2016; 50: 564-591.

[7]  Bert F, Paget DZ, Scaioli G. A social way to experience a scientific event: Twitter use at the 7th European Public Health Conference. Scandinavian Journal of Public Health, 2016; 44: 130–133

[8] Roland D, May N, Body R, et al. Emerg Med J 2015;32:412–413.

[9] Stuntz R, Clontz R. An Evaluation of Emergency Medicine Core Content Covered by Free Open Access Medical Education Resources. Ann Emerg Med. 2016 May;67(5):649-653.e2. doi: 10.1016/j.annemergmed.2015.12.020. Epub 2016 Feb 11.

The Road to Academic Emergency Medicine

Authors: Brit Long, MD (@long_brit, EM Attending Physician at SAUSHEC), Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital), and Jennifer Robertson, MD, MSEd (Assistant Professor, Emory University, Atlanta GA)

Emergency physicians train to be highly proficient in the resuscitation and management of acutely ill patients.  In addition, all emergency medicine (EM) training programs focus on preparing physicians to care for these patients in community practice settings. While most EM graduates go on to practice in community settings, academic EM is an option for interested physicians.

In general, academic EM was established to provide the teaching, research, and leadership goals of the specialty. For current residents and community doctors, specific pathways for practicing academic EM are now available, which allow new graduates to directly enter academic EM from residency or transition from community to academic EM.

The decision to practice academic or community practice can be a difficult one to make, as there are perks and drawbacks in both settings. This post will evaluate the road to academic emergency medicine, the positives and negatives, and provide tips for success. However, before we start, we need to understand the difference between academic and community EM.

What is academic emergency medicine?

An academic emergency medicine practice is defined by its providers spending the majority of their time in resident education/supervision, along with scholarly activity (academic writing, teaching, or research).1-5 This focus came into existence in order to meet the teaching, research, administrative, and educational aspects of emergency medicine. The majority of academic providers are associated with a teaching hospital, and many have time protected for academic pursuits. Over 40% of current residents are interested in pursuing an academic career, but the road to determining whether an academic or community practice is right for you can be difficult.1

Unfortunately, many graduating residents feel ill prepared to begin a career in academics, and program directors agree. A survey of EM residency directors found that only 29% feel their program graduates are prepared for an academic career involving original research.2 Obstacles include insufficient research training and resident difficulty in finding knowledgeable collaborators and mentors.

What is community practice?

Community EM refers to practices based mostly on clinical medicine. In community EM, providers spend the majority of their time on clinical duties (usually shifts), rather than supervising and educating residents. Providers may have other obligations such as administrative tasks, but their primary focus is direct patient care. However, the actual amount of patient care duties will vary within individual departments, hospitals, and even parts of the country. Pay is often based on the number of shifts and relative value units (RVUs) per shift. However, overall pay can be also be affected by partnerships, bonuses based on productivity, patient satisfaction, and quality measures.

 Why academic EM?

Academic medicine seeks to pursue scholarship, expand knowledge, and pass on that knowledge. This is most commonly done through resident education and supervision. Education and scholarly activity are ultimately the goals, though these can take several forms. Academics provides career diversity, expertise development, formation of educational philosophy and techniques, specialty advancement, networking and formation of relationships, and research development. It can allow physicians to influence hospital and institution practices, and provide a bit of control in his or her schedule. Best of all, academic EM gives physicians the chance to affect and improve the care of many patients through resident education and scholarly activity.

There are several negative factors associated with academic EM. You will likely work more hours combined, make less money, work fewer clinical hours, and experience more pressure to be scholarly productive (we will cover this later), as compared to community practice.

We know the decision is difficult.

Residency rotations in both settings can provide glimpses of both types of practice. Hybrid programs are also in existence, and it is never too late to switch from one to the other.

In the meantime, how should a resident prepare for academic EM? Residency is the time to obtain several important skills.

1) The first is the most fundamental and important: clinical competency. Excellence in patient care is fine-tuned during residency. Every patient encounter, lecture, and time spent studying should focus on learning and enhancing clinical evaluation and management.

2) The next skill is teaching and knowledge dissemination. This is primarily learned via supervising junior residents or medical students at the bedside or by mentorship. In addition, lecture-based learning and teaching are also paramount.

3) Research skills are essential, no matter what environment you will practice in. Experience in reviewing the literature, establishing research questions and study designs, data collection/analysis, and presentation of data is important.  This can be difficult to obtain through journal clubs only, and some form of higher education is often beneficial for developing key research skills.

4) Expressing ideas and disseminating your knowledge are important, not only for abstracts, papers, and grants, but for hospital protocols and committees.

5) Administrative skills are helpful for both community and academic settings.

6) As most physicians (especially in EM) know, “people” skills are essential, not only to your clinical practice but also in forming long-lasting relationships and collaborations. Whether you go into academic or community EM, these skills are critical.

7) Finally, developing a personal learning strategy is important for continued clinical development.

Ok, so academic EM sounds like your thing… Now what?

There are several aspects of career planning that will help you find the best fit and succeed in academic EM. Each of the following components summarize key information for not only academic survival, but also for long term success.

Preparing for Academics

  1. The importance of a mentor – Mentorship is a key component of a healthy career. Forming a healthy mentoring relationship leads to academic success and career satisfaction, especially when formal postgraduate training is not completed.15-19 Look for mentors within the department, your institution, other institutions, prior training places, and from regional/national meetings. Mentors assist in setting and achieving goals, providing feedback on performance, building confidence and moral support, helping you get involved in committee work, introducing mentees to leaders in your field, protecting you and your interests, and keeping you on track. Your mentor is your advocate.   When choosing a mentor, there are several considerations. These include ensuring the mentor has a track record in the area of your interest, has available time and interest, possesses a personality that fits, and does not possess conflicts of interest. More than one mentor can be helpful, and mentors outside of EM can provide a different viewpoint for you.
  1. Setting time goals: 1, 3, 5, 10 years – Short and long term goals are necessary for a successful career, as a resident and faculty member. You have probably been setting goals all of your life, and just like before, it is important to possess concrete and obtainable goals. A career plan should be established, with each year broken down into separate goals that work toward achieving the long term goal. Keep in mind these may need to be revised, and these goals should be used as a guide for feedback/evaluation sessions. These goals should be discussed with your mentor, with regular meetings and feedback sessions to keep you on track.
  1. Finding your niche – Even though EM is a broad specialty, the majority of academic leaders are known for expertise in one or several areas of knowledge. This is essential for those forming a career: determine what interests or excites you and what opportunities are available to focus on these interests. Ask yourself what your passion is and what excites you. Another key is to consider what you do not enjoy. When you recognize what you like and dislike, then seek to get involved in your area of interest, with a goal of academic productivity (through research, lectures, or publishing). Research projects should also focus on this. Because of EM’s broad spectrum, some may want to target what’s currently available at their institution. Others may take too much on, spreading themselves too thin. It can be difficult to focus on one or two areas, but do your best to choose what interests you the most.
  1. Keep an academic portfolio and curriculum vitae – As most know, a curriculum vitae (CV) is a necessity. Even though different formats may be used, all contain the same information. Your mentor and senior department leadership can provide valuable assistance in forming and fine-tuning your CV. A personal academic profile or portfolio should also be maintained, as this summarizes your teaching, compiles your awards and evaluations, and should also contain examples of lectures and other academic achievements. Both are vital for academic success and promotion.
  1. Join an EM organization – Several emergency medicine societies are available, and each can provide significant benefits. Organizations include AAEM, ACEP, SAEM, CORD, NAEMSP, and several others. These organizations provide valuable networking and socializing opportunities for residents and faculty of all levels. Many of these organizations also have committees, which provide opportunities to improve nonclinical educational skills, form relationships with physicians with similar interests, and contribute to EM. If you can, attend meetings that allow open attendance. You will gain valuable skills in learning how to manage meetings and conferences by watching those in charge.
  1. Networking – There are several aspects to networking. Joining a committee or task force can be helpful and provide links to other departments and senior leaders. Speaking with everyone in the department, from interns to department chair, can form relationships that last. Everyone in EM has lessons learned or advice they can offer. Ask senior department members for connections or to introduce you to other leaders.
  1. Remember your colleagues and provide assistance to others – An academic physician with goals will develop and advance. As you begin to grow in your career, seek to help and mentor others. You obtained your success with the assistance of others, including your mentor and family, and you need to extend this same courtesy to others around you. Involve others in your projects and educational goals. By seeking the advancement of other EM colleagues, you form friendships and long-lasting relationships. If you switched programs, remember those back home and acknowledge them in your success.

