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Authors: Tim Montrief, MD MPH and Mehruba Anwar Parris, MD FAAEM
AAEM/RSA Publications & Social Media Committee and Common Sense Assistant Editor 
Originally published: Common Sense May/June 2019

A 25-year-old Caucasian male with no significant known past medical history presented to a community emergency department via EMS with palpitations and altered mental status while on vacation at a friend’s bachelor party. Per the patient’s friend, he had been drinking alcohol all day and accidentally ingested a large amount of smokeless tobacco one hour prior to arrival, with subsequent nausea, vomiting, and excessive salivation. His friend denied any co-ingestions or drug use. The patient was found to be somnolent but arousable to voice, without any focal neurologic deficits and normal point of care blood glucose. The initial physical exam was remarkable for new-onset atrial fibrillation with a heart rate in the 160’s, blood pressure of 102/56 mmHg, respiratory rate of 16 breaths per minute, and saturating 100% on room air. Aside from atrial fibrillation with rapid ventricular response, the electrocardiogram was unremarkable (Figure 1). Additionally, the chest X-ray showed no evidence of cardiopulmonary pathology. Further testing revealed normal troponin, T4, and TSH levels. He had an elevated serum alcohol level of 191 mg/dL, and a negative urine drug screen. Initial cotinine and nicotine levels were not available. The patient was given a diltiazem bolus and drip, as well as four liters of lactated ringers, with subsequent heart rates in the low 100’s, with corresponding blood pressures in the 120’s/80’s. The patient was admitted to the ICU, and spontaneously converted back to a normal sinus rhythm within 24 hours of his initial presentation. The patient was discharged the next day with close outpatient follow-up.

Figure 1. Initial ECG, showing atrial fibrillation with rapid ventricular response at a rate of 150 beats per minute, and normal PR/QT/QRS intervals.

What do we know about smokeless tobacco and nicotine toxicity?
Smokeless tobacco products contain either air- or fire-cured tobacco that is powdered or ground for use as nasal or oral snuff, cut and grated for use as oral snuff, or stripped and compacted for use as chewing tobacco. These products routinely include formaldehyde, various sugars (most commonly sucrose, fructose, sorbitol, molasses, or dried fruit), water, sodium chloride, ammonium chloride, licorice, menthol, paraffin oil, and glycerol, in addition to tobacco-specific nitrosamines.[1] Tobacco also contains nicotine, which acts on both the parasympathetic and sympathetic nervous systems by binding to acetylcholine receptors. Nicotine is readily absorbed through the lungs, skin, GI tract, and mucous membranes. While ingestion is the most common route of exposure for accidental overdoses, exposure can also occur through the dermal, ocular, and inhalational routes. Compared to smoked tobacco, smokeless tobacco produces a much slower onset and much lower peak concentration of nicotine in the blood with the same total daily dose of nicotine.[2] However, studies comparing the use of smokeless versus smoked tobacco have demonstrated qualitatively similar magnitude of effects on the sympathetic nervous system from nicotine.[2]

Although nicotine toxicity is not a new phenomenon, the recent emergence of electronic cigarettes has spawned a market for highly concentrated liquid nicotine, resulting in unprecedented access to potentially toxic doses of nicotine and other harmful compounds in the home. Calls to Poison Centers regarding tobacco products have rapidly increased since 2010, resulting in an average of 200 calls per day in early 2014.[3]

A recent comprehensive review by Mayer suggests an LD50 of 6.5-13 mg/kg (approximately 500-1000 mg for adults), which is more consistent with reported values in case reports of actual fatalities.4 However, clinically significant symptoms of nicotine toxicity can occur in children with doses as low as 1 mg and in adults with doses as low as 2-5 mg.[4] For comparison, one cigarette has about 20-30 mg of nicotine, and the typical systemic dose from a single exposure to a cigarette, snuff or chewing tobacco is estimated to be 2 to 3 mg.[5]

What are the clinical features of nicotine toxicity?
Acute nicotine poisoning has a strongly biphasic pattern, owing to its short half life of one to four hours (Figure 2). The early clinical phase occurs most commonly within the first hour of exposure, and is characterized by excessive nicotinic stimulation. Patients may present with nausea, vomiting,
pallor, abdominal pain, salivation, bronchorrhea, tachypnea, hypertension, tachycardia, miosis, ataxia, tremor, fasciculations, arrhythmias (including atrial fibrillation), and seizures.[6] The delayed phase consists of central nervous system, as well as respiratory depression, and most commonly occurs greater than one hour after ingestion. These patients present with severe dyspnea, bradycardia, hypotension, shock, mydriasis, weakness, muscle paralysis, coma, and death. Signs and symptoms after ingestion of nicotine appear to be dose related, with lower doses stimulating the neural and cardiovascular systems, while higher doses suppress the central nervous and respiratory systems.

Figure 2. The clinical features of nicotine toxicity by organ system, in the early (<1 hour after ingestion) and delayed (>1 hour after ingestion) phases.

What treatments are available for nicotine toxicity?
Treatment of nicotine poisoning is usually supportive (Figure 3). The patient should have cardiorespiratory monitoring, intravenous access, and be observed closely. Immediate treatment should be initiated whenever nicotine toxicity is suspected, primarily focusing on resuscitating the patient and correcting any life-threatening symptoms, including respiratory support with mechanical ventilation if necessary. Anticholinergic drugs such as atropine can be given to counteract bradycardia, bronchorrhea, excessive salivation, and wheezing.6 Benzodiazepines may be given for seizures, and antiemetics may be given for nausea or vomiting. Decontamination by washing the skin and removing clothes is necessary for dermal exposures. Use of activated charcoal is an option for patients who present within an hour of ingestion, but it is infrequently used, and close consultation with your local Poison Control Center is recommended. Multi-dose activate charcoal may be beneficial to remove Figure 3. Treatments for nicotine toxicity by clinical manifestation. it from enterohepatic circulation. Likewise, gastric decontamination may be initiated if recommended by poison control experts. Although nicotinic stimulation, including hypertension and tachycardia, is usually treated with adrenergic antagonists during the early phase, this treatment is not recommended, as this may exacerbate any hypotension during the delayed phase.7 Hemodialysis may also theoretically enhance elimination due to its low protein binding and small volume of distribution but evidence supporting its use is sparse. While nicotine toxicity is commonly a clinical diagnosis, blood tests may be indicated, particularly if the patient is unstable, has an unclear history, ingestion was an attempted suicide, or if the toxidrome is inconsistent. Serum nicotine and cotinine (a nicotine metabolite) levels are not generally available and may not result in a timeframe that is practical in the ED. It may be useful to confirm exposure and toxicity.8 Generally, a minimum observation time after oral or dermal exposure is four to six hours, although longer observation periods may be warranted for large ingestions involving intact nicotine patches or plant material.

Figure 3. Treatments for nicotine toxicity by clinical manifestation.

As tobacco delivery devices, particularly e-cigarettes, are becoming more widespread in the United States, more patients are presenting with sequelae of their toxicity. While most providers already know the classic presentation of nicotine toxicity, it is important for us to be aware of the other complications, including dysrhythmias, and their appropriate treatment.


1. Hoffmann D, Adams JD, Lisk D, Fisenne I, Brunnemann KD. Toxic and carcinogenic agents in dry and moist snuff. J Natl Cancer Inst. 1987;79(6):1281-6.

2. Benowitz NL. Cardiovascular toxicity of nicotine: pharmacokinetic and pharmacodynamic considerations. In: Benowitz NL, ed. Nicotine Safety and Toxicity. New York, NY: Oxford University Press Inc; 1998:19–28.

3. Chatham-Stephens K, MD1, Law R, Taylor E, et al (2014). Notes from the Field: Calls to Poison Centers for Exposures to Electronic Cigarettes — United States, September 2010–February 2014 Weekly. 63(13); 292-293.

4. Mayer B. How much nicotine kills a human? Tracing back the generally accepted lethal dose to dubious self-experiments in the nineteenth century. Arch Toxicol. 2014;88(1):5-7.

5. Hukkanen J, Jacob P, Benowitz NL. Metabolism and disposition kinetics of nicotine. Pharmacol Rev. 2005;57(1):79-115.

6. Mishra A, Chaturvedi P, Datta S, Sinukumar S, Joshi P, Garg A. Harmful effects of nicotine. Indian J Med Paediatr Oncol. 2015;36(1):24-31.

7. Karaconji IB. Facts about nicotine toxicity. Arh Hig Rada Toksikol. 2005;56(4):363-71.

8. Raja M, Garg A, Yadav P, Jha K, Handa S. Diagnostic Methods for Detection of Cotinine Level in Tobacco Users: A Review. J Clin Diagn Res. 2016;10(3):ZE04-6.
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Author: James Keaney, MD MPH MAAEM FAAEM
First President of AAEM

The Current Climate of EM – How Did We Get Here?
There are several recurrent phrases making their way into the vernacular of emergency medicine including transmutation, Joe the Plummer, the Leviathan Levy, and tumbleweed doctors.

The transmutation of clinically generated fees into management money is the theme of this talk revolving around the misallocation of Medicare-approved, clinically generated fees by practicing doctors into administrative wealth. The premise of the talk is this transmutation not only provides zero-point-zero real benefit to the physician, possibly even has negative effects, but also represents a public health detriment to the communities in which the hospitals are located. Many of you will ultimately work in community hospitals. Ideally, you will find an independent group with a fair road to full partnership and equitable distribution of nights, weekends and holiday shifts. However, independent groups are rapidly losing their natural habitat meaning most of you will likely work for a large contract management group (CMG) which has scores of contracts with hospitals and then subcontracts with a hundred, or hundreds, or maybe even many hundreds of emergency physicians, most of them residency-trained like yourselves.

When you graduate, you will make three to five hundred thousand dollars a year give or take. For the right to work in a CMG you will be required to tithe 25% of your collected fees to the mothership receiving a prorated number of shillings in return depending on your longevity and fealty to the CULTure of the CMG.

Fifty to seventy-five grand from ten doctors staffing an ED multiplied by ten contracted hospitals adds up to some pretty serious coin. Leasing the one-eighth of an acre on the hospital’s first floor, otherwise known as the emergency department (ED), makes the ED the most expensive piece of real estate in any district with many barracudas in the tank vying for these lucrative leases.

Until very recently, the three-square-yard footage of terra firma in front of the operating table occupied by the anesthesiologist was not for sale, nor the chair in front of the view box by the radiologist, only God’s little acreage in the ED.

What’s a CMG to do with all those Krugerands accumulating in the vault? Well, they could give it back to the clinicians who earned it, but rarely. Instead it goes to unconscionable sums distributed to directors, regional directors, COOs, CFOs, CEOs, and various well-remunerated vice presidents, all of them just a few years ago fellow clinicians working in the foxhole next to you before their rise in the management ranks to partake of the largesse, the same boys and girls now wearing different hats, a bizarre phenomenon not existing in other medical specialties. The neurosurgeon who clips the most aneurysms and removes the most brain tumors has the highest income. In emergency medicine, unlike any other specialty, the emergency physicians seeing the fewest emergencies make the most money.

Yes, twenty grand a month is a common stipend for the director of an emergency department with an annual census of thirty-thousand visits a year. That’s a quarter-of-a-million bucks before they even see a patient. Bear in mind, the chief of staff of the whole hospital has a stipend of twenty grand a year. How ‘bout fifty grand a month for being a regional director, doing the hard work of taking hospital administrators to Michelin restaurants, golf courses, maybe even St. Andrews to secure a high-stakes hospital contract. As one regional director of a California CMG wrote, “you just don’t know what hard work it is dealing with these administrators.” It’s certainly difficult to find time to do clinical work after eighteen holes. In fact, most regional directors only see patients at the point of a bayonet, and even then, just in urgent care clinics taking out a few stitches here and there. There are also fluff positions for loyal buddies, like vice presidents of education, government affairs (what surgery group-practice has their own vice president for government affairs?), leadership, and most importantly vice presidents for mergers and acquisitions where some potentially astounding salary and commission money is to be made especially if a buyout occurs or an IPO emerges. The physician CEOs and others are generously paid, “work” in opulent offices, and receive lavish golden parachutes, sometimes the golden watch worth millions of departing money for their “valuable services,” all originating from the Medicare-approved, clinically generated fees of the yeomanry. Everything about emergency medicine “management” is luxuriant, and again, only in emergency medicine not the other twenty-three formally recognized medical specialties by the American Board of Medical Specialties (ABMS).

What to do with the rest of the rapidly accumulating loot? Logically, one turns to the vice president of mergers-and-acquisitions. But there are only five thousand emergency departments in the nation and more than half of these are in rural areas, or academic centers, Kaisers, VAs, or military hospitals so there is a limited quarry to excavate. After continuing efforts to torpedo the other CMG’s ED contracts, the next logical prey is right in the neighborhood, the square yardage in front of the operating table. Given that, one of best ways to metabolize all the mounting cash is to acquire, mainly purchase, the nearest investable asset which would be an anesthesia group, and voila — expansion bonanza by annexation — and now on to that chair in front of the PACS machine in the radiology cave. The triple play offers the complete package, an Amazonification with the whole enchilada from one CMG, one-stop shopping for hospital administrators. Large corporations, having nothing to do with emergency medicine, have taken note of the high-profit margins by skimming off of the fees of emergency physicians with bigger fish gobbling the barracudas purchasing ED groups creating handsome dividends for their shareholders. Unbelievably, a Moby Dick hedge fund has recently gone into the sweepstakes as well, and a neologism, “the Leviathan Levy” on emergency physicians has been created for the mega-wealthy.

It is self-evident when Joe the Plumber takes his daughter into the emergency department at 3:00am for an earache and pays his fee to the residency-trained board-certified emergency physician, Joe is unaware a portion of his fee, the Leviathan Levy is going to a well-rested investor comfortably in bed. It is equally self-evident Joe the Plumber would find displeasure with this fiscal arrangement with the moneychangers in the temple.

Emergency physicians also work in disjointedness from the internists, surgeons, and pediatricians, physicians who usually settle in one locale for a lifetime of work with continuity-of-care for their patients. These doctors have due process rights which fall within the purview of the governance of the hospital medical staff. If a dispute occurs with hospital administration, the administrator cannot single-handedly remove a physician. Administrators can request a judicial review where the medical staff doctors themselves, and only the medical staff doctors, make the final decision on staff discipline. However, CMGs make all emergency physicians sign lengthy contracts, the forty-page contracts being masterpieces of complexification also assuring the hospital administrations the CMGs will kindly handle all due process adjudications with their own in-house extrajudicial Star Chamber complete with kangaroo courts, show trials and hanging judges. Administrators remind emergency physicians in so many words they can be removed if the color of their ties is not to their liking.

You also have gag orders other specialists don’t, and this in today’s world, represents a public health detriment to the community. The no-fly zones for emergency physicians are safety suggestions to administration that cost money. Do not complain about the carbon-dated ultrasound machine with a missing probe gifted from the radiology toolshed. Never criticize the hospital policy to cotton-candy the (insured) drug addicts who waste an inordinate amount of time and resources to get their daily fix. And whatever you do, don’t suggest the obvious like extra nurses for the understaffed evening shift. A good CMG director will inform you ahead of time not to express such verboten thoughts at staff meetings. The director will inform you these suggestions can only be brought by the permanent cardiac or orthopedic rainmakers, not subcontractors with ninety-day no-cause termination contracts. You will soon realize the indignity of knowing all the other specialists at the table are fully aware you’re the only doctor that can be here today and gone tomorrow. “Whatever happened to …?”

You are also the community canary in the coal mine warning about unusual infectious disease patterns especially meningitis and other notifiable diseases, or messaging the public of a higher grade of heroin on the street or a local food-poisoning epidemic, and as well, unfortunately, have to act the constable for on-call doctors who don’t respond appropriately. You are also the de facto primary care doctors to many locals especially the recently uninsured. Party loyalist regional directors have the eye of an ornithologist making sure any birds singing out of school are neutralized. If you are a responsible town crier but don’t color within the lines you could find yourself absent on next month’s schedule tumbleweeding to a new CMG located in another zip code.

The work-a-day of a national CMG begins with the daily check of a map of the country showing all existing ED contracts with red pins showing the contracts soon to expire. The situation room looks like the headquarters of NORAD with the bloodhounds on red-hot scents for any new contracts up for grabs. Next the printing presses are heated up. Thousands of beautiful, slick, Madison Avenue-designed brochures, printed on glossy, very-expensive papyrus tsunami the offices of hospital administrators. If the CEO bites, the marketing team is sent for the presentation. If you ever get the opportunity to attend a presentation, jump at it, even if it’s short notice and you realize they only want to showcase a tokenized scrub like yourself. Be their preforming seal and be dazzled by the ringmaster orchestrating the men in crisp blue suits and red ties accompanied by the Saks Fifth Avenue ladies in high heels “shocking and aweing” hospital administrators with their technicolor bar graphs and pie charts demonstrating how their doctors are providers of “peer-reviewed, evidence-based, best practices to offer the highest quality emergency care at the lowest price making your institution a Center of Excellence with one-hundred per cent CUSTOMER SATISFACTION!”

Then the tyranny of the meaningless metrics, and ah yes, the metrics of productivity are the darling of the marketing departments with the MBAs from the best schools who excel with Excel. You must embrace that this side of the room sees 2.4 patients per hour but this side sees only 2.1 patients per hour. Might not seem like much except the taxi-meter runs 24-7-365 and the cash the 2.4s generate adds-up, possibly enough to buy another anesthesiology group. Now, of course, it may be the 2.1s are more meticulous with their suturing, likely to take their time sewing up a vertically oriented facial laceration in a child too deep to Dermabond. The 2.4s would rather unwrap a thick 4-0 nylon thread with a large fishhook needle and get it over with, maybe even whip out a staple gun and get themselves up to 2.5. Hedge funds only want productivity from the rapid-through-put assembly lines since insurance only pays for the length of the laceration not the final cosmetic outcome.

All CMGs will then claim they have trade secrets revealed only to the exclusivists and their Fellows. Emergency medicine is the only specialty offering a Fellowship in Management! A madrassa in “management?” Could someone please tell me what trade secrets are in emergency medicine? They’re obviously pretty well-kept secrets since no stool pigeon has ever told me what they are. What about proprietary information, copyrights, trademarks? What’s the secret sauce here and how come nobody’s spilled it? Keeping the contract at all costs, regardless of morality is clearly the single biggest trade secret which is common knowledge to all in the subculture. But how far does the information warfare and nefariousness go to poach ED contracts from other CMGs? Hacking tools perhaps?

After the show’s main event winds down, you will realize that you, the clinician who evaluates and treats the patients of America, are the sideshow, the bit player, a movie extra utilized for window dressing. You may be invited to the Loch-Ness-Monster-Lobster lunch, but the magicians still do not reveal their secrets. You will not be invited to where the deals are solidified, an Area 51 where the perks are announced to the administrator. You will also not be invited to the champagne cork popping if the CMG successfully hit the mother lode by outmaneuvering and capsizing the existing contract holder, dropkicking the current emergency physicians out of town to be proselytized into a brand-new CULTure. Someday, when the curtain of contract acquisition is finally pulled back, the Wizard of Oz-like figure will appear.

Most unfortunately, the American College of Emergency Physicians (ACEP) has been dominated by the wealth and exploitation of the original founders and many past presidents who were never emergency physicians to begin with but were highly motivated by the riches of a plantation economy. Their strict radio silence disguised as laissez-faire has betrayed the innocent blood of newly graduated residents, willfully neglecting individual physician rights along with the community welfare, and aiding and abetting the power of the abusive corporations. The litmus test for management advancement in CMGs is active involvement in ACEP at national and state levels. Most CMGs pay the dues money of their subcontracted physicians utilizing a tax deduction to massively boost ACEP’s treasure chest indirectly.

What about the general medical societies, national and local? They will not, I repeat, be of any help. Don’t get me wrong, they perform their tasks extremely well, but they are not constituted in such a fashion to champion an explosive issue especially when some of their CMG-embedded dues-paying, office-holding, cocktail-party buddies are involved.

What will happen this time when reforms are proposed? There will be a perfunctory public reading of the mission statement and other pieties, “We are here to protect the health of the Blah, blah, blah.” Then the faux outrage will demand a committee be formed, yes of course, a committee with all the stakeholders present to hammer out a suitable solution fair to all parties for this perplexing dilemma. Committee is medical code for delay until the fuss dies down. Joe the Plummer is in no need of such head scratching. If Joe applies too much external pressure they will announce not just a committee but convene a Blue-Ribbon Commission to issue a White Paper “for the protection the public.”

There’s still an elephant in the room my friends in the national medical societies. When the one-eighth of an acre on the hospital’s first floor is being leased for the price of Fabergé Eggs, and clinically generated physician fees are alchemized into obscene “physician-owned-and-managed” salaries and bonuses, all of medicine is losing ground. Surgeons don’t pay their office managers more than themselves, and cardiology groups don’t pay fifty-thousand dollars a month for managers to handle schedules, retirement plans, health insurance, and go golfing with administrators on weekends in Hawaii. There’s no reason not to pay management doctors a fair hourly for his or her time that is equal to the clinicians seeing and treating the patients rather than the current tapeworms envisioning themselves as a bizarre new form of captains of industry even though they created no industry. Other than raw exploitation there is no economic justification for excessive nonclinical, laughable bonuses ruled by the now rather visible hand of the market place, paying clinicians “whatever the market will bear” while keeping the rest for themselves.

Ossified brains sipping Grand Marnier in executive dining rooms will harrumph, “Isn’t this capitalism? What do those apparatchiks want, Bolshevism? Although Joe the Plumber never read Marx and Engels, and never sipped Grand Marnier in an executive dining room, it would again be self-evident that collectivized labor in a Worker’s Paradise with a Five-Year-Plan by a Central Committee with no Glasnost or Perestroika, and with untold riches going to the politburo is not entrepreneurialism but worthy of a May Day parade.

Not to be totally exculpatory to the old guard but the embryonic specialty of emergency medicine didn’t even exist just thirty-five years ago. Most older doctors know only of serving a tour of duty in the ED as a resident or as a moonlighter, and many still say, “I used to be an ER doc.” Many physicians who were full time moonlighters were bidding their time until a dermatology residency or a gastroenterology fellowship opened up. Others had medical or substance abuse problems such as the orthopedic surgeon who developed rheumatoid arthritis. Some were just ski-and-scuba bums taking a gap year making pocket money doing shifts here and there. More than a few were post-sixties Jesus lookalikes wearing sandals and flowing robes to work. Many who attended the first emergency medicine conferences in the 1980’s looked like characters who’d just stepped out of the Old Testament or Greek Mythology with this image still persisting.

However, a new paradigm in American medicine has emerged, happening so rapidly many physicians haven’t realized the seismic shift, an epochal medical advancement as important as the CAT scan or MRI. Emergency medicine needs a new Tabula Rasa (clean slate). Today’s emergency departments need to have professional physicians staffing the department as integral members of the medical staff for a lifetime of continuity of community care. Organized medicine has to embrace this model rather than the current greed-based musical chair policy where whole ED staffs are replaced en masse by marauding CMGs with their new set of provisional physicians parachuting into town. No longer can it be ignored. If general medical societies really want new clinician members they can’t walk between the raindrops forever pretending to be the piano player in the whorehouse not knowing what’s going on upstairs.

The Solution
There’s an obvious common-sense solution. I propose the Emergency Medicine Antiprofitering Act (EMAPA) which includes four elements:
  1. A percentage cap on management fees
  2. Interdiction of the sales of emergency department contracts for any form of consideration
  3. Elimination of coterminous clauses where physicians automatically lose hospital privileges when the CMG loses its contract
  4. Strengthening due process rights for real-estate-based physicians.
In reality, with a simple percentage cap on management fees the rest will fall into line with the cap being the core of the reverse engineering that needs to be done. Until there is a cap, the last rites cannot be administered to the current blight of the CMGs.

Although I’m not the greatest fan of Obamacare, one clause peaked my attention — the clause limiting the administrative costs of health insurance companies to 15% of the premiums, requiring 85% go directly to patient care. Why can’t we clinicians have a law capping the percentage any organization or individual expropriates for their so-called management? Ironically, the oligarchies justify their incomes because of the excessive amount of resources spent on the cutthroat competition fending off the other jackals for the lucrative spoils of a new contract.