What about postgraduate training?

Postgraduate training can help through providing focus on future work, as well as training in teaching, writing, research, and funding. Unfortunately, medical school and residency often do not prepare physicians for an academic career. Though not mandatory for an academic position, postgraduate training can facilitate academic training, enhance career satisfaction, and increase chances of academic success. This training also assists mentoring relationships and collaborative relationships. Dedicated postgraduate training may be the only means of obtaining truly protected time to develop academic skills. Interestingly, fellowship or postgraduate-trained physicians are more likely to obtain success and career satisfaction if involved in an academic program. This training provides increased job mastery, leading to less stress, greater certainty, and improved vision of career goals. Fellowships include pediatric EM, toxicology, undersea and hyperbaric medicine, sports medicine, ultrasound, palliative care, EMS, critical care, and several others. However, further training does delay maximum salary potential.

If you are considering a fellowship, look at each program’s expected clinical time, training value, access to mentors, research opportunities, and total experience. The vast majority of EM fellowship programs offer complete, valuable experiences. If interested in education, fellowship training necessity is less defined. This fellowship is growing, but many departments offer formal, structured, multiyear educational training opportunities. For more information on fellowships, please see EMRA’s complete guide at:

The nuts and bolts for success in academic EM

What roles are there? Academic EM is comprised of many positions, and each institution and program will vary. Research roles include director, clinical trial director, research advisor, and research assistants’ program director. Educational roles can be residency director, associate residency director, medical student director, medical school leadership (dean), rotating resident director, fellowship director, CME director, hospital committee director, and others. There are also specialty roles such as ultrasound, hyperbaric chamber, chest pain, etc. Administrative roles include chief/chair, EMS director, operations director, pediatric ED director, CQI/Risk management director, and others.

Finding the right program – A program that will provide the environment and tools to help you flourish is important. First, characterize the institution, and evaluate what the program rewards (publications, lectures, clinical throughput). Are you just another cog in a vast machine? What would happen if you leave the program? You should ensure true opportunities to advance clinically and professionally exist in the program. Ultimately, look at what the institution and the program can do for you, rather than what you can do for the institution/program.  

Several program types or models possess different attributes. The egalitarian model treats everyone the same, regardless of specific talents or interests. Faculty work similar numbers of shifts, teach a similar number of lectures, carry similar administrate duties, and are expected to have similar productivity. The specialization model demonstrates a more team-based approach. All faculty work clinically, but the department can modify career development to better match faculty member strengths, weaknesses, interests, and dislikes. Shift numbers can vary based on faculty member roles and productivity.

Promotion and tenure – There are progressive ranks with timelines for academic physicians including assistant professor, associate professor, and full professor. Many are based on specific criteria such as publications, grants, regional/national recognition, teaching portfolios, and clinical productivity. An area of focus or niche can be helpful. This should be discussed with your department/program leadership and mentor. A mark of a strong program is a definitive track for career advancement, so you must inquire about this component of the academic program. Many offer workshops or provide further faculty development, which can significantly improve your advancement.

Research – Research is one of the fundamental means of growth for EM. The research environment physicians experience during residency often shapes future interest in research.1,4  At its core, research involves formulating a question, addressing the question with appropriate study design, collection and interpretation of data, and presenting the results in a peer-reviewed journal. This is often a long process, requiring time, effort, and mentorship for residents. Faculty have several goals when it comes to research: conducting research themselves, educating residents on scientific study, and/or how to conduct a study.

A large number of relevant areas of study are in existence. The majority of academic centers will desire their physicians to be “academically productive,” or obtain clinically relevant publications or grants. Research topics can be clinical, basic science, education, policy, or clinical operations. Mentorship and senior physician assistance to residents and new faculty seeking a research track are essential. Properly forming a research question and designing a protocol can be challenging, and thus, the more experience you can obtain, the better.

Teaching – Education is one of the key factors in an academic position. All physicians teach, whether the audience is nurses, technicians, or other physicians. One major component of an academic program is working with residents. Most programs expect academic clinicians to teach on shift as well as present lectures at conferences several times per year. This aspect is often one of the most fulfilling aspects of academic medicine, as you have the opportunity to affect the growth of future EM physicians. You may also work with students and off-service residents, and your relationship with these learners can have significant impact on their education, patient care, and relationships with the emergency department in their future careers.

Residency provides valuable time for honing educational skills. Some programs have dedicated programs for teaching, while others expect those interested in teaching to pick up the skills on their own. Focusing on shift teaching, presentation skills, and creation of lectures are great places to start for residents and new faculty. In emergency medicine, it can be difficult to work on your teaching skills, as there are so many options for teaching and so many different learners. Many adult learners seek information that will directly and positively impact their future careers. Thus, it is important to focus on how individuals learn and how you can make a difference in their learning experiences.

Teaching involves the ability to observe, question, and review trainee performance in actual patient care settings. When developing your own education techniques, look at the educators around you. New faculty and senior residents should pay close attention to those teachers who demonstrate master education skills. At the same time, strongly consider providers who are working on their own deficiencies. You should seek to recognize and understand these deficiencies so you can avoid them. Recognizing these skills and one’s own shortcomings will allow you to grow as an educator.

Scholarly Activity – One major aspect of an academic career is scholarly activity. In the past this included writing, either book chapters, original research, or review articles. The majority of academic programs still rely on clinical research and formal publication in medical journals. The academic environment is evolving, with several other opportunities. Free Open Access Medical Education (FOAMed) is one of these, with a growth of blogs and podcasts. Many academic physicians have now based their career on this avenue. Other options include ACEP’s Critical Decisions in Emergency Medicine, case reports, images, and specialty organization newsletters. Most programs will ask for at least one lecture per academic year, often grand rounds. However, speaking at regional, national, or international meetings is another means of scholarly productivity.