We can justify a congressionally enacted federal law since so many of the payments come from government sources. Taxpayer Joe should know exactly where his fee is going. Representative Pete Stark, while in congress, would lecture us that Medicare ran on a four per cent overhead while indemnity insurance ran on 35% overhead. Capping management fees to 4% excluding the hard cost of billing and malpractice would eliminate all interest in acquiring an ED contract except for those wanting to work in a hospital and live in a community for a lifetime career. The Barnum and Bailey Circus of emergency medicine would come to a screeching halt with no more avalanches of glossies to administrators, restaurants, golf, top-shelf liquors, Waterford crystal or Steuben Glass. Emergency medicine needs to codify the ancient doctrine of “Render unto Caesar.”

The second approach, and I believe the better one, is the Thurgood Marshall strategy. Who would have ever thought the little elementary schoolgirl in Topeka, Kansas would overturn the sixty-year precedent of Plessy v. Ferguson eliminating the charade of separate but equal? The Centers for Medicare and Medicaid are in clear violation of the original intent of the Medicare Act. The Medicare system has become the unwitting supplier of the river of money oiling the scam artists sometimes creating fast-buck millionaires overnight, essentially a federally sanctioned money laundering scheme enriching unnecessary third-party middlemen. They have been shameful stewards of the taxpayer money designated to provide healthcare to the Joe-the-Plumbers of America. Even Ginsberg and Kavanaugh would need no head scratching on that one. For that matter, even Trump and Ocasio-Cortez wouldn’t need to committee it. It’s time for the Common Sense Emergency Physicians versus United States of America.

Thomas Carlyle said, “No lie can live forever.” Eventually payers will catch on to this bizarre falsity existing in only one specialty. It would be far better for us emergency physicians to bring it to the public’s attention rather than an outside group doing it for us. It would be most embarrassing for a public interest group to do the dirty work because of our inaction. At a minimum, we must Paul Revere the nation. Two lanterns in the belfry and Leviathan is coming your way.

These are high-stakes issues that big money is going to fight to the death, but my fellow emergency physicians, this is a good fight and the issues are far from insurmountable. Corporations will threaten us with what I call the three lawsuits of the last refuge of scoundrels – libel, slander, and antitrust. CMGs know they will be laughed out of open court when they say that contract management groups place patients above dividends and bonuses. District by district, state by state, we can expose them, removing the stranglehold existing in only one medical specialty. We need to fight with an organization interested in long-term career emergency physicians serving a community throughout their tenure, dedication, and offering true quality assurance for the populace. We would no longer have to choose between the Oath of Maimonides or the bottom-line dictums of Bernie Madoff.

It’s best for our patients, and it’s best for us.

James Keaney is a former president of the American Academy of Emergency Medicine (AAEM).

AAEM was formed in 1993 as the emergency physician’s alternative to ACEP, and now has eight thousand members. AAEM is the only organization of board-certified emergency medicine physicians that promotes the right of every American to be served by a qualified emergency physician and the right of every physician to serve those patients with full autonomy without corporate interference, and with all the obligations, duties, and due process rights of the entire hospital medical staff.

James K. Keaney, MD MPH, a clinical emergency physician for the past 43 years, is solely responsible for the contents of this article.

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Authors: Akilesh Honasoge, MD MA; Robert Brown, MD; Sharleen Yuan, MD PhD MA
Editors: Kami M. Hu, MD FAAEM and Kelly Maurelus, MD FAAEM
Originally Published: Common Sense May/June 2019

Clinical Question:
Can high sensitivity troponin meaningfully contribute to an acute coronary syndrome evaluation?

Traditional 4th-generation troponin assays are part of the standard cardiac evaluation when there is suspicion of acute coronary syndrome (ACS). Patients presenting to emergency departments with chest pain are typically risk stratified using a combination of historical risk factors, electrocardiogram (ECG) findings, troponin testing, and clinical suspicion. Patients are discharged from the emergency department if their risk is determined to be low while higher risk patients are usually admitted for further observation or testing. Recent data suggests, however, that high sensitivity troponin (hsTrop) testing could supplement or even replace current methods such as clinical risk scores when used in specific protocolized serial testing pathways. High sensitivity troponins first became available in the United States in 2017, but their use has not yet reached widespread acceptance. The test offers detection of cardiac troponin approximately 1,000 times more sensitive than standard 4th-generation cardiac troponin testing. With this higher sensitivity come questions regarding reliability and specificity in certain comorbidities such as chronic kidney disease and underlying coronary artery disease. Some studies also explore the use of computed tomography (CT) coronary angiography when used in conjunction with hsTrop. Here we explore a few studies that evaluate the role of hsTrop in the evaluation of potential ACS.

Chapman A, Hesse K, Andrews J et al. High-Sensitivity Cardiac Troponin I and Clinical Risk Scores in Patients with Suspected Acute Coronary Syndrome. Circulation. 2018;138:1654-65.
The authors of this study sought to determine whether the addition of hsTrop to previously developed clinical risk scores would alter their negative predictive value (NPV) for ruling out ACS in low-risk patients. They evaluated two hsTrop ACS rule-out protocols: the European Society of Cardiology 3-hour pathway (ESC) and the High-Sensitivity Troponin in the Evaluations of patients with Acute Coronary Syndrome (High- STEACS) pathway. For both pathways, myocardial infarction is ruled in if the hsTrop concentration rises above the 99th percentile.

The ESC pathway rules out ACS in patients with symptoms lasting longer than six hours and a non-ischemic ECG if the initial hsTrop level is below the 99th percentile. For patients with symptoms lasting less than six hours, a second hsTrop is collected three hours after presentation, and if it remains below the 99th percentile and changes by less than half the threshold for the 99th percentile, ACS is ruled out.

By comparison, the High-STEACS pathway rules out ACS in patients with symptoms lasting two or more hours, without ischemic changes on ECG, with a hsTrop < 5ng/L at presentation. If the patient is within two hours of symptom onset a second hsTrop is collected at three hours after presentation and if it remains below the 99th percentile and there is no change (Δ <3ng/L), ACS is ruled out. For patients with a presenting hsTrop > 5ng/L but below the 99th percentile, a re-test is performed three hours later and if there is no change (Δ <3ng/L) then the patient is considered ruled out for ACS. Of note, the 5ng/dL threshold to rule out ACS at presentation was derived and then validated using consecutive suspected ACS cases at hospitals in Scotland.

The authors compared the sensitivity and negative predictive value for ACS of these protocols both with and without the following additional clinical risk scores: Thrombolysis in Myocardial Infarction (TIMI), Global Registry of Acute Coronary Events (GRACE), Emergency Department Assessment of Chest Pain Score (EDACS), and the History, ECG, Age, Risk Factors, Troponin (HEART) score.

This was a prospective observational cohort study of 1,935 consecutive suspected ACS cases at a tertiary care center in Scotland. The primary outcome was the composite outcome of myocardial infarction (MI) due to ACS or death due to MI, dysrhythmia, or heart failure at either presentation or 30 days later. Diagnoses were adjudicated by 2 independent cardiologists. The authors achieved 100% follow up via individual patient calls as well as regional and national registries.

The primary outcome occurred in 276 patients (14.3%). The ESC 3-hour pathway NPV was 97.9% (95% CI: 97.1-98.6) but with a sensitivity of only 89.9% (95% CI: 86.3-93.4), corresponding to a pathway-based rule-out of 70% of patients, with 27 missed events. When combined with clinical decision rules there was a significant (p<0.001) improvement of the NPV (99% or greater in each case) but the proportion of patients characterized as “low risk” decreased dramatically to 25% with the addition of the HEART score, 42% with EDACS, 43% with TIMI, and 49% with GRACE.

The High-STEACS pathway ruled out a similar proportion of patients (65%) but with a better NPV (99.7% CI: 99.4-99.9) and sensitivity (98.7%, CI: 97.4-99.8), corresponding to 3 missed events. When combined with clinical decision tools there was no significant improvement in the NPV but the proportion of patients able to be categorized as low-risk fell significantly to 24.3% for the HEART score, 41% for EDACS, 44% for TIMI, and 47% for GRACE with p<0.001 for each.

Although the High-STEACS protocol outperformed the ESC pathway, there are important limitations to this data. The actual High-STEACS pathway was derived from the first 1,218 patients used for this study, which derived its patients from a single large academic center. Therefore, it is without broad multi-centered validation. The study also notes that there is a high coefficient of variance surrounding the reference limits of the hsTrop testing of about 12.6% across 33 devices. This study also requires replication to ensure the generalizability of using a 5ng/L cutoff for hsTrop.

The High-STEACS highly sensitive troponin pathway appears to offeran effective method of ACS evaluation that is not significantly improved when combined with clinical risk score such as the HEART score. However, hsTrop pathways require more studies with different study populations, further specification of reference limits, and actual data on the effects of utilizing said pathways before there can be widespread adoption.

Kraus D, von Jeinsen B, Tzikas S, et al. Cardiac Troponins for the Diagnosis of Acute Myocardial Infarction in Chronic Kidney Disease. J Am Heart Assoc. 2018;7:e008032.
Chronic kidney disease (CKD) is associated with an increased risk for myocardial infarction, but the utility of cardiac troponins in evaluating for ACS is hindered by the fact that patients with CKD often have elevations in troponin even in the absence of myocardial ischemia. In this study, the authors hypothesized that although the performance of high sensitivity troponins I and T (hereby referred to only as “hsTrop”) to diagnose ACS is confounded by the presence of CKD, dynamic changes in hsTrop may outperform static cutoffs in the diagnosis of NSTEMIs in CKD patients. The authors proposed an algorithm using hsTrop levels to increase specificity in CKD patients.

The authors included two patient cohorts including over 8,500 patients in their analysis. The first was a prospective cohort that enrolled 1,818 patients with suspected ACS. They excluded dialysis-dependent patients but included 280 with CKD. The second was a retrospective cohort of patients with hsTrop testing in clinically-suspected ACS. Dialysis patients were again excluded, and it was narrowed to 5,478 patients without CKD and 1,581 patients with CKD after exclusion criteria. Important exclusion criteria included dialysis dependence, pregnancy, recent surgery, IV drug abuse, and anemia. The authors used this data to calculate the appropriate initial and 3-hour hsTrop level that would optimize both positive predictive value (PPV) and negative predictive value (NPV) for ACS in patients with CKD. The final diagnosis of ACS was made by two independent cardiologists after thorough chart review.

For the prospective cohort, the average GFR of patients with CKD was 46 mL/min/1.73 m2, while in patients without CKD the GFR was 85 mL/min/1.73 m2. The prospective cohort resulted in an NSTEMI rate of 17% (without CKD: 15%, with CKD: 26%). The retrospective cohort had a similar 19% overall rate of NSTEMI (without CKD: 17%, with CKD: 28%). The high sensitivity troponin levels were overall higher in patients with CKD (measured in ng/L). In the prospective cohort, for example, the initial hsTrop on average was 5.[6] (CI: 3.0-18.2) in patients without CKD and 14.7 (CI: 6.5-76.9) in patients with CKD.

The authors derived optimized cutoffs for both absolute and relative changes for their hsTrop algorithms. The two main thresholds used were the 99th percentile and another “very high” level. This “very high” hsTrop level was calculated to reach an equivalent specificity for ACS in CKD patients when compared to an initial hsTrop in a patient without CKD based on the 99th percentile cutoff. This “very high” level maintains the sensitivity of hsTrop I while dropping the sensitivity of hsTrop T. Based on these cutoffs, the authors established three different algorithmic criteria upon which to rule ACS in or out, making the following statements:

If the initial hsTrop level at presentation falls below the 99th percentile with no more than a 2.8x increase in hsTrop after three hours, ACS in patients with CKD can be ruled out (NPV=98%, CI=94-100%). Any increases past this level should prompt at least inpatient observation.

If the initial hsTrop is above the 99th percentile and increases more than 2.8x for hsTrop I after three hours, ACS is ruled in (PPV=89%, CI=65- 99%). If they increase after three hours, but do not exceed the 2.8x cutoff, ACS is still possible, and the patient should be observed.

If the initial hsTrop level is above the very high level, ACS is ruled in without need for further troponin measurement in the emergency department (PPV=74%, CI not given).

Based on these cutoffs, when applied to the two cohorts being studied, the authors found the rule out approach described above had a sensitivity of 100% (CI=94-100%) for the diagnosis of ACS.