Once you have a project, seek to present the results in multiple settings and formats. Start with presenting an abstract at a conference, then seek publishing in a peer-reviewed journal. A FOAMed blog publication is also an option. Presenting this further at other functions, such as a grand rounds lecture, offers another avenue.  Publication in this format develops writing skills, develops an area of expertise, and advances your career. Remember, most programs still focus productivity on peer-reviewed publications.

The Literature – Residency programs usually promote some form of literature understanding through several formats: journal clubs, evidence-based medicine projects, and education on clinical shifts. Faculty may lead discussions or projects for literature awareness, aimed at promoting a deeper understanding of EM studies. For faculty, a key component of academics is staying abreast of the current literature, as well as “classic” studies. This can be difficult with all of your other duties and clinical shifts, but this is vital to your own education. There are multiple means of remaining current, from subscriptions to journals (Annals of EM, American Journal of EM, Journal of EM, etc.), podcasts (EM:RAP, EMA, EMCrit), and blogs (ALiEM, emDocs, Core EM, EM Updates, REBEL EM). FOAMed has revolutionized medical learning, and residents and faculty can use FOAMed to remain abreast of new, exciting medical updates.

Goals and Persistence – Specific goals with a timeline are a necessity for success in academic medicine, and they must be written down to solidify their importance. The act of setting the goal with timeline, verbalizing it, and writing it creates a commitment. Remember, academic medicine can be and will be difficult. There will be setbacks, but do not be discouraged. You will have papers and grants rejected. Make changes and keep going.

Collaboration – Finding others interested in your niche or topic can benefit. With our schedules, it can be difficult to frequently meet with your mentor to discuss areas of interest. This is where collaboration can help. Team members can provide skills and perspectives that will improve the quality of projects. Just make sure you set specific goals for the project, with a timeline.

Other Specifics – Determine what percentage of your work week should be clinical and what should be given to the rest of your academic pursuits. You should consider what you want to be doing in 5-10 years. Where do you see yourself? Saying “no” is ok if you have too much on your plate.

I think I know how to succeed, but what can I mess up?

There are many pitfalls in academics. These include not enough protection from other duties (working too many clinical shifts with the expectation for academic productivity), not enough training for an academic career (research focus without training on research question and protocol formation), failure to have a mentor (one of the cornerstones of academic success), failure to form a plan/timeline of goals, lack of balance (which leads to burnout), biting off too much, and not listening to feedback.

Importance of Balance – Maintain balance and block off time for your family and hobbies. Success takes time, and it will not occur overnight. Recent years have seen an emphasis on physician health. This really comes down to balancing many aspects of life including your shifts, academics, community activities, exercise, hobbies, family, religious/spiritual concerns, friends, and future plans. Pushing too hard and too fast with too much will lead to burnout.

The Decision – Residency is a great time to explore academics and community practice. Rotations in both settings can help you determine which practice is the best fit for you. You can always switch settings, or in other words, it is never too late to go from community to academic practice. Work on perfecting your clinical skills and management early, as this is essential to both academic and community medicine.

Thanks for reading. For more, please see the resident section of the CORD website at

Please comment below with other tips or questions!

References/Further Reading

  1. Stern SA, Kim HM, Neacy K, Dronen SC, Mertz M. The impact of environmental factors on emergency medicine resident career choice. Acad Emerg Med. 1999 Apr;6(4):262-70.
  2. Neacy K, Stern SA, Kim HM, Dronen SC. Resident perception of academic skills training and impact on academic career choice. Acad Emerg Med. 2000; 7:1408–15.
  3. Aycock RD, Weizberg M, Hahn B, Weiserbs KF, Ardolic B. A survey of academic emergency medicine department chairs on hiring new attending physicians. J Emerg Med. 2014 Jul;47(1):92-8.
  4. Sanders AB, Fulginiti JV, Witzke DB, Bangs KA. Characteristics influencing career decisions of academic and nonacademic emergency physicians. Ann Emerg Med. 1994;23:81–7
  5. Clinton JE. Educating academic emergency physicians. Acad Emerg Med. 1999;6:260–1.
  6. Stead LG, Sadosty AT, Decker WW. Academic career development for emergency medicine residents: a road map. Acad Emerg Med 2005 May;12(5):412-16.
  7. Hobgood C, Zink B (eds). Emergency Medicine: An Academic Career Guide, ed 2. Lansing, MI: Society for Academic Emergency Medicine; 2000.
  8. Faculty Development Web site. Available at: facdev/fac_dev_handbook/. Accessed Nov 10, 2016.
  9. Cydulka C. Preparing for a career in academics. Emergency Medicine: An Academic Career Guide. Available at: http:// Accessed Sep 18, 2001.
  10. Hall KN, Wakeman MA. Residency-trained emergency physicians: their demographics, practice evolution and attrition from emergency medicine. J Emerg Med. 1999;17(1):7-15.
  11. Reinhart MA, Munger BS, Rund DA. American Board of Emergency Medicine Longitudinal Study of Emergency Physicians. Ann Emerg Med 1999;33(1):22-32.
  12. Kellerman AL. Are you considering an academic career? EMRA. Available at Accessed 04 November 2016.
  13. Pines JM. The young physician in academic emergency medicine: tips for success. AAEM. Available at Accessed 04 November 2016.
  14. Sokolove P, Stern S, Baren J. An academic career: is it right for you? 2008 SAEM Annual Meeting, May 2008. Available at Accessed 04 November 2016.
  15. Taylor JS. Academic Medicine 2001;76:366-372.
  16. Stack SJ, Watson MJ. Enriching the resident-faculty relationship. Ann Emerg Med. 2001; 38:336–8.
  17. Osborn TM, Waeckerle JF, Perina D, Keyes LE. Mentorship: through the looking glass into our future. Ann Emerg Med. 1999; 34:285–9.
  18. Hazzard WR. Mentoring across the professional lifespan in academic geriatrics. J Am Geriatr Soc. 1999; 47:1466–70.
  19. Peluchette JV, Jeanquart S. Professionals’ use of different mentor sources at various career stages: implications for career success. J Soc Psychol. 2000; 140:549–64.
  20. Holmboe ES, Ward DS, Reznick RK, Katsufrakis PJ, Leslie KM, Patel VL, Ray DD, Nelson EA. Faculty development in assessment: the missing link in competency-based medical education. Acad Med. 2011; 86(4):460-7.