Limitations of the study include its use of initial serum creatinine at time of measurement of hsTrop rather than evaluation of the patient’s baseline creatinine clearance, which may damage the inherent validity of this study, as conditions like acute kidney injury offer a different pathophysiology and inherent ACS risk than chronic disease. The determination of final diagnosis of ACS was made by independent cardiologists in the prospective cohort, however the retrospective cohort established the final diagnosis of ACS from the patient’s evaluating provider. The study cohorts also excluded patients on dialysis, limiting the generalizability to that population.

Using a cutoff for hsTrop change, rather than absolute values, in the ACS evaluation of patients with CKD may have a place at some point in the future, however there is not enough data to make an adequate assessment on the validity of this approach at this time.

Ferencik M, Liu T, Mayrhofer T, et al. hs-Troponin I Followed by CT Angiography Improves Acute Coronary Syndrome Risk Stratification Accuracy and Work-Up in Acute Chest Pain Patients: Results from ROMICAT II Trial. JACC Cardiovasc Imaging. 2015;8(11):1272-81.
The ROMICAT II trial (Rule Out Myocardial Infarction/Ischemia using Computer Assisted Tomography) explored the effects of supplementing standard troponin testing with standard coronary computed tomography angiogram (CTA) to reduce hospital admissions and further testing. This study is a nested observational cohort of the larger ROMICAT II trial that evaluates the outcomes of combining hsTrop testing with advanced coronary CTA.

The study population included patients aged 40-75 years with at least two cardiac risk factors, in sinus rhythm, who presented to the ED with at least five minutes of chest pain or an anginal equivalent concerning for ACS. Notable exclusion criteria include a positive initial standard troponin, serum creatinine >1.5mg/dL, or an ECG with diagnostic ischemic changes such as ST elevations or depressions >1mm or T wave inversions >4 mm in two anatomically adjacent leads. This study narrowed the 501 members of the CTA arm of the ROMICAT II trial to those who also had hsTrop testing, which lead to a total study population of 160 patients.

The patients were divided into three main categories based on their initial hsTrop: low risk (below the level of detection, <0.5pg/mL), intermediate risk (0.5-0.49pg/mL), and high risk (above the 99th percentile, >0.49pg/mL). Coronary CTA findings stratified levels of coronary stenosis to define presence of coronary artery disease (CAD) defined as: no CAD (0%), non-obstructive CAD (1-49%), and obstructive CAD (>50%). Advanced evaluation of coronary CTA analyzed high-risk features of coronary artery plaque (remodeling index >1.1, plaque with low CT attenuation <30 HU, napkin-ring sign, and spotty calcium) independently of the level of underlying coronary artery stenosis. The eventual diagnosis of ACS was based on an independent committee review of the patient’s hospital or after-discharge course.

The overall presence of ACS in this cohort was 11.9%. In patients stratified by hsTrop level, 5.6% were deemed to be low risk and 7.5% were deemed to be high risk, with a 0% and 58.3% rate of diagnosed ACS respectively, independent of CTA testing. The 86.9% of patients with intermediate-risk hsTrop levels had an ACS rate of 8.6%. All patients with an eventual diagnosis of ACS had at least one high-risk feature on advanced CTA independent of the presence of obstructive CAD. No patient with an absolutely negative CTA (no CAD and no high-risk plaque) developed ACS, while patients with both obstructive CAD and high-risk plaque had an ACS rate of 69.2%.

The authors proposed an ACS evaluation algorithm that first stratifies patients based on initial hsTrop and associated rate of ACS (noted in parentheses): see Figure 1.
  1. Patients with low-risk hsTrop levels (ACS=0%) would be deemed appropriate for ED discharge without a need for a coronary CTA.
  2. Patients with intermediate-risk hsTrop levels (ACS=8.6%) would subsequently receive an advanced coronary CTA for further risk stratification. If no obstructive CAD and no high-risk plaques are found (ACS=0%), the patient is low risk. If either CAD or high-risk plaque is found, they are defined as intermediate risk (ACS=7.7%). If both are found the patient is deemed to be high risk (ACS=69.2%).
  3. Patients with high-risk levels (ACS=58.3%) would go on to further inpatient evaluation without need for additional ED risk stratification with coronary CTA.
Figure 1: Combined hsTrop and Advanced Coronary CTA algorithm for ED evaluation of ACS derived from the ROMICAT II Trial[7]

Ferencik M, Liu T, Mayrhofer T, et al. hs-Troponin I Followed by CT Angiography Improves Acute Coronary Syndrome Risk Stratification Accuracy and Work-Up in Acute Chest Pain Patients: Results From ROMICAT II Trial. JACC Cardiovasc Imaging. 2015;8(11):1272-81.
The author’s overall conclusion is that use of hsTrop and advanced coronary CTA maintains the 100% (95% CI: 82.4-100.0%) sensitivity of ACS when compared to standard troponin and standard coronary CTA. However, it improves the specificity from 48.2% (95% CI: 39.7-56.8%) to 68.1% (95% CI: 59.7-75.7%).

This study is a small study (n=160) with no direct control or comparison group. Its generalizability is limited by excluding patients not in sinus rhythm and with chronic kidney disease, which may confound the hsTrop level determinations, even if it is sensible that physicians are not likely obtaining coronary CTAs in patients with CKD.

The use of sequential high sensitivity troponin and coronary CTA with assessment of advanced plaque features has potential to be an improved objective tool for stratifying ACS risk, potentially allowing discharge of patients who would otherwise fall into the intermediate risk category. Evaluation of high-risk plaque features on coronary CTA has the potential to change our approach to ischemia evaluation via stress testing and potentially even invasive angiography. Additional studies are required, however, to validate this proposal, and physicians will need to keep in mind the cohort of patients excluded due to limitations in the use of coronary CTA.

Shah ASV, Anand A, Strachan FE, et al. High-sensitivity troponin in the evaluation of patients with suspected acute coronary syndrome: a stepped-wedge, cluster-randomised controlled trial. Lancet. 2018; 392(10151):918-28.
The High-STEACS investigators sought to determine whether utilization of a hsTrop assay with a sex-specific threshold above the 99th percentile would decrease the rate of subsequent MI or cardiac death in patients with suspected ACS. A cluster-randomized, stepped-wedge trial across ten hospitals in Scotland over three years, the study included patients presenting to the ED with suspected ACS, collecting both a standard and high-sensitivity troponin at initial presentation and again at six or 12 hours after the onset of symptoms, at the attending physician’s discretion. The study was broken up into a six-month validation phase during which treating physicians were blinded to the hsTrop level, and an implementation phase during which the hsTrop level was known but the standard troponin level was masked to treating physicians.

The primary outcome was subsequent MI (type 1 or 4b) or cardiovascular death within a year of initial presentation to the hospital. Secondary outcomes were duration of hospital stay, type 1 or 4b MI, unplanned coronary revascularization, hospital admission for heart failure, ischemic stroke, major hemorrhage, unplanned hospital admission, and all-cause death. Diagnosis of MI was made by two physicians blinded to the study phase who determined that there was myocardial injury (hsTrop level above the 99th percentile) in the context of suspected ACS with consistent symptoms or signs on ECG or stent thrombosis at angiography.

A total of 48,282 patients were enrolled, with 10,360 (21%) having hsTrop concentrations above the 99th percentile and meeting criteria for myocardial injury at presentation. 1,771 (17%) patients had not been initially identified by the standard troponin assay and were reclassified based on the hsTrop. At one year, 2,586 (5%) patients overall had MI or cardiovascular death. Patients who demonstrated myocardial injury by troponin level were more likely to meet the primary outcome, although there was no difference in rate of primary outcome between implementation or validation phase. Of the 1,771 patients reclassified with myocardial injury by hsTrop, only a third were diagnosed with subsequent myocardial infarction, but these patients were more likely to undergo coronary angiography (11 vs 4%) without increase in percutaneous coronary intervention, be prescribed additional anti-platelet therapy, ace inhibitors, statins, and/or beta-blockers, and had a longer hospital stay. In patients without evidence of myocardial injury, the duration of hospital stay was decreased from a median of seven to four hours.

Some caveats to the study findings include its before-and-after study design, which may include inherent confounding from changes in practice or treating physicians at the various locations over time. Also, some argue that the benefits of additional medical therapy may not be seen within a year’s follow-up, leading to premature acceptance that there was no decrease in primary outcome. The authors also comment that they did not make adjustments to the threshold for renal dysfunction. Identification of higher risk patients with positive hsTrops did not translate to improved outcomes in this study, but the data leaves room to speculate on improved ability to discharge from the ED.

The use of high sensitivity troponin pathways or protocols appear to circumvent some of the pitfalls of isolated hsTrop testing. The current data suggests a higher number of patients may be able to be discharged safely from the emergency department which may be able to lower health care costs, but the high sensitivity of the test puts physicians and patients at risk of increased testing, medication, and cost without apparent benefit. Research suggests that a result below the level of detection can effectively rule out ACS in emergency department visits regardless of underlying historical risk factors, however the small percentage of patients in which these levels occur limit the test’s utility in busy EDs, where confounding factors such as the presence of chronic kidney disease lead to an elevated level of high sensitivity troponin regardless of the patient’s underlying cardiac pathology. A variety of testing algorithms appear to suggest that serial testing in the emergency department with a high sensitivity troponin or use in conjunction with other cardiac testing such as advanced coronary CTA can lead to even better specificity than traditional methods while maintaining tremendous sensitivity for acute coronary syndrome. Serial testing algorithms may allow EM physicians to eliminate the subjectivity of currently accepted clinical risk stratification scores, such as the HEART score while combined use with coronary CTA may be able to recategorize intermediate risk patients to allow for discharge from the emergency department rather than admission. For the moment, however, the lack of an established laboratory standard, limited prospective data, and current ease of use and widespread acceptance of the HEART score limit the current implementation of the high sensitivity troponin.

Current data on high sensitivity troponin pathways suggest they may be able to offer a more simplified and objective approach to ACS evaluation. However, due to the confounding factors of hsTrop, these pathways are not ready for general use and much more data is needed before widespread adoption can be considered.


1. U.S. Food and Drug Administration. 510(k) Premarket Notification. https://www.accessdata.fda.gov/scripts/cdrh/cfdocs/cfPMN/pmn.cfm?ID=K162895. Accessed February 19, 2019.

2. Giannitsis E, Kurz K, Hallermayer K, Jarausch J, Jaffe AS, Katus HA. Analytical validation of a high-sensitivity cardiac troponin T assay. Clin Chem. 2010;56(2):254-61.
3. Roffi M, Patrono C, Collet JP, et al. 2015 ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation: Task Force for the Management of Acute Coronary Syndromes in Patients Presenting without Persistent ST-Segment Elevation of the European Society of Cardiology (ESC). Eur Heart J. 2016;37(3):267-315.

4. Chapman AR, Anand A, Boeddinghaus J, et al. Comparison of the..
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Image Credit: Common Sense
Author: Molly Estes, MD FAAEM
YPS Board of Directors
Originally published: Common Sense January/February 2019

We’ve all seen our waiting rooms on an “average day.” And we’ve all read the studies about annual census numbers. And we all dread every approaching flu season with increasing levels of anxiety as we try to imagine seeing even more patients with no beds or room to speak of. And in the middle of the administration meetings about flow, setting up tents and triage units in parking lots and hallways, and trying to prevent patients from dying in the waiting room, those of us who work at academic institutions are also expected to impart our hard-fought knowledge onto the next generation. Now how in the world is that possible?

For those who work in academics, we tend to have some kind of special soft spot for the learner, whether that be a medical student, PA or nursing student, EM or off-service resident. Part of us likes the challenge of trying to get our learner to understand a concept and takes joy when the lightbulb moment of realization occurs. And yet, we are under ever increasing pressure to move our departments, to see higher and higher patient volumes and meet door-to-disposition times. One would think that these two desires, to do well at our jobs and to fill the role of teacher, to be in opposition to each other. After all, explaining something to another person takes longer than just doing it yourself. There is some truth to this, it does take extra time to engage in the teaching process. But I would like to make the argument that it doesn’t have to completely disrupt your day. Here are some tips and tricks to continue your instructor legacy while making hospital admins happy.