Cervical Collars for C-Spine Trauma: The Facts

Authors: Joshua Bucher, MD (@JBucherMD – EMS Fellow and Attending Physician, Morristown Medical Center) and Joslyn Joseph, DO (@EMDocJos – EM Resident Physician, Morristown Medical Center) // Edited by: Alex Koyfman, MD (@EMHighAK – Editor-in-Chief; EM Attending Physician, UT Southwestern Medical Center / Parkland Memorial Hospital) and Manpreet Singh, MD (@MPrizzleER – Associate Editor-in-Chief; Assistant Professor in Emergency Medicine / Department of Emergency Medicine – Harbor-UCLA Medical Center)

Case: A 42-year-old male comes in complaining of neck pain and difficulty moving his upper extremities after trauma. The patient was involved in a motor vehicle collision where he was in the front passenger seat and was hit from that side. The patient had a loss of consciousness and complains of nausea, headache, vomiting, and trouble with motor function of his arms. He also complains of decreased sensation.

On exam, the patient has decreased sensation of bilateral upper extremities as well as 3 out of 5 strength in his upper extremities. What is the best method to immobilize the patient’s spine?

Introduction: A few months ago we covered an article considering the evidence and myths surrounding the pre-hospital use of the long backboard for spinal immobilization in trauma patients with suspected spinal cord injuries (  This time, we will consider the utility of another device reflexively applied to these patients – the rigid cervical collar.  From the NAEMT to PHTLS and ATLS, c-spine stabilization is considered a major priority after the ABCs.  Pre-hospital EMS protocols dictate that whenever a patient admits to neck pain or any neurological symptoms following trauma, applying a rigid plastic, often ill-fitting, uncomfortable cervical collar is mandatory.   The purpose of these devices is to prevent further motion of the cervical spine by maintaining in-line stabilization that could theoretically worsen a c-spine injury, convert a partially unstable fracture into an unstable fracture or a convert a partial spinal cord injury into a complete spinal cord transection.  This bears us to ask the question – what evidence exists to support the use of these devices?

  1. Can small voluntary spinal movements cause harm?
    • There is a fear that any movement of the cervical spine will cause further injury or worsen already existing spinal fractures or injury; however, there is no evidence that slight movement of the cervical spine will cause worsening injury. Maiman et al performed a study on cadavers involving applying forces to their necks vertically, forward and rearward to attempt to cause ligamentous injury and fracture. The loads required to cause an injury ranged from 645 to 7,439 Newtons of force.1 This study sets precedent that it may not be movement of the spine, but the force from a strong impact that causes injury. Therefore, the fear of movement, such as minimal head turning, flexion and extension of the cervical spine, or movement during airway management causing worsening injury appears to be somewhat unfounded.
  1. Do cervical collars truly immobilize the cervical spine?
    • Again, we can turn to cadaver studies as well as biomechanical analysis of live patients during extrications to answer this question. Horodyski et al tested axes of cervical motion in all planes in lightly embalmed cadavers both with an intact c-spine and induced global instability at C5-C6.  Motion was tested in five cadavers using EMG sensors applied to the C5-C6 vertebral bodies, comparing no collar, to a one-piece extrication collar (Ambu), and two-piece (Aspen) collar in repeated measures.  The results of this study indicated that though significantly more motion occurred in the unstable cadaver c-spine, no significant difference in motion occurred with the application of either cervical collar compared to the no intervention group.  Even more surprising, a similar cadaver study with induced unstable C-spine fractures by Lador et al documented increased intervertebral motion in both the axial and cranial-caudal planes in the one-piece rigid collar group compared to no intervention as well as the creation of a “pivot point” of enhanced motion where the collar contacts the TMJ and shoulder areas (we will mention this later).2 Finally, a study by Dixon et al extricating healthy volunteers from a simulated motor vehicle crash in a RCT comparing conventional equipment and manual aided techniques including the cervical collar showed four times as much motion using equipment as opposed to controlled self-extrication with no collar.3
  1. Does the cervical collar positively affect the neurological outcomes of patients with spinal cord injuries?
    • There are no prospective, randomized patient studies that look at the use of cervical collars versus placebo. Hauswald et al. performed a retrospective cohort study comparing blunt trauma patients in two different systems, the United States (which routinely immobilizes patients) and Malaysia (which does not routinely immobilize patients). They compared patients with and without spinal immobilization and performed multivariate logistic regression analyses. They found that there was less neurologic disability in the unimmobilized patients from Malaysia (OR 2.03, 95% CI 1.03-3.99; p=0.04).4 This supports the possibility that immobilization may actually be harmful.
  1. Can cervical collars cause further harm to the trauma patient?
  • C-collars can potentially increase intracranial pressure. Stone et al. took healthy volunteers and placed them in cervical collars. Their internal jugular vein cross-sectional area was measured before and after cervical collar application, and showed a mean percentage increase of 37% with the collar applied.5 Theoretically, the decreased venous return may increase intracranial pressure, which is something we want to avoid in patients with intracranial injury.
  • The neck pivot-shift phenomenon was demonstrated by Lador et al. in a study performed on cadavers. Intervertebral movements were measured based on CT imaging after application of cervical collars. It was found that “pivot points” shifted the center of rotation lateral to the spine and worsened motion between vertebrae. These points can cause stress on the c-spine due to the use of the collar.
  • The cervical collar can lead to increased intracranial pressure. A prospective study found that CSF pressure increased by approximately 25 mm H20 in a group pre- and post c-collar application in patients undergoing lumbar puncture.6

Based on the available data, it does not appear that cervical collars have any appreciable positive effect on patient care. However, at this point in time, they are the recommended treatment option. Hopefully this knowledge will help your daily practice by understanding the effects of cervical immobilization.

Case Resolution: The patient is carefully placed into a rigid, padded collar and asked not to move his neck in any direction. He undergoes appropriate imaging and management per the trauma and spinal surgery teams.

References / Further Reading

  1. Maiman DJ, Sances A, Jr., Myklebust JB, et al. Compression injuries of the cervical spine: a biomechanical analysis. Neurosurgery. 1983;13(3):254-260.
  2. Lador R, Ben-Galim P, Hipp JA. Motion within the unstable cervical spine during patient maneuvering: the neck pivot-shift phenomenon. The Journal of trauma. 2011;70(1):247-250; discussion 250-241.
  3. Dixon M, O’Halloran J, Cummins NM. Biomechanical analysis of spinal immobilisation during prehospital extrication: a proof of concept study. Emergency medicine journal: EMJ. 2014;31(9):745-749.
  4. Hauswald M, Ong G, Tandberg D, Omar Z. Out-of-hospital spinal immobilization: its effect on neurologic injury. Academic emergency medicine: official journal of the Society for Academic Emergency Medicine. 1998;5(3):214-219.
  5. Stone MB, Tubridy CM, Curran R. The effect of rigid cervical collars on internal jugular vein dimensions. Academic emergency medicine: official journal of the Society for Academic Emergency Medicine. 2010;17(1):100-102.
  6. Kolb JC, Summers RL, Galli RL. Cervical collar-induced changes in intracranial pressure. The American journal of emergency medicine. 1999;17(2):135-137.