Think bigger, teach smaller.
When presented with a broad topic, most of our inclinations is to settle in to a thorough explanation. “What is on your differential for chest pain? Well, let me tell you about the six can’t-miss differential diagnoses for chest pain, compare and contrast PERC and Wells, explain how the HEART score relates to cardiac events, and discuss patient disposition depending on access to stress testing.” In the busy department, this is waaayyy too much information and takes too much time. Instead, try breaking your go-to lectures into mini, bite-sized pieces. Piece #1: what are the absolutely top, 100% can’t miss diagnoses for chest pain? Piece #2: what is the HEART score? Piece #3: how is the HEART score calculated? By doing this, you can stretch one single massive discussion into tiny pieces that take no longer than 60 seconds each to discuss.

Teach one person and then have them teach the next. 
See one, do one, teach one, is still a mantra of emergency medicine. Why shouldn’t we also apply it to teaching? Especially in a department with a mix of residents and students, this can be a valuable technique for getting more distance out of a single teaching moment. Take one to two minutes to explain to one learner your teaching point. Then, when another learner needs the same information, call out your first learner to teach it to them. It will reinforce your teaching as well as save you a few minutes until you can cross-check their explanation. Rally the troops. If a great case rolls through the door, capitalize on a few minutes to do a general teaching session. Quickly call for all your learners in the vicinity, spend two to three minutes talking about what makes this presentation, lab result, image, etc. so special, then send everyone on their way. You will save time in trying to share the awesomeness on an individual level.

Have a handout or picture.
The saying, “a picture is worth a thousand words,” absolutely applies to many standard teaching topics. Find a blog or podcast about one of your favorite teaching topics. For example, Life In The Fast Lane’s blog post on how to read a chest X-ray. Then, when presented with the chance to discuss the topic, refer your learner to the post, handout, picture, etc. You can briefly discuss the topic afterwards, but it won’t take as much time as teaching de novo.

Have the learner look it up.
The tried and true method of high school teachers everywhere. There is nothing wrong with encouraging your learner to find the answer to their question themselves. Check their results but have them teach themselves.

Assign “homework.”

Inevitably one of your learners will find a broad topic or complex management question that is simply impossible to address in the middle of a busy shift. In that case, it is completely fine to admit you don’t have time to discuss the answer. Give them the short pearl of knowledge, then ask them to look up or read more about it after the shift. You can even refer them to a journal article, blog post, or book chapter that you yourself have used to learn the topic. Then you can continue the discussion either on your next shift, next conference day, or via email. This way you encourage their learning while giving the time needed for the complexity of the topic.

Hopefully these ideas will help you fulfill your teaching role at the same time as helping you keep your sanity in the midst of the ever-crazier months to come.
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Image Source: Pexels
Author: Madhu Hardasmalani, MD FAAEM
AAEM Physician Wellness and Burnout Prevention Committee
Originally Published: Common Sense November/December 2017

Resilience is the ability to bounce back from an adverse life situation. Some individuals are born with this trait and we are all envious. However, the majority of us need a little help. Even those individuals with the inborn resilience trait, need help maintaining it.

Now having and maintaining this trait is not very simple — there is no magic “resilience pill.” The key is lifestyle changes, which may initially be a bit daunting, but can better equip us to meet life’s challenges head on without breaking down.

The basic lifestyle factor is diet. You are what you eat. What you eat effects how you will feel. Eat junk, feel junk. Eat healthy, feel healthy. It’s as simple as that.

Making healthy “clean” food choices should be a priority. Including more fruits and vegetables and less red meat in our diet is known as the “Mediterranean diet” which is known to be anti-inflammatory and is the key in maintaining healthy physical and mental health.[1] Junk food is processed food. Processed meats and frozen entrees that we grab-and-go are heavily laden with pesticides, endocrine disruptors, and poorly laden with nutrients. This will soon make our bodies nutrient deficient and when this happens symptoms of anxiety, feeling overwhelmed, and depression develop.

An important food component that is detrimental to our brain health is sugar.[2] Sugar, especially the simple sugars such as glucose, cause rapid increase in blood sugar are very inflammatory to every cell including neurons. Complex sugars, on the other hand like beans, lentils, sweet potatoes are beneficial because they do not cause acute rise of blood sugars and hence less inflammation.

So, making this choice of not consuming processed and sugar laden foods but instead spending a little time doing some grocery shopping and cooking is investing in long-term physical and mental wellbeing. And this wellbeing will translate to longevity of our careers. Isn’t this what we want?

In addition to eating wholesome foods, are there any food/supplements that can help us maintain our body and mind? Few supplements are proven to support our mind and body effectively.

One of these is probiotics. Probiotics are healthy bacteria or actually life enhancing bacteria. These bacteria are present in our digestive tracts in abundance, about 100 trillion of them. These not only line up our GI tract intestinal walls, but research has now proven that these little creatures secrete substances that are transported to the brain where they exert anti-anxiety, anti-depressive effects. This gut-brain connection is truly a two way street.[3] In fact this is the basis of nutritional psychiatry — an exciting new field to manage mental disorders. Their presence in each of us is individualized and is based on genetics, diet, age, and guess what? Stress! So even if we are born with the most robust microbiome, the stress we experience, especially circadian disruption, can kill tons of these. It is important to replenish these little bugs with probiotics. Now probiotics can be in the form of supplement but better is food. Foods like plain yogurt, not the sugar laden “fruit at the bottom” kind, unsweetened kefir, fermented foods like kimchi, sauerkraut, and pickles all will replenish our microbiota so that we function optimally. If getting these healthy probiotics feels like a chore, then by all means at least take the supplement which there are plenty in the market.

Another nutrient that is essential for our brain health are fatty acids. Now for decades we were made to believe that fats are bad for us but sugars are ok. Now since the research has been exposed, we know that the reverse is true. Fats are good for us. In fact phospholipids form the wall of each and every cell in our body. By fats, I mean healthy fats, both saturated and unsaturated in moderation. Trans-fats are pro-inflammatory and are bad fats, but good fats are olive oil, butter, coconut oil, avocados and ghee. So don’t eliminate fat from your diet but consume these good fats in moderation and improve cognition and emotional health.

Brain is 80% lipids and 30% of these lipids are polyunsaturated fatty acids (PUFA) and these are known to significantly modulate our neuronal function. These PUFA are essential (EFA) since these are exclusively obtained from our diet. Omega 3 primarily the DHA and EPA and Omega 6 mainly arachidonic acid are the principal CNS EFA’s. Both Omega 3 and 6 are essential but the ratio needs to 3:1; unfortunately, our typical western diet has significantly reversed this ratio and hence the rise of mental illness in our country. Bottom line, increase intake of Omega 3 fatty acids.[4] These acids are abundantly found in fish, walnuts, chia and flax seeds. Include these rich foods in your diet for healthy brains.

In summary, what you eat is how you feel. Include a rainbow of fruits, vegetables, unprocessed grains and fish in your diet. Supplement with probiotics and essential fatty acids.


1. Anti-inflammatory effects of the Mediterranean diet: the experience of the PREDIMED study, Estruch R, Proc Nutr Soc 2010, Aug69(3):333-40

2. Sugar- and artificially sweetened beverages and the risks of incident stroke and dementia, A prospective cohort study, Matthew P Pase et al, Stroke April 2017.

3. The Gut Microbiome and the Brain, Leo Galland, Journal of Medicinal Food, J Med Food, Dec 2014;17 (12), 1261-1272.

4. Essential Fatty Acids and the Brain, Marianne Haag, Can J of Psychiatry, Vol 2003;48: 195-203.
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Image Credit: Common Sense
Author: Ashely Alker, MD MSc
AAEM/RSA 2017-2018 President

Whether it is Women in EM (WiEM), AWAEM, FeminEM or Shemergency, women in emergency medicine are uniting to advance shared goals, including equal pay and access to leadership opportunities. This comes at a time when women across many disciplines, from Hollywood actors to D.C. politicians, are standing up against inequality.

Women have been undervalued since before they entered the workplace. A Washington Post article determined that the value of a homemaker’s labor is equivalent to an annual salary of $96,261.[1] This is not an inconsequential sum, as the United States Census Bureau quotes the median household income as $55,322.[2] Meanwhile, a woman with an advanced degree earns $65,000, which is $30,000 less than the median income of a man with the same degree.[3]

Today, the reality is that despite 75% of the health care labor force being women, only 26% of hospital CEOs are women.[4] Moreover, a 2016 survey of Fortune 500 health care companies showed women make up only 21% of executive roles and 21% of board members.4 Men and women are far from equal in the workplace.

It is essential to recognize and overcome the insidious sentiment that opposes true gender equality: fear. For example, one may fear that increased women in leadership roles means that men must lose leadership opportunities. And from a place of fear come falsehoods concerning men being superior leaders to women.

A recent Critical Care Medicine Article, “Influence of Gender on the Performance of Cardiopulmonary Rescue Teams,” exemplifies this false narrative. This article concludes that female code leaders did not perform as well as male code leaders. A critical care powerhouse team across three specialties from the University of California, San Diego, including emergency medicine’s Radhika Sundararajan, MD PhD, wrote a forceful rebuttal. The rebuttal evaluated the study’s serious systemic flaws, including the use of medical students with no code experience as code leaders, and equating assertiveness with leadership. Cognizant of the repercussions from bad research linking vaccines and autism, we must be critical of all research-drawn correlations, especially those which propagate negative stereotypes.

It is important to acknowledge we still live in a patriarchal society, from the simple convention of a woman taking a husband’s last name to the male predominance in our leadership. We are assigned our gender roles and without realizing it, we become accustomed to sexism. However, recent events, including the social media #metoo and #dresslikeawoman campaigns, demonstrate that our society is demanding a new normal. The most qualified candidate should get the job, but this necessitates open access resources and opportunities to bring forward the most competent candidates from all backgrounds. This is the philosophy of emergency medicine gender equality guru, Dara Kass, MD FAAEM.

Sceptics Guide to Emergency Medicine (SGEM) deemed 2017 the year of females in emergency medicine, with the number one slot going to Dara Kass, MD FAAEM, the driving force behind FeminEM. One of the crowning achievements of FeminEM being the FeminEM Idea Exchange (FIX conference), held October 2017 in New York City. The RSA Diversity and Inclusion Committee was excited to host the resident networking coffee hour event at FIX. The FIX conference boasted speakers from many backgrounds, enthusiastically including men. Talks highlighted overcoming imposter syndrome, leadership, finance, branding, maternity leave, and mentorship.

RSA’s podcast also interviewed Dr. Kass, who stated FeminEM was created because there was, “no place to park the issues related to women in emergency medicine consistently that was not governed by an overarching organization.” When Dara Kass speaks about equality, she purposefully includes both men and women in the discussion, stating that one of her worst days in academic medicine was “seeing my resident at work 24 hours after his wife gave birth and their baby was under bili lights.” Dr. Kass calls for options-based solutions for both men and women. “There is no right way to be a physician. Anyone can choose to be at home or at work, but the decision should be yours.” What is Dr. Kass’ ultimate goal for the FeminEm organization? “For there to be no need for it to exist.” Because that means we are truly equal.

RSA has many opportunities for you to support equality in emergency medicine through our Diversity And Inclusion Committee, and the Women in EM (WiEM) Committee. Or, just start by listening to our FeminEM podcast with trailblazer, Dara Kass, MD FAAEM. The next FeminEM FIX conference will take place October 16-18, 2018, in New York City.

1. D'Arcy, Janice. “A Homemaker's Real Salary.” The Washington Post, WP Company, 1 Feb. 2012, www.washingtonpost.com/blogs/on-parenting/post/a-homemakers-real-salary/2012/02/01/gIQAh7czhQ_blog.html?utm_term=.037d5ce26f63.

2. Bureau, US Census. “Search Results.” Results, 18 Apr. 2015, www.census.gov/search-results.html?q=medain%2Bhousehold%2Bincome&search.x=0&search.y=0&search=submit&page=1&stateGeo=none&searchtype=web&cssp=SERP.

3. Generational Earnings and Education. Unites States Census Bureau, 3) https://www.census.gov/content/dam/Census/library/visualizations/2016/comm/cb16-203_graphic_earnings_education.pdf.