Dr. Strangelove or How I Learned to Stop Worrying and Sit on the qSOFA: A pathophysiologic approach to qSOFA

Author: Nikolai Schnittke, MD (@nikolaischnittk, EM Resident Physician, Berbee Walsh Department of Emergency Medicine, University of Wisconsin Hospital and Clinics) // Edited by: Alex Koyfman, MD (@EMHighAK) and Brit Long, MD (@long_brit)


The last few months have seen an enormous amount of controversy in the press, in the FOAMsphere, and in our ED hallways regarding the new consensus sepsis definition1,2. The goal of this post is not to rehash the strengths and weaknesses of Sepsis 3, but rather to explore the pathophysiologic basis of the simplified clinical features of sepsis outlined in the qSOFA score, which might explain why the definition shook out the way it did. Hopefully, such an understanding will help us apply lessons learned from the derivation of Sepsis 3 to the management of these profoundly sick patients.

So what is Sepsis 3? In his “biography of cancer”, The Emperor of all Maladies, Siddhartha Mukherjee writes about how in the mid 1800s Virchow set out to “describe human diseases in simple cellular terms”3. This need for a pathophysiologic, cellular, and molecular explanation of human disease has permeated many of the advances of modern medicine, but has been curiously lacking from our understanding of sepsis. While past definitions sought to define sepsis as a clinical syndrome based on clinical features (SIRS)4, Sepsis 3 seeks to define sepsis as a pathophysiologic entity. This was predicated on research done in the past few decades yielding a considerable, albeit still elementary body of scientific study revealing sepsis to be correlated with a dysregulated metabolic5,6, immunologic7, and microvascular response to infection8, which leads to organ failure. Thus, the authors defined sepsis as “a life-threatening organ dysfunction caused by a dysregulated host response to infection”.

This cerebral definition, while scholarly and useful in our conceptualization of the essence of sepsis, seems to do little to help the clinician recognize and treat sepsis. After over two decades of consensus sepsis definitions most clinicians have grown familiar and comfortable using SIRS. The three sepsis mega-trials: PROCESS9, ARISE10, and PROMISE11 seem to have validated a simplified approach to identification and treatment of sepsis using SIRS criteria. The authors of Sepsis 3 however, argue that SIRS has unsatisfactory sensitivity and specificity (best demonstrated by the Area Under the Receiver Operating Curve or AUROC) when it comes to the identification of a life threatening disease. That point was hammered home with disturbing force by a study in the NEJM in 2015, which used a large EMR database to check the sensitivity of SIRS in detecting downstream organ failure caused by infection, and found that SIRS missed 1 out of 8 patients (12%) with severe sepsis or septic shock12.

Moreover the mortality rate for sepsis remains high despite the significant advances of the last three decades. Indeed, the sepsis mega-trials consistently demonstrated a 90 day mortality in the range of 20-30%, which while significantly better than the 46% baseline mortality rate of Dr. Rivers’ initial EGDT trial13, is a shockingly high mortality for a disease whose prevalence continues to increase14. For comparison, consider that as of 2010, 30-day mortality rate for STEMI by one estimate is down to ~4.4%15. In an attempt to translate Sepsis 3 into a clinically helpful entity, the authors then worked backwards in a statistical tour de force to define the clinical features that might correlate with mortality in sepsis.

This behemoth retrospective derivation from 1.3 million EMR charts and subsequent validation of 700 thousand charts revealed three clinical variables that were strongly correlated with mortality: RR>21, Altered mental status[1], and SBP<100. The AUROC for situations where two of these variables were present was comparable to or better than that of SIRS in both ICU and non-ICU settings2. Thus, Sepsis 3 provides not only a pathophysiologic definition of sepsis, but also the first evidence based description of its clinical features, which are predictive of mortality. The goal of this post is to explore how these two realms fit. In other words, why are these three clinical changes so predictive of mortality secondary to organ dysfunction caused by a dysregulated host response to infection?

 1. Altered mental status

Consider the following case seen recently at Janus General:

An 89 year old man is brought to the ED unresponsive to painful stimuli. His VS are: HR 72, BP 112/54, RR 24, SpO2 96% on 2L NC, FSBG 112. This is his third visit to the ED in three days. During each of these visits, neighbors called EMS, because the patient was found on the floor of his trailer. During the last two visits, he would have his eyes closed, moan occasionally, and would not respond to painful stimuli. After about 30-60 minutes he would wake up, curse out the staff, and demand to be discharged home. Because his labs, CXR, and CT head were all within normal limits, he was discharged home.

This visit is not different from the past two days, except you note that he seems to moan a bit more when your press on his abdomen, but is otherwise unresponsive to sternal rub or nasal trumpet. The patient has a history of dementia, and review of recent admissions indicate that he has a habit of becoming belligerent when admitted, cursing at staff and driving several nurses to tears with insensitive and aggressive comments.


Altered mental status has long been recognized as a feature of sepsis where it has gone by other monikers such as Sepsis Associated Encephalopathy and Sepsis Associated Delirium18. The concept of “delirium” may be particularly useful in understanding this phenomenon and our relationship to it in the ED.

The DSM-5 defines delirium as an acute change in consciousness not explained by a previous neurocognitive disorder, and thought to be due to a medical or toxicologic condition19.  As sepsis is a medical condition, the alterations in mentation, which often accompany it can be classified as a subset of a broader delirium syndrome.

The pathophysiology of the delirium syndrome is complex and involves neurotransmitter balances (the cholinergic and dopaminergic axes are strongly implicated), underlying dementia (as with any organ failure, the chronic brain failure of dementia is a strong risk factor for developing acute exacerbations of delirium), vasculopathic changes, and inflammatory changes20.  The latter two are very strongly implicated in sepsis associated delirium, and are the same pathophysiologic changes that cause inflammatory and microangiopathic organ dysfunction during sepsis21.  Thus, sepsis associated delirium is a powerful indicator of life-threatening organ dysfunction. While other organs require labwork (creatinine, troponin, liver enzymes) to evaluate for damage, the CNS is the one organ whose function is assessed at the bedside.

This seems like a no-brainer: infection is always at the top of our differential when it comes to altered mental status. However, it turns out that EPs are notoriously poor at picking up delirium when “altered mental status” is not listed as the chief complaint. Several studies place us at around 30% sensitivity in the recognition of delirium and many of these patients are discharged home with no specific plan with regard to their mental status22,23.  This, despite findings that delirium in the ED is likely an independent risk factor for mortality24. Why is it so difficult to recognize a clinical feature, which requires no additional invasive tests and has such a high predictive value for morbidity and mortality? Of course many of these patients are elderly, with dementia at baseline, and it is difficult to establish how truly different from baseline they are at the time of our evaluation. There are few things as frustrating as being on hold with a nursing home while a nurse who knows the patient’s baseline can be found. Moreover subtle changes in attention can require a full assessment such as a Confusion Assessment Method (CAM), which takes several minutes. And yet, this is perhaps the most powerful clinical lesson we can glean from the sepsis 3 derivation:

We cannot afford to miss altered mentation: a clinical state of organ dysfunction that can be assessed at the bedside.

Identifying mental status aberrations is often as simple as paying attention to this part of the clinical exam. In cases where we are not sure if a patient is altered, the following steps might be helpful in assessing altered mentation in the busy ED setting:

I) Obtain the patient’s baseline. It’s impossible to know if the patient is altered without knowing where the patient usually is. This often means contacting family and/or nursing home staff. If you do not have time on a busy shift to be on hold with the nursing home, it’s ok to delegate this step to a nurse or a tech. Do not rely on hospital admission records to establish the patient’s baseline: many of these patients are not at baseline when in the hospital.

II) Use a cognitive forcing strategy. Too often we see documented exams of intubated patients who are “AOx3”. Force yourself to think of the diagnosis of delirium by documenting the mental status appropriately in the exam. If the patient is AOx3, that’s ok, but if you didn’t ask them to tell you the date, don’t write AOx3.

III) Screening test. Han et al designed a Delirium Triage Screen (DTS) outlined in Figure 125 . This screen can be done in about 20 seconds and when compared to a 30 min psychiatrist evaluation, the sensitivity of the DTS was 98%. This quick screen performs just as well, regardless of whether it is done by a physician or a non-MD research assistant.

Screen Shot 2016-07-04 at 11.55.20 AMIV) Confirmation test. While the DTS is very sensitive, it is only ~55%  specific. In order to confirm delirium use a modified brief Confusion Assessment Method (bCAM), which has a specificity ~96% (Figure 2). This method is a bit more involved, but still takes about 1-2 minutes. Again if you don’t have time, ask the nurse/tech/med student.

Screen Shot 2016-07-04 at 11.54.59 AM

 Remember, these two tests are aids to help guide your clinical assessment. You don’t need to do this with every nursing home resident, but if you’re on the fence, it may well be worth the 2 minutes to validate your concerns. On the other hand, you might be surprised: a nursing home resident who hasn’t had to go to a meeting in twenty years might not know the date, but can still be sharp as a tack.

2. Tachypnea

This is the only carryover from SIRS, and yet it continues to get almost no clinical respect in the ED setting. Pathophysiologically, tachypnea is a respiratory regulatory response to increased metabolic stress and primary metabolic acidosis. The metabolic profile of septic patients is rather complex as it seems to be characterized by both an increased level of cellular respiration as well as mitochondrial dysfunction 26,27. The net balance of these two opposing forces appears to be an increase in the overall energy expenditure through both aerobic and anaerobic pathways26. These pathways result in net overproduction of CO2 and lactic acid, and subsequent respiratory compensation through tachypnea.

Increased energy expenditure in sepsis seems to be an early feature of the septic response and is mediated by endocrine mechanisms including increased corticosteroid and catecholamine production. As sepsis proceeds to more severe organ failure and shock, energy expenditure actually appears to decrease as a result of mitochondrial shutdown27,28. The lactate that we measure in the early risk stratification of septic patients is most likely not due to anaerobic glycolysis alone, but rather is a marker of overall increased metabolic demand and sympathetic overdrive29. Adding a lactate level did not seem to add significantly to the predictive value of qSOFA2,30. This may be because, pathophysiologically, tachypnea addresses the same metabolic processes as the lactate level.

Like altered mental status, and unlike lactate, tachypnea does not require a blood test. Instead, it requires careful measurement of the respiratory rate, an activity that takes an ENTIRE MINUTE, yet, once again gives us immediate information about the patient’s metabolic status with prognostic value comparable to the lactate level. This brings us to the second most powerful clinical lesson of Sepsis 3:

The respiratory rate is the most important vital sign when you think a patient might be sick, but can’t quite tell yet.

3. Hypotension 

This is perhaps the most straightforward clinical feature. All EPs are acutely aware of hypotension and will treat it aggressively. Even in Sepsis 3, persistent hypotension requiring vasopressors is still classified as septic shock with even worse prognostic value than the qSOFA score2,31. But what about transient hypotension? In trauma patients, we have known for some time that transient hypotension in the field is correlated with increased mortality32. More recently, transient hypotension has been correlated with increased mortality in all comers to the ED, and a small study in 2009 showed that this effect may be more pronounced in septic patients33,34.  qSOFA now solidifies sepsis as a disease state in which transient hypotension is correlated with adverse outcomes. Yet, when we admit the pneumonia patient with a presenting SBP of 80/40 who responded to IV fluids, we often hear from our medicine colleagues: “great he can go to the obs unit”. Or worse: “sounds like you fixed her, she can follow up with her PCP tomorrow”.

There are at least three pathophysiologic mechanisms which can contribute to hypotension in sepsis: distributive vasodilation, relative hypovolemia due to poor PO intake and potential insensible losses, and sepsis associated cardiomyopathy. When we talk about volume responsiveness, we are referring to the heart’s ability to improve cardiac output when we fill a relatively depleted and functionally expanded tank35. While volume responsiveness is reassuring (it means the heart can still keep up and is a defining difference between sepsis and the more deadly septic shock), it does little in and of itself to improve the process that got the tank empty and dilated enough to cause a drop in blood pressure. Moreover, the observation that a patient was volume responsive in the ED may result in downstream aggressive volume resuscitation, and delay in initiating vasopressor therapy, which can lead to worse patient outcomes. For more on the physiology and dangers of IV fluid therapy in sepsis see these two excellently researched and referenced emdocs posts36,37. Thus, transient hypotension is a marker of the life-threatening organ dysfunction of sepsis, and should be taken seriously even if the blood pressure improves with initial volume resuscitation.

 Case resolution:

The patient woke up and began to berate staff. While this appeared consistent with his recent presentation during admission for UTI, his daughter informed the ED team over the phone, that he is usually belligerent only when he has health problems, and he normally does not act this way. At this time his total bilirubin came back at 4.1, AST 156, ALT 163, alkaline phosphatase 377. Right upper quadrant ultrasound showed cholecystitis with biliary tree dilatation concerning for cholangitis. He continued to have waxing and waning mental status throughout his stay in the ED, tearing off his clothes, cursing at staff, demanding discharge, and then falling asleep. He was admitted to the ICU for IV antibiotics and ERCP in the morning.

Closing thoughts

For centuries, we have defined sepsis in terms of its clinical features. Sepsis 3 takes a radically different approach: it defines the physiologic essence of sepsis and works backwards to define the clinical features of sepsis. While the resultant clinical features of qSOFA seem intuitive, they are pathophysiologically complex: a complexity that is congruent with the definition of life-threatening organ dysfunction caused by infection.

Although this consortium of critical care physicians “unanimously considered SIRS to be unhelpful”, it is difficult to abandon SIRS altogether. SIRS will continue to help us suspect significant infection and it will be a component of CMS sepsis core measures for some time, however it does not identify life-threatening organ dysfunction very specifically. In order to understand how sick a patient captured by the broad net of SIRS might be, qSOFA provides us with a tool to judge the severity of illness in these patients38. While prospective validation is needed to assess its utility in guiding clinical decision making, this tool includes several key features, which are grounded in pathophysiology. These features are frequently overlooked in the ED setting, and it’s up to us to start taking these symptoms seriously.