4. Castellucci, Maria. “Inequality in the C-Suite Has Gotten the Attention of Healthcare Organizations Looking to Diversify.” Modern Healthcare, 25 Feb. 2017, www.modernhealthcare.com/article/20170225/MAGAZINE/302259983www.modernhealthcare.com/article/20170225/MAGAZINE/302259983.
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Image Credit: Heather Star Krause, MD MPH(c)
Author: Heather Star Krause, MD MPH(c), 2019 EM Residency Candidate
AAEM Diversity and Inclusion Committee
Originally Published: Common Sense November/December 2018

In the bend of the south Texas coast, a community comes together to reflect on a year gone by since
many lost everything. We danced in the streets, honored one another’s hardships and congratulated each other’s resilience, and I reflect on my own experience.

The last move my husband and I made before evacuating with our toddler and seven-month-old was to throw an anchor from our sailboat, sitting on its trailer, in the front yard, a hundred feet from the water’s edge. “Maybe that will keep her from surfing into the neighbor’s second story living room,” my husband half-heartedly joked as he climbed into our small RV, wet from the first bands of the storm blowing ashore. At 5:30am, we left our home, driving in 20-minute shifts, exhausted from a day and a night of increasingly frantic preparation. Less than 12 hours later, the eye-wall of Hurricane Harvey made landfall directly on our small hometown of Rockport, Texas.

We returned to “The Charm of the Texas Coast” two days after the storm. Half of the structures were damaged beyond repair, the electrical grid was a tangle of wires and snapped poles, there was no running water, and overnight there was a new homeless population. The nearest hospital was destroyed and the majority of doctors’ offices closed due to damage. Rockport (Aransas County), Texas, was already designated a Medically Underserved Area. Like so many coastal communities, it is a glaring example of wealth inequality and social stratification; vacation homes and trailer homes. The storm’s destruction exacerbated an already failing safety net of health care and left our vulnerable population struggling with added mental and physical stress, financial devastation, and decreased access to primary care resources. It was obvious that the community needed a local medical response. After a short and self-guided course on legal protections for volunteer medical professionals in disaster zones, approval from the city Emergency Manager, and crucial support, both on the ground and remote, from a small group of graduates of the Latin American School of Medicine, I founded the Rockport Strong Mobile Medical Unit (RSMMU). For four months, RSMMU served as a pop-up urgent care clinic, staffed with volunteer physicians, nurses, and
community health workers, operating out of the same RV in which my family had evacuated. Working alongside Emergency Management and FEMA, we provided free medical attention to over 400 patients.

Our team conducted a survey analysis to determine some characteristics of the population seeking our services. Some of the more important questions we asked our patients were if they had a primary care provider (61.5% reported they did not) and if they had health insurance (68% said no). And to the question, “Do you use the ED as your primary care provider?” 34% said they did. Of note, 74% of patients reported negative effects of the storm on their physical and/or mental health. The stories of the people represented in these figures were just as disconcerting: “I lost everything. I didn’t qualify for assistance. I don’t have a spare dollar to my name. My house is molding. I can’t afford my prescriptions.”

A year later, tattered blue tarps fail to cover the holes in roofs spaced throughout the community. Whose roof, though? Well, this is a diversity and inclusion column, so I bet you can guess. First, let’s talk about disaster vulnerability and how social conditions and location lend to the potential for greater harm to some social groups during a disaster and in the immediate aftermath. Social class factors force the poor to live in substandard housing, often located in physically vulnerable areas such
as flood zones and in proximity to industrial sites, and reduce the ability to undertake loss-reduction measures (boarding windows, stockpiling supplies). In the U.S., race and ethnicity are strongly correlated with social class and are also associated with increased vulnerability to disaster.[1]

In the intermediate phase of disaster recovery, the same differential presents itself. Research conducted in the months following Hurricane Harvey found that the population affected differs by geography, race/ethnicity, and income, the largest impact felt by Blacks, Hispanics, and those with a self-reported income <100% FPL.[2] Loss of income and employment disruption had a larger effect on Hispanic, Black, and lower-income residents. Among those with home damage, low-income, Black and Hispanic residents were less likely to have had insurance. Blacks and low-income residents also reported in higher percentages that they were not getting the help they needed. Language barriers arose as a contributing factor to sluggish recovery. Three in ten individuals answering a survey in Spanish reported that it was very or somewhat difficult to find information in Spanish regarding recovery assistance. The study also conveyed that undocumented migrants are particularly vulnerable to the effects of natural disasters, in part out of fear of exposing themselves or family member’s immigration status, and in another part due to ineligibility for benefits.

Now let’s look at long-term recovery and what has recently come to light. A study published in August (2018) concludes that wealth inequality increases along the lines of race, education, and homeownership in counties badly hit by natural disasters.[3] In areas with at least $10 billion in damages, Black, Hispanic, and Asian communities saw their wealth decrease by an amount between $10,000 and $29,000, while white communities increased their wealth by an average of $126,000. The study suggests that the money follows the higher levels of reinvestment via infrastructure improvements and low-interest loans after a disaster occurs, as more privileged residents gain access to new resources. Meanwhile, low-income and non-property owners are more likely to experience financial strain from losing one’s job, moving, paying higher rents due to housing shortages, and depleting savings trying to compensate. Contrary to an often repeated myth, this data does not support the idea of disasters being “great equalizers.” It does however bring attention to the fact that for some people the resources which flow into disaster zones can be a silver lining to a universally bad situation. I witnessed this in Rockport as it became a temporary boomtown for construction contractors, clean-up crews, and donation sites across town. The issue is that the silver doesn’t seem to be making it into all folk’s pockets, especially for people of color.

What can we do? Disasters are great disruptors, and where there is disruption, there is room for innovation. After Hurricane Mitch slammed Honduras in 1998, Cuba responded by founding an international medical school, The Latin American School of Medicine (Escuela Latinoamericana de Medicina), designed to train doctors from lesser-developed countries, mostly people of color, who would return to their medically underserved area when they graduate so that these communities would be healthier and more prepared for disasters in the future. This plan obviously took a very long view of disaster response, as the first graduates would have returned home some seven years after Mitch made landfall. It’s an example of a long-term disaster response that promotes inclusion and diversity in terms of both the medical profession and access to health care. The free mobile clinic in Rockport was a much smaller and shorter-term response, but was still a successful innovation
that brought resources to a medically underserved disaster zone. It is a model that can easily be recreated when the need presents.

The scientific community warns us that our warming planet will make high-magnitude weather events like hurricanes Katrina, Harvey, and Maria more frequent over the coming years. What does this mean for the health of communities of color exposed to these forces of destruction? Unfortunately, if disaster recovery maintains the pattern of reinforcing gaps in wealth along racial lines and the strong correlation between socio-economic status and individual health is also maintained, it’s likely that the health of communities of color will disproportionately suffer. While the issues are systemic, there are roles that individual physicians can take to immediately address some of the social determinants of health at play in post-disaster communities. Here are three suggestions:

  1. Set up a free clinic or volunteer to staff if one is already operating.
  2. Consider in-kind donations of medical equipment.
  3. Get involved with Emergency Management and advocate for the funding of programs that will improve access to health care (a community health center, for example).
Innovate. We need to change the trajectory of who gets to recovery from a disaster. The resilience and diversity of our communities depend on it.

1. Tierney, Kathleen. (2006). Social inequality, hazards, and disasters. On Risk and Disaster: Lessons from Hurricane Katrina. 109-128.
2. Hamel, L. et al. (2017). An Early Assessment of Hurricane Harvey’s Impact on Vulnerable Texans in the Gulf Coast Region: Their Voices and Priorities to Inform Rebuilding Efforts. Kaiser Family Foundation and Episcopal Health Foundation. http://www.episcopalhealth.org/files/7315/1240/4311/An_Early_Assessment_of_Hurricane_Harveys_Impact.pdf

3. Junia Howell, James R Elliott. (2018). Damages Done: The Longitudinal Impacts of Natural Hazards on Wealth Inequality in the United States, Social 2Problems, spy016, https://doi.org/10.1093/socpro/spy016
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Image Credit: Wikipedia
This post was peer reviewed.
Click to learn more.

Author: Mary E. Blaha, DO
Indiana University School of Medicine
AAEM/RSA Publications and Social Media Committe

Calcium channel blocker (CCB) overdose is a potentially lethal toxicity with multiple management options available. Intravenous lipid emulsion (ILE) therapy is a potential treatment that is being used with more frequency. This review will discuss the management of CCB overdose focusing on the available ILE literature.

CCB Toxicity Overview
CCBs are commonly prescribed to manage hypertension and arrhythmias. When implicated in accidental or intentional overdose, CCBs carry a high potential for toxicity that can ultimately lead to severe cardiovascular injury.[1,2] Specificlly, dihydropyridine CCBs, which include amlodipine and nicardipine, act primarily on arterial smooth muscle L-type calcium channels, which can lead to reflex tachycardia. Nondihydropyridine CCBs, which include diltiazem and verapamil, act primarily on cardiac myocyte L-type calcium channels, which can lead to cardiogenic shock.
Therapies Used in CCB Overdose
Because CCBs are so dangerous when ingested in overdose, emergency medicine physicians should be well-versed in treatment options.[3]
  • Atropine (often tried first)
  • High-dose insulin with intravenous dextrose
  • Glucagon
  • Intravenous calcium
  • Pacemaker placement
  • Vasopressors with beta-1 agonist activity
  • Extracorporeal Membrane Oxygenation (ECMO)
  • ILE
ILE: Suggested Mechanisms of Action
ILE consists of phospholipids, glycerin, and soybean oil and is used in parenteral nutrition.[2] Although classically used as an antidote for local anesthetic poisoning, it has been tried as a treatment in toxicity of lipophilic drugs such as CCBs. Potential ILE mechanisms include the following:
  • Lipid sink theory: ILE introduces a lipid phase in the blood, forming a concentration gradient to pull toxic drugs from tissues.[2]
  • Enhanced metabolism theory: ILE acts as an energy source for myocytes under toxic conditions.[4]
  • Positive inotrope theory: ILE opens voltage-gated calcium channels, leading to increased cardiac contractility.[5]
  • ILE provides cardioprotection from cell damage.[6]
ILE dosing
The optimal dosing for toxicities caused by drugs other than local anesthetics has not been determined and there are conflicting recommendations. Micromedex recommends a 1.5 mL/kg of 20% lipid emulsion (Intralipid) bolus given over 2-3 minutes followed by a continuous drip 0.25 mL/kg/min[7]

When Should ILE be Used in CCB Overdose and is it Effective?
There is limited guidance from animal studies, observational studies, and case reports on the utility of ILE in CCB overdose. The literature is conflicting, with mixed reports of successes and failures, and reports of failure outnumber the reports of success. Much of the literature recommends ILE only after trying standard treatments or in extreme cases. In case reports, ILE was usually administered after other treatments were tried and it is difficult to determine whether there is a synergistic effect with other therapies on board.[8-11] Clinical toxicologists recommend ILE therapy if the patient is refractory to first-line treatments, in refractory shock, and in periarrest situations.[12] Evidence-based recommendations put forth in Clinical Toxicology state that ILE should never be used as a first-line therapy in CCB overdose.[13]

As with anything in medicine, there are potential side effects of using ILE, including acute respiratory distress syndrome (ARDS), pancreatitis, allergic reactions, and fat overload syndrome. ILE administration can cause interference with laboratory results including complete blood count (CBC), lipid studies, troponins, electrolytes, and liver transaminases. ILE may also interfere with beneficial therapies such as vasopressors, insulin, and ECMO.[10,13]

CCBs are commonly prescribed drugs that can be extremely harmful in overdose. There are many ways to treat these kinds of overdoses. The data remains inconclusive about the effectiveness of ILE and expert recommendations are weak due to the lack of robust clinical trials. Based on review of the literature, it appears to be acceptable to start ILE in a critically-ill patient with CCB overdose once other treatments have been utilized. If unsure, do not hesitate to consult specialists.


1. Kang C, Kim D, Kim S, et al. The effects of intravenous lipid emulsion on prolongation of survival in a rate model of calcium channel blocker toxicity. Clin Toxicol. 2015;53(6):540-4.

2. Kryshtal D, Dawling S, Seger D, Knollmann, B. In vitro studies indicate intravenous lipid emulsion acts as lipid sink in verapamil poisoning. J Med Toxicol. 2016;12(2):165-71.

3. Rietjens S, De Lange D, Donker D, Meulenbelt J. Practical recommendations for calcium channel antagonist poisoning. Neth J Med. 2016;74(2):60-7.

4. Muller S, et al. Intralipid emulsion rescue therapy: emerging therapeutic indications in medical practice. J La State Med Soc. 2016;168(3):101.

5. Murphy C, Williams C, Quinn M, et al. Pilot trial of intravenous lipid emulsion treatment for severe nifedipine-induced shock. J Med Toxicol. 2016;12(4): 380-5.

6. Walter E, McKinlay J, Corbett J, Kirk-Bayley J. Review of management in cardiotoxic overdose and efficacy of delayed intralipid use. J Intensive Care Soc. 2018;19(1):50-5.

7. IBM Micromedex Drug Reference: Verapamil. Greenwood Village, CO: Truven Health Analytics; 2019. https://www.micromedexsolutions.com. Accessed January 28th, 2019.

8. Mithani S, Dong K, Wilmott A, et al. A cohort study of unstable overdose patients treated with intravenous lipid emulsion therapy. CJEM. 2017;19(4):256-64.

9. Karbek Akarca F, Akceylan E, Kıyan S. Treatment of amlodipine intoxication with intravenous lipid emulsion therapy: A case report and review of the literature. Cardiovasc Toxicol. 2017;17(4):482-6.

10. Smolinske S, Hoffman RS, Villeneuve E, et al. Utilization of lipid emulsion therapy in fatal overdose cases: an observational study. Clin Toxicol. 2018;27:1-6.

11. St-Onge, M, Anseeuw, K, Cantrell FL, et al. Experts Consensus Recommendations for the Management of Calcium Channel Blocker Poisoning in Adults. Crit Care Med. 2017;45(3):306-15.

12. Gosselin, S, Stellpflug, S, Hayes, B, et al. Evidence-based recommendations on the use of intravenous lipid emulsion therapy in poisoning. Clin Toxicol. 2016;54(10):899-923.

13. Martin C, Gonzalez H, Ruiz S, Ribes D, Franchitto N, Minville V. Acute respiratory distress syndrome following verapamil overdose treated with intravenous lipid emulsion: a rare, life-threatening complication. Ann Fr Anesth Reanim. 2014;33(6):e101-2.
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Authors: Ted Segarra, MD; Taylor Conrad, MD; Rithvik Balakrishnan, MD; Taylor M. Douglas, MD
Editors: Kami Hu, MD FAAEM and Kelly Maurelus, MD FAAEM
Originally published: Common Sense March/April 2019

Respiratory distress is a common presentation in both the pediatric and adult emergency department (ED). Community acquired pneumonia (CAP) is a common cause for this distress, and carries the potential for high morbidity and mortality if inadequately treated. In a fast-moving and potentially resource-limited ED, however, it can sometimes be difficult to decide which patients require further imaging to differentiate CAP from the myriad of other potential etiologies for respiratory distress such as bronchiolitis, asthma, chronic obstructive pulmonary disease (COPD), heart failure, and pulmonary embolism. Although both the British Thoracic Society (BTS) and Infectious Disease Society of America (IDSA) state that bacterial CAP is a clinical diagnosis based on persistent fever, retractions, and tachypnea, they agree that radiographic imaging should be obtained in any patient requiring hospital admission or with significant clinical uncertainty.[1,2] Unfortunately, even if the ED provider decides to pursue chest X-ray (CXR) imaging, he or she may still miss the diagnosis, as CXR has been shown in several studies to have a notable false negative rate (FNR) and high inter-observer variability in the diagnosis of CAP.[3,4,5,6] The limitations and inherent radiation exposure of CXR, in combination with the increasing availability of and familiarity with bedside lung ultrasound (LUS) imaging, have prompted many ED physicians to begin looking to LUS as a potential alternative in the evaluation of patients with suspected CAP.
  1. What is the level of sensitivity and specificity of LUS compared to traditional CXR and clinical findings in the diagnosis of CAP?
  2. Do other aspects of bedside LUS (i.e. lack of ionizing radiation, speed of assessment, easy repeatability, ability to monitor progression of disease, cost) make LUS a more feasible alternative in resource-limited environments?
Patel CJ, Bhatt HB, Parikh SN, et al. Bedside lung ultrasound in emergency protocol as a diagnostic tool in patients of acute respiratory distress presenting to emergency department. J Emerg Trauma Shock. 2018;11(2):125-9.
Studies have shown that ultrasound has the capability to diagnose pneumonia along with many other thoracic pathologies, and several researchers have worked to design and study a standardized approach to lung evaluation, especially in the critically-ill patient.[7] The bedside lung ultrasound in emergency (BLUE) protocol is an attempt at creating this standard approach that, in prior studies, has been shown to have a diagnostic accuracy of approximately 90%.[8,9] This process defines characteristics of different profiles that represent various disease states. Four anterior upper and lower left chest points are used, along with the posterolateral alveolar and/or pleural syndrome (PLAPS) point, which is essentially the posterolateral lung base. Several characteristic profiles are described and are listed in Table 1. The ultrasound findings that make up these characteristics include the following: A-lines, B-lines, absence or presence of lung sliding, lung point, C-lines or consolidated lung, PLAPS (presence of small pleural effusion and/or lung consolidation at the PLAPS point), and the presence of venous thromboembolism. The application and resulting pathologies associated are described in Figure 1.

Table 1: The characteristics of each profile.[7]
Figure 1: BLUE Protocol starting with evaluation of the four anterior points.
VTE is venous-thromboembolism. Adapted from Lichtenstein.[7]
Patel, et al., attempted to replicate the prior BLUE protocol studies to determine the accuracy of the protocol when applied in the ED. This study was a small (n = 50), prospective observational study with patients over the age of 12 admitted to the intensive care unit (ICU) with acute respiratory distress. The patients were enrolled over a span of two months. The ED provider responsible for the ED care and disposition was the ultrasonographer; ICU teams were blinded to the ultrasound results and images. The prior mentioned BLUE protocol was utilized, and the patient’s ultimate diagnosis was compared to the initial presumptive diagnosis determined by the protocol. Non-standardized means of determining the final diagnosis were used and included patient history, treatment response, laboratory findings, X-rays and computed tomography (CT) scans. Specifically for pneumonia, when all profiles were considered, the authors report a sensitivity (Sn) of 94.1% and specificity (Sp) of 93.9%, corresponding to a positive likelihood ratio of approximately 15. The results were similar to prior findings by Lichtenstein and Dexheimer.[8,9]

This study is important in its attempt to replicate the results of previous studies and determine the protocol’s applicability in the ED. Numerous limitations exist, however, severely dampening any potential impact this study might have. The small size and fact that it is at a single center limits its generalizability. Additionally, the fact the ultrasonographer is also the treating ED provider introduces multiple biases and likely influences the future diagnosis, which in this study had no standardized method of being concluded. It is also important to note that only ICU patients were evaluated. Nevertheless, the bottom-line argument that LUS is an ever increasingly useful tool likely still holds. It is important to continue research into the utility of ultrasound and its application as a rule-in diagnostic tool for pneumonia and other lung pathologies.

Balk DS, Lee C, Schafer J, et al. Lung ultrasound compared to chest X-ray for diagnosis of pediatric pneumonia: a meta-analysis. Pediatr Pulmonol. 2018;53(8):1130-9.
Balk, et al., performed a systematic review and meta-analysis to compare the accuracy of LUS to CXR in the diagnosis of pediatric community acquired pneumonia (pCAP), searching PubMed, EMBASE, and Web of Science using the keywords “pneumonia,” “lung ultrasound,” and “pediatric population.” The authors required that these studies include pediatric patients, assess for bacterial pediatric CAP (pCAP), use both CXR and LUS, and use a gold standard of expert pediatrician clinical diagnosis for the ultimate diagnosis of pCAP. They initially identified 784 potential studies, which were then further screened and narrowed using Preferred Reporting Items for Systematic Reviews and Meta-analyses (PRISMA) followed by a 14-item Quality Assessment of Diagnostic Accuracy Studies (QUADAS) tool to screen for relevant and unbiased studies. A final 12 studies including 1510 patients were ultimately selected for data extraction, and the authors used Freeman Tukey transformation of the data to calculate Sn, Sp, positive predictive value (PPV), and negative predictive value (NPV). Heterogeneity was assessed using Forest plots and calculations of inconsistency (I2) and Cochrane Q.

The 12 studies spanned 10 years (2008-2017) with a majority being prospective studies (9/12), half of which were from Italy with the remainder based in the USA, Turkey, India, Greece, Russia, and Taiwan. The study locations were equally split between the ED and inpatient floors. Four
studies relied solely on expert clinical diagnosis as the gold standard for pCAP, while the remaining eight studies used a combination of expert clinical diagnosis and CXR. In regard to the sonographic diagnosis of pCAP, all 12 studies used trained sonographers, eight of which used only experts. Of the remaining four studies, two did not specify sonographer experience level, one used novice radiologists, and one used both pediatric ED residents and expert sonographers. Ten studies used a 12-view lung evaluation, while the remaining two studies used an eight-view evaluation. LUS exams were considered positive for bacterial pCAP if they showed a) consolidation with or without air or fluid bronchograms (12 of 12 studies), b) focal B lines (4 of 12 studies), and c) pleural line abnormalities (1 of 12 studies).

The authors noted a significantly higher pooled Sn of LUS compared to CXR [95.5% (95% CI 93.6-97.1%) with no significant heterogeneity vs 86.8% (95% CI 83.3-90%) with significant heterogeneity]. Both LUS and CXR showed similarly high Sp (95.3% and 98.2%, respectively; with no significant heterogeneity between studies). There were no significant differences between LUS and CXR in PPV (99% and 99.6%, respectively) or NPV (63.1% and 43.6%, respectively).

Though overall a well-designed study demonstrating results consistent with prior literature, this meta-analysis contains a few notable limitations with regard to patient demographics and inter-study heterogeneity. All 12 study populations had a relatively high prevalence of disease and pretest
probability of pCAP, which likely explains the equally high PPVs and low NPVs across both study groups. This high prevalence of disease also limits extrapolation to populations without an equally high pretest probability of disease. In addition, since half of the studies were performed in Italy, the results may not be applicable to other patient demographics. Furthermore, there was notable heterogeneity between studies regarding both the clinical and sonographic diagnostic criteria of pCAP, which could skew the number of false positives and negatives. Despite these limitations, however, the authors found no significant heterogeneity in the final calculations of LUS Sn, LUS Sp, and CXR Sp, indicating that LUS may indeed be significantly more Sn in diagnosing pCAP, while sharing a similarly high Sp with CXR.

Amatya Y, Rupp J, Russell FM, et al. Diagnostic use of lung ultrasound compared to chest radiograph for suspected pneumonia in a resource-limited setting. Int J Emerg Med. 2018;11(1):8.
All studies prior to this one had been conducted in high- or mediumincome settings, and that factor spurred Amatya et al. to implement this method in Nepal. The importance of studying LUS in a resource-limited setting, in addition to the low generalizability of other research study results in this setting, is the truth that cheap, fast testing has a particularly important role when patients pay out-of-pocket and often must be transported by their family members for any tests ordered.

Criteria for inclusion in the study included age of 18 years or older with at least three of the following clinical characteristics: temperature >38°C, history of fever, cough, dyspnea, respiratory rate >20, and oxygen saturation <92%, in accordance with both the BTS and the European Society for Clinical Microbiology and Infectious Diseases (ESCMID) definitions of suspected CAP as well as criteria used in other studies.[2,10] After training physicians to perform LUS, they identified a convenience sample of patients with these characteristics whenever an ultrasound-trained physician was available. All enrolled patients received a Posterior-Anterior CXR as per usual care in this hospital and then also had a LUS exam and a CT scan of the chest (at no extra cost to the patient). Lateral views on X-ray were not included as they, in daily practice, incur an additional cost to the patient, further demonstrating the importance of cost in care in Nepal but also limiting the diagnostic value of the X-rays in the study.

A positive LUS exam was defined as the presence of unilateral B lines (A/B-profile) or subpleural lung consolidation (C-profile). Whether or not other BLUE protocol profiles were taught or evaluated is not mentioned, but these definitions are in accordance with the above and other BLUE protocol-based studies. Patients with positive radiologic exams were compared to patients with the same clinical characteristics who had negative radiologic exams. No comparison was made to patients who did not have the same clinical presentation, although this would be a valuable comparison due to the high prevalence of TB and chronic lung disease.