Finally, Sepsis 3 and qSOFA have many weaknesses spelled out elsewhere39,40. However, this is a strong attempt to bring the understanding of sepsis into the modern era of medicine. An era that demands an understanding of the underlying mechanisms of disease. As our understanding becomes more sophisticated we should be able to improve on this definition. Despite its flaws, Sepsis 3 still provides a significant improvement over older definitions, and should not be ignored just because our current “usual care” is just as good as “aggressive care” in losing a quarter of the lives affected by this life-threatening condition.

Acknowledgements: I’d like to thank Jamie Santistevan (@jamie_rae_EMdoc) and Matt Anderson (@CCInquisitivist) for their amazing and detailed comments and suggestions for this post.

[1]Note: The qSOFA derivation actually used a GCS of 13 or less as the formal criteria for AMS2, however the GCS has known problems of interobserver concordance and qSOFA has been widely interpreted by the medical community and its authors to include altered mentation in general, or GCS<15.16,17


References / Further Reading:

  1. Singer, M. et al. The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA 315, 801–810 (2016).
  2. Seymour, C. W. et al. Assessment of Clinical Criteria for Sepsis: For the Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA 315, 762–774 (2016).
  3. Mukherjee, S. The Emperor of All Maladies: A Biography of Cancer. (Simon and Schuster, 2010).
  4. Bone, R. C. et al. Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. The ACCP/SCCM Consensus Conference Committee. American College of Chest Physicians/Society of Critical Care Medicine. Chest 101, 1644–1655 (1992).
  5. Zolfaghari, P. S., Pinto, B. B., Dyson, A. & Singer, M. The metabolic phenotype of rodent sepsis: cause for concern? Intensive Care Med Exp 1, 25 (2013).
  6. Singer, M., De Santis, V., Vitale, D. & Jeffcoate, W. Multiorgan failure is an adaptive, endocrinemediated, metabolic response to overwhelming systemic inflammation. Lancet 364, 545–548 (2004).
  7. Aziz, M., Jacob, A., Yang, W.-L., Matsuda, A. & Wang, P. Current trends in inflammatory and immunomodulatory mediators in sepsis. J. Leukoc. Biol. 93, 329–342 (2013).
  8. Trzeciak, S. et al. Early microcirculatory perfusion derangements in patients with severe sepsis and septic shock: Relationship to hemodynamics, oxygen transport, and survival. Ann. Emerg. Med. 49, 88–98.e2 (2007).
  9. ProCESS Investigators et al. A randomized trial of protocolbased care for early septic shock. N. Engl. J. Med. 370, 1683–1693 (2014).
  10. ARISE Investigators et al. Goaldirected resuscitation for patients with early septic shock. N. Engl. J. Med. 371, 1496–1506 (2014).
  11. Mouncey, P. R. et al. Protocolised Management In Sepsis (ProMISe): a multicentre randomised controlled trial of the clinical effectiveness and costeffectiveness of early, goaldirected, protocolised resuscitation for emerging septic shock. Health Technol. Assess. 19, ixxv, 1–150 (2015).
  12. Kaukonen, K.-M. et al. Systemic Inflammatory Response Syndrome Criteria in Defining Severe Sepsis. N. Engl. J. Med. 372, 1629–1638 (2015).
  13. Rivers, E. et al. Early GoalDirected Therapy in the Treatment of Severe Sepsis and Septic Shock. N. Engl. J. Med. 345, 1368–1377 (2001).
  14. ProductsData BriefsNumber 62 – June 2011. Available at: (Accessed: 28th June 2016)
  15. Puymirat, E. et al. Association of changes in clinical characteristics and management with improvement in survival among patients with STelevation myocardial infarction. JAMA 308, 998–1006 (2012).
  16. Reith, F. C. M., Van den Brande, R., Synnot, A., Gruen, R. & Maas, A. I. R. The reliability of the Glasgow Coma Scale: a systematic review. Intensive Care Med. 42, 3–15 (2016).
  17. qSOFA :: quick Sepsis Related Organ Failure Assessment. Available at: (Accessed: 24th June 2016)
  18. Tsuruta, R. & Oda, Y. A clinical perspective of sepsisassociated delirium. J. Intensive Care Med. 4, 18 (2016).
  19. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders (DSM-5®). (American Psychiatric Pub, 2013).
  20. Inouye, S. K., Westendorp, R. G. J. & Saczynski, J. S. Delirium in elderly people. Lancet 383, 911–922 (2014).
  21. Zampieri, F. G., Marcelo, P., Machado, F. S. & Azevedo, L. C. P. Sepsisassociated encephalopathy: not just delirium. Clinics 66, 1825–1831 (2011).
  22. Han, J. H. et al. Delirium in older emergency department patients: recognition, risk factors, and psychomotor subtypes. Acad. Emerg. Med. 16, 193–200 (2009).
  23. Elie, M. et al. Prevalence and detection of delirium in elderly emergency department patients. CMAJ 163, 977–981 (2000).
  24. Han, J. H. et al. Delirium in the Emergency Department: An Independent Predictor of Death Within 6 Months. Ann. Emerg. Med. 56, 244–252.e1 (2010).
  25. Han, J. H. et al. Diagnosing delirium in older emergency department patients: validity and reliability of the delirium triage screen and the brief confusion assessment method. Ann. Emerg. Med. 62, 457–465 (2013).
  26. Chioléro, R., René, C., JeanPierre, R. & Luc, T. Energy metabolism in sepsis and injury. Nutrition 13, 45–51 (1997).
  27. Brealey, D. et al. Association between mitochondrial dysfunction and severity and outcome of septic shock. Lancet 360, 219–223 (2002).
  28. Kreymann, G. et al. Oxygen consumption and resting metabolic rate in sepsis, sepsis syndrome, and septic shock. Crit. Care Med. 21, 1012–1019 (1993).
  29. Marik PE, B. R. Lactate clearance as a target of therapy in sepsis: A flawed paradigm. OA Critical Care 1, (2013).
  30. EMCrit, A., Weingart, S. & Crew, T. E. WeeCliff Deutschman with Additional Thoughts on Sepsis 3.0. EMCrit (2016). Available at: (Accessed: 17th June 2016)
  31. ShankarHari, M. et al. Developing a New Definition and Assessing New Clinical Criteria for Septic Shock: For the Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA 315, 775–787 (2016).
  32. Chan, L., Lisa, C., Bartfield, J. M. & Reilly, K. M. The Significance of Outofhospital Hypotension in Blunt Trauma Patients. Acad. Emerg. Med. 4, 785–788 (1997).
  33. Marion, M. & Matthew, M. Emergency department hypotension predicts sudden unexpected inhospital mortality: A prospective cohort study. J. Emerg. Med. 32, 225–226 (2007).
  34. Marchick, M. R., Kline, J. A. & Jones, A. E. The significance of nonsustained hypotension in emergency department patients with sepsis. Intensive Care Med. 35, 1261–1264 (2009).
  35. Marik, P. & Bellomo, R. A rational approach to fluid therapy in sepsis. Br. J. Anaesth. 116, 339–349 (2016).
  36. Long, B. Resuscitation in Sepsis: How Much is Too Much? – emdocs. emdocs (2015). Available at: (Accessed: 17th June 2016)
  37. Long, A. The Dangers of OverResuscitation in Sepsisemdocs. emdocs (2016). Available at: (Accessed: 17th June 2016)
  38. Moskowitz, A., Andersen, L. W., Cocchi, M. & Donnino, M. W. The Misapplication of SeverityofIllness Scores Toward Clinical Decision Making. Am. J. Respir. Crit. Care Med. (2016). doi:10.1164/rccm.201605-1005ED
  39. EMCrit, A., Farkas, J. & Crew, T. E. PulmCritTop ten problems with the new sepsis definition. EMCrit (2016). Available at: (Accessed: 15th June 2016)
  40. Morgenstern, J. Sepsis 3.0 – No thank you. First10EM (2016). Available at: (Accessed: 15th June 2016)