The incidence of pneumonia in the study, using CT as the diagnostic standard, was 71%, similar to rates seen in other studies. LUS demonstrated higher sensitivity for pneumonia than CXR (91 vs 73%, respectively, p=0.01) with no difference in specificity (61 vs 50%, respectively, p=0.62). Both CXR and LUS missed the same four cases of pneumonia, all in the middle of the lung parenchyma, deep to the pleura. The sensitivities of each modality are consistent with prior studies and meta-analyses in high-income and middle-income countries, however the specificities seen in this study are much lower, which the authors attribute to the higher prevalence of chronic lung disease and TB leading to more false positives. Importantly, LUS was faster (patients would not have to wait the two hours for transport, film acquisition, as well as preparation and interpretation of the image) and was performed at low/no cost to the patient, two factors that were not quantitatively measured but are inherent to LUS.

The major limitations of this study are its small size and inadequate power, convenience sample design, and lack of blinding of the ultrasonographers. It also left some questions unanswered regarding the design and results. One limitation in study design is that patients with these characteristics who presented when no trained physician was present were not identified or discussed, providing no evidence that this sample was not biased for an unidentified reason. Additionally, the lack of a lateral view potentially limited the performance of CXR, although inclusion of the lateral view would have increased cost to the patients, opposite the researchers’ goal. The authors also mention in the study protocol that if pneumonia was not clearly addressed in the radiologist interpretation then they were asked specifically to comment upon it. These studies could have been indeterminate or very obviously negative, however this distinction was not made or discussed so it is unknown if this would have affected results.

Notably, the study was not actually powered to evaluate specificity, so although there was no statistically-significant difference between the two groups, the outcome would perhaps change in a larger, appropriately powered study, and the authors also make a valid argument regarding false positives and subsequent lower specificity due to lung disease. They also admit their results are limited because they were in a single hospital in an urban area, but the same existing issues of out-of pocket costs, high pneumonia incidence, and high prevalence of chronic lung diseases and tuberculosis (TB) help make results seen in this setting applicable to other low-resource areas. Finally, one should consider the possibility that, in populations with a high prevalence of TB, it may be unwise to abandon CXR in favor of only LUS. This study, the first of its kind in a resourcelimited setting, provides a jumping-off point for future studies but does not represent definitive evidence that LUS for pneumonia will become the diagnostic method of choice in such areas.

While CAP and pCAP are considered clinical diagnoses, research and practice demonstrates that imaging is frequently used as an adjunct in cases with diagnostic uncertainty or unstable patients. LUS has most recently been proposed as a cheap, fast, bedside, radiation-free method to evaluate for CAP and pCAP. Various LUS criteria have been tested to determine what ultrasound characteristics should be used to diagnose CAP and pCAP, and the BLUE protocol has been demonstrated to be a well-defined set of criteria that could be used to standardize future research. The studies reviewed above present encouraging results, despite the heterogeneity and variability in clinical definition of CAP and pCAP, ability of ultrasonographers, and comparators (clinical decision vs CT vs CXR). The current research provides support for future studies into LUS as it compares to clinical decision-making, CXR, and CT as methods of identifying pCAP and CAP.

Now we return to the questions posed in the introduction:
1. What is the diagnostic accuracy of LUS compared to traditional CXR in the diagnosis of CAP?
The studies detailed in this article find LUS to have high sensitivity and specificity identifying CAP as compared to other modalities, such as CXR and clinical findings alone, but is dependent on sonographers’ level of experience and expertise. Specificity was lower in a resource-poor setting with high prevalence of other lung pathologies.

2. Do other aspects of bedside LUS (lack of ionizing radiation, speed of assessment, easy repeatability, ability to monitor progression of disease, cost) make LUS a more feasible alternative in resource-limited environments? 
While these aspects of LUS make it an intuitively more appealing alternative on the surface, no current studies quantitatively assess them, and considerations have to be made regarding the need for well-trained ultrasonographers as well as the diagnostic value of the CXR in cases of TB, another lung disease prevalent in resourcelimited environment. More research is needed to fully evaluate the impact of LUS replacing CXR in this setting.

1. Balk DS, Lee C, Schafer J, et al. Lung ultrasound compared to chest X-ray for diagnosis of pediatric pneumonia: a meta-analysis. Pediatr Pulmonol. 2018;53(8):1130-9.
2. Lim WS, Baudouin SV, George RC, et al. BTS guidelines for the management of community acquired pneumonia in adults: update 2009. Thorax. 2009;64:iii1-iii55.

3. Davies HD, Want EE, Manson D, et al. Reliability of the chest radiograph in the diagnosis of lower respiratory infections in young children. Pediatr Infect Dis J. 1996;15:600–4.

4. Swingler GH. Observer variation in chest radiography of acute lower respiratory infections in children: a systematic review. BMC Med Imaging. 2001;1.

5. Young M, Marrie TJ. Interobserver variability in the interpretation of chest roentgenograms of patients with possible pneumonia. Arch Intern Med. 1994;154:2729–32.

6. Maughan BC, Asselin N, Carey JL, et al. False-negative chest radiographs in the emergency department diagnosis of pneumonia. R I Med J. 2014;97:20–3.
7. Lichtenstein DA. BLUE-protocol and FALLS-protocol: two applications of lung ultrasound in the critically ill. Chest. 2015;147(6):1659-70.
8. Lichtenstein DA, Meziere GA. Relevance of lung ultrasound in the diagnosis of acute respiratory failure: the BLUE protocol. Chest. 2008;134(1):117-25.

9. Dexheimer Neto FL, Andrade JM, Raupp AC, et al. Diagnostic accuracy of the Bedside Lung Ultrasound in Emergency protocol for the diagnosis of acute respiratory failure in spontaneously breathing patients. J Bras Pneumol. 2015;41(1):58-64.
10. Woodhead M, Blasi F, Garau J, et al. Guidelines for the management of adult lower respiratory tract infections - Full version. Clin Microbiol Infect. 2011;17(6):E1-E59.
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Image Credit: Pexels
Author: Deniece Boothe, DO
Originally Published: Common Sense March/April 2019

The terms “hospice” and “palliative care” remain synonymous for many health care providers. Despite the intertwined relationship, it is important that we understand the differences in an effort to provide appropriate resources for our patients facing serious, life-limiting illness. Palliative care, also known as palliative medicine, is specialized medical care for people living with serious illness. It focuses on providing relief from the symptoms and stress of a serious illness whatever the diagnosis. The goal is to improve quality of life for both the patient and the family.[1] Hospice care is designed to give supportive care to people in the final phase of a terminal illness and focus on comfort and quality of life, rather than cure. Those with a prognosis of six months or less meet criteria for hospice. A Center to Advance Palliative Care survey found that most health care professionals erroneously equated palliative care with end-of-life (EOL) care.[1] This lack of understanding leads to ineffective communication between the provider and patient or health care proxy.

Let us look at two cases where hospice vs. palliative care is appropriate.

Case 1
Mrs. A, a 35-year-old female with recent diagnosis of ovarian cancer is your next patient to be seen. You review her vital signs and note that she is tachycardic: HR 116BPM, BP 124/80, RR 16, O2 sat 100% on room air, temp 98.4. The patient states that she has persistent abdominal pain despite using her short acting morphine 5mg every four hours over the past two weeks. She admits to nausea and constipation as well. Her overall functional status is fair. She recently started chemotherapy and has tolerated treatment thus far with minimal symptoms. Her workup in the ED reveals progression of disease in the liver, a negative study for pulmonary emboli and labs are within normal limits. She receives a total of 2mg of Dilaudid in the ED and reports that her pain has subsided from a level 10 to level 4. The patient is discharged home and advised to continue with morphine prn, to follow up with her PCP and oncologist as soon as possible.

Case 2
Mr. B is an 89-year-old male with hx of HTN, CVA, and advanced dementia. He presents to the ED from a long term care facility in respiratory distress. The documents accompanying the patient state that he was found to be less responsive today, hypoxic - sat’s 70’s, improved with oxygen prior to arrival. You note that the patient had three prior visits resulting in admissions over the past six months for sepsis secondary to pneumonia, UTI. On exam the patient is contracted, with noted bi-temporal wasting and is minimally responsive to painful stimuli. Respirations are labored, oxygen saturation remains at 90% on venti mask. Additional vitals: BP 80/40, HR 120 - irregular, RR 30, temp 103.4. You sift through the documents from the facility and note that the patient does not have an advanced directive or POLST document. Family members arrive at bedside. You identify his wife as his legal next of kin and inform her that the patient will require intubation due to respiratory failure as well as a central line to administer pressors. You express concern for septic shock and explain that the patient will be admitted to the intensive care unit for further management.

Hospice or Palliative Care?
Patient A is an appropriate patient for palliative care services. Patients with a serious illness often experience substantial physical burden due to pain and symptoms such as fatigue, anorexia, nausea, and dyspnea. Anxiety and depression are also common after the diagnosis of a life threatening illness. Any of these symptoms may alter a person’s ability to fulfill roles critical to self-identity.[2] Early integration of palliative care services in the emergency department will allow for improved quality of life. The patient requires appropriate pain management i.e., incorporation of a long acting opiate vs. adjuncts for adequate pain control. A bowel regimen should be instituted and persistent nausea should be addressed. Additional palliative care services should incorporate symptom management, support and establish the patient’s goals in the setting of advanced disease. Patient B is appropriate for hospice services. It is essential that the treatment goals are established in the ED setting prior to aggressive interventions if possible. Further discussion with the patient’s health care proxy or legal next of kin may lead to a decision directed towards comfort care vs. initiating life sustaining measures. An understanding of advanced dementia and the trajectory of illness will serve as an important foundation for the physician when addressing the goals of care.

In both cases the conversation should incorporate the following:

  1. Eliciting the understanding of illness
  2. Assessing willingness to hear information
  3. Provide information and options of care
  4. Respond to emotions
  5. Review and summarize
Proper identification and disposition of the hospice vs. palliative care patient is essential to our practice in the field of emergency medicine. ED providers may serve as the sole source of information for patients facing serious illness. The primary goal when meeting with these patients is to ensure quality of life. “Quality” is defined by the patient, health care proxy or legal next of kin. Each has an ideal definition of quality of life. One that is specific to that individual. It is important that this is recognized as this definition will be what drives the conversation and ultimately define the goals of care.


1. Center to Advance Palliative Care. About palliative care. https:// www.capc.org/about/palliative-care/. Accessed December 1, 2018.

2. Mayo Clin Proc. n February 2017;92(2):280-286 n http://dx.doi.org/10.1016/j.mayocp.2016.11.007 www.mayoclinicproceedings.org n ª 2016 Mayo Foundation for Medical Education and Research

3. Buss MK, Rock LK, McCarthy EP. Understanding Palliative Care and Hospice: A Review for Primary Care Providers. Mayo Clin. Proc. 2017; 92:280-286.

4. Goett, R. Fetzer, M. Aberger, K. Rosenberg, M. (2015, June). Why Palliative Care? Why Now? ACEP Now. 36(4). Retrieved fromhttp://www.acepnow.com/article/emergency-physicians-should-provide-palliative-care-options/
5. Rosenberg, M. Parker, R. (2014, Jan). Emergency Physicians Can Help Ensure Patients Receive Quality End-of-Life Care. ACEP Now. 33(1). Retrieved from http://www.acepnow.com/article/emergency-physicians-can-help-ensure-patients-receive-quality-end-life-care/
6. Fried, T.R. Bradley, E.H. Towle, V.R. Allore, H. Understanding the treatment preferences of seriously ill patients. N Engl J Med, Vol. 346, No. 14. 1061–1066.
7. Shearer, F.M. Rogers, I.R. Monterosso, L. Ross-Adjie, G. Rogers, J.R. Understanding emergency department staff needs and perceptions in the provision of palliative care. Em Med Australasia. 2014;26(3):249–255.
8. Smith, A.K et al. Am I Doing the Right Thing? Provider Perspectives on Improving. Palliative Care in the Emergency Department. Ann of Em Med. 2009;54(1):86–93.
9. Bakitas M, Lyons KD, Hegel MT, et al. E!ects of a palliative care intervention on clinical outcomes in patients with advanced cancer: the Project ENABLE II randomized controlled trial. JAMA. 2009;302(7):741-749.

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