Teaching When There is No Time

Author: Robert Cooney, MD (@EMEducation – EM Associate Program Director / Attending Physician, Geisinger Medical Center) // Edited by: Alex Koyfman, MD (@EMHighAK – EM Attending Physician, UTSW / Parkland Memorial Hospital) and Brit Long, MD (@long_brit – EM Chief Resident at SAUSHEC, USAF)

As you walk into your shift, the familiar din that made you fall in love with emergency medicine greets you.  You’ve barely sat down and logged into the EMR, when Jake, one of the interns, asks if he can present a patient.  As he presents, 2 other residents sit down and you can tell from their impatient looks that they too have patients to present.  A quick glance at the board confirms that the waiting room is 20 deep, the ED is holding 50% of its beds with admitted patients, and there are at least another half dozen expected arrivals.  “Well,” you think to yourself, “It’s another day in paradise,” and you begin to prompt Jake along so that you can get him and the other residents back to work.  After taking the 3 presentations, you pause to wonder, “Is there a better way to teach when it’s so busy?”

Between 1993 and 2003, total hospital beds declined by 198,000 while ED visits increased from 90.3 million to 113.9 million and continue to rise.  This loss of capacity within hospitals has caused the burden of care for patients needing admission to fall to the ED.  Academic emergency departments are particularly prone to this problem as they serve as receiving centers for patients in need of critical interventions and specialist evaluation.  Whether overcrowding affects resident education is a matter of debate. Berger et al1 found that productivity and teaching evaluations were not related; and surprisingly, the most productive attendings were also highly rated teachers.  Kelly et al2 found that clinical workload did not affect teaching scores.  Finally, Pines et al3 found no association between crowding and teacher-learner interactions.

While overcrowding may not have an effect on the quality of teaching, the Berger study did find that attending physicians did perceive the workload to interfere with the ability to teach well.  When it gets busy, seasoned educators will often rely on tried and true methods to accomplish effective teaching with minimal time.  Bandier et al4  identified methods that award-winning educators felt made the difference for their teaching.  These include:

Tailor teaching to the learner:

A few minutes spent at the beginning of the shift getting to know your learners is an investment that pays dividends.  This is especially true when working with medical students and off-service residents who are new to the department.  This helps to establish the relationship, determine their learning needs and goals, and you can also establish expectations.  Knowing the learner’s “story” will help you to tailor the teaching as the shift progresses.  Is the student going into radiology? Coaching them on image interpretation for all of their patients reinforces that you understand their interests.

Optimize faculty-learner interaction:

Once you know your learners, you can much more effectively tailor your teaching.  Learning to ask questions properly ( allows you to “diagnose” your learner’s level and can guide your learner through the case, improve retention, and structure their learning.  Going to the bedside is another way to optimize the interaction. Muck et al6 found that bedside rounding increased the amount of discussion about differential diagnosis, overall questions, and led to changes in diagnostic workup compared to board rounds.  While it did take longer to complete bedside rounds (4 minutes), the efficiency gained by a more appropriate patient work-up likely negates the time cost.  A full discussion of bedside teaching is outside the scope of this article.  If interested, Twelve Tips to improve Bedside Teaching by Subha Ramani7 is an excellent starting point.

Tailor teaching to the situation and actively involve the learner:

When it gets really busy during a shift, it becomes too easy to dismiss learning opportunities for the sake of speed.  Two tricks can be used when this situation arises.  First, the 1-minute preceptor8 ((Paucis Verbis Card) (  After listening to the learner’s presentation, the educator will:

  • Probe for commitment: “What do you think is going on with this patient?”
  • Probe for evidence: “Why; what else are you considering?”
  • Teach a general rule: “The key to making this diagnosis is…”
  • Reinforce what’s right: “Your differential included the key conditions that I worry about when a patient presents with a complaint of…”
  • Correct mistake: “Prior to ordering a d-dimer, make sure that the patient’s pretest risk is in the correct range.”

Another simple way to teach quick pearls is the use the “What if…” question.  This question can change a routine simple case into a learning opportunity.  For example, if a person has URI symptoms, as “What if this person was just traveling in Yosemite (Hanta), or Africa (Ebola), or Puerto Rico (Chikungunya).  A simple case suddenly becomes a hit-and-run learning experience.

Actively seek opportunities to teach:

While on a busy shift, learners often are pulled in multiple directions to see patients, document, deal with consultants, perform procedures, and the list goes on.  Always being aware of the department can help you tailor the learning.  Perhaps you’ve taken a presentation for a patient that will require a more uncommon procedure.  Bring multiple learners into the situation.  What if it’s not busy?  Keep a teaching file.  I use a combination of Evernote and a USB drive filled with images to offer learners the opportunity to review cool cases when the time presents itself.

Whether we like to acknowledge it or not, there will always be impediments to good teaching in the Emergency Department.  Whether competing demands, lack of time and/or resources, or trainee issues such as lack of interest or knowledge deficits, we can use the above simple tricks to improve our teaching.  Our patients will be better for it.

References/Further Reading:

  1. Berger, Todd J., et al. “The impact of the demand for clinical productivity on student teaching in academic emergency departments.” Academic emergency medicine 11.12 (2004): 1364-1367.
  2. Kelly, Sean P., et al. “The effects of clinical workload on teaching in the emergency department.” Academic Emergency Medicine 14.6 (2007): 526-531.
  3. Pines, Jesse M., et al. “The effect of ED crowding on education.” The American journal of emergency medicine 28.2 (2010): 217-220.
  4. Bandiera, Glen, Shirley Lee, and Richard Tiberius. “Creating effective learning in today’s emergency departments: how accomplished teachers get it done.” Annals of emergency medicine 45.3 (2005): 253-261.
  5. Cooney, Robert. “Article Review: Use of Effective Questioning” Available at:
  6. Muck, Andrew, et al. “Bedside rounds versus board rounds in an emergency department.” The clinical teacher 12.2 (2015): 94-98.
  7. Ramani, Subha. “Twelve tips to improve bedside teaching.” Medical teacher25.2 (2003): 112-115.
  8. Neher, Jon O., et al. “A five-step “microskills” model of clinical teaching.” The Journal of the American Board of Family Practice 5.4 (1992): 419-424.
  9. Sudario, Gabe. “PV Card: One Minute Preceptor – NERDS mneumonic.” Available at: