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Wednesday, September 11, 2019

Is There an EM Residency Glut?

BY THOMAS COOK, MD

Seventy-seven emergency medicine residency programs received their initial accreditation by the Accreditation Council for Graduate Medical Education since 2016, and the overall number of positions increased by 37 percent, which begs the question, Is the profession being glutted?

The American Academy for Emergency Medicine thinks so; it released a statement earlier this year expressing concern that current trends may produce more emergency physicians than are needed. (AAEM Position Statement, Spring 2019; http://bit.ly/2EQPDd9.)

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Some of that increase can be attributed to osteopathic programs previously accredited by the American Osteopathic Association changing over to the ACGME. But even if we take that into account, the number of new programs opening their doors still substantially outpaced the previous three decades.

The AAEM statement also expressed concern that "the vast majority of new emergency medicine residencies are sponsored by national contract management groups or by national hospital networks that may have a vested interest in creating an oversupply of emergency physicians."

Are large contract groups such as US Acute Care Solutions and TeamHealth and large health care organizations such as HCA responsible for a significant component of the surge in emergency medicine training opportunities?

University Affiliation
US Acute Care Solutions is a contract management group that staffs more than 220 emergency departments; it was launched in 2015 in partnership with Welsh, Carson, Anderson & Stowe, a private equity firm, according to its website. (http://bit.ly/2TVqDrl.) Various sources say the company has more than 1000 employees and an annual revenue of more than $500 million, but USACS did not respond to EMN's request for confirmation. The company's website says, however, that their physicians manage eight EM residency programs in seven states, three of which started after 2015.

TeamHealth, a subsidiary of the Blackstone Group, also a private equity firm, is a much larger organization with more than 18,000 physicians, physician assistants, nurse practitioners, and nurses in 3,400 civilian and military hospitals, clinics, and physician groups in 47 states, according to their 2015 filing to the Securities and Exchange Commission. That filing also reported nearly $83 million in net earnings on $3.6 billion in revenue in 2015. (http://bit.ly/2HkzIVL.)

The company generated some controversy in 2003 when the company staffed the new EM program in Tampa, and they are currently involved with several other EM programs. It has also diversified beyond emergency medicine into a variety of other specialties. TeamHealth does not list the EM programs they staff online.

HCA has a gross annual revenue of $46.7 billion and 262,000 employees, according to its 2018 annual report (http://bit.ly/2YZuEkm). It entered the EM residency business in 2016. At that time, I reported in this column my conversation with a member of the HCA recruiting staff about their intent to train and retain emergency physicians. (EMN. 2017;39[1]:1; http://bit.ly/2ZhrF6k.) They opened 11 residencies between 2016 and 2018, eight in Florida and one each in California, Nevada, and South Carolina. (HCA; http://bit.ly/2MqGKwl.) Each program has at least 12 residents per class, a total of 135. HCA is responsible for nearly 20 percent of the 667 new residency positions created in the United States since 2016. This is from a company that had no experience in managing an emergency medicine residency five years before.

It is also interesting to note how the traditional providers of residency training, the university-affiliated medical centers, appear to be less inclined to develop new programs. Only 19 of the 27 new EM programs since 2016 have an affiliation with a university medical school. Around 60 percent of the programs that started before 2016 have a university affiliation.

Corporate Medicine
What should we make of this? Providing training to attract skilled employees is nothing new for any business, whether it is plumbers and electricians or nurses and doctors. My training occurred at a small community hospital where we were the only residents. The goal of my employer (the United States Army) was to have as many EPs as possible because we are the most suited for battlefield medical care.

The company I work for now is a relatively small contract management group that covers five hospitals in a small city. It goes without saying that when we identify a talented resident and have an open position, we speak with him about sticking around the mothership (and many of them do). My point is that everyone does this, so what's the beef?

If only it were that simple. When massive companies apply their vast resources to a problem (in this case, getting enough emergency physicians to staff their EDs), it generates a lot of disruption, causing unintended consequences. The corporations want a stable workforce, and even though building an emergency medicine program from scratch is expensive, it is much more cost-effective in the long run. But this is done to the detriment of new residency grads taking on huge loan debt. How will it feel for them to pay back $250,000 while huge, highly profitable health care organizations increase their bottom line by slowly nibbling away at their paycheck?

This dilemma will not go away anytime soon. Cash-strapped public universities and profit-driven private medical schools are not going to decrease tuition. They will keep pushing the price up until they bleed all the money they can from a student's wallet.

Will corporate medicine pay off their loans without an equally effective financial incentive for them? Perhaps the future of medical school education will be to apply to a large health care company immediately after college to receive medical school tuition in exchange for multiple years of service at reduced pay. Many nontraditional formats for financing a career in medicine may be forthcoming, and the implications of corporate medicine flexing its muscles in the realm of residency training will have a huge impact.

Dr. Cook is the program director of the emergency medicine residency at Palmetto Health Richland in Columbia, SC. He is also the founder of 3rd Rock Ultrasound (http://emergencyultrasound.com). Friend him at www.facebook.com/3rdRockUltrasound, follow him on Twitter @3rdRockUS, and read his past columns at http://bit.ly/EMN-Match.


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Wednesday, September 4, 2019

Transfusions Stuck in an Endless Cycle of Denial

BY RORY SPIEGEL, MD

Each publication from Maitland, et al., gives us a glimpse of a greater medical truth, but our view is obstructed by questions about external validity.

This group published the landmark FEAST trial that questioned the safety and utility of one of the most ubiquitous interventions in medicine today, the fluid bolus. (N Engl J Med. 2011;364[26]:2483; http://bit.ly/2L0ozdO.) The authors enrolled 3141 pediatric sepsis patients at six clinical centers in Africa, and patients were randomized to receive an IV fluid bolus (saline or albumin) plus a continuous infusion or infusion alone.

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The results were surprising, to say the least. The trial was stopped premature of its 3600 predetermined sample size because of an increased rate of 48-hour mortality, 10.6 percent, 10.5 percent, and 7.3 percent in the albumin-bolus, saline-bolus, and no bolus control groups, respectively. This was the first trial empirically examining the efficacy of a fluid bolus for septic shock, and the authors found that IV fluid boluses were associated with increased 48-hour and 28-day mortality.

Yet, eight years later, rapid fluid administration is still paramount in managing septic shock. Many argue that these results may not be externally valid outside the context in which they were tested. Are fluid boluses detrimental when used in critically ill adults with access to ICU care? I previously wrote about the growing body of evidence suggesting Maitland's results are applicable more broadly than originally considered (EMN. 2019;41[5]:1; http://bit.ly/2J46WKK), but concerns about the FEAST trial's external validity have limited its influence on managing sepsis and septic shock.

Long-held Practice
Now, the TRACT trial by Maitland, et al., asks us to consider the validity of another long-held medical practice. (N Engl J Med. 2019;381[5]:407; http://bit.ly/2KT2aPi.) Much like administering IV crystalloid, the current management of severe anemia is, in theory, fairly straightforward. Maitland was guided by the TRICC trial, in which critically ill ICU patients with no signs of active hemorrhage were randomized to different transfusion thresholds, 7 g/dL or 10 g/dL. (N Engl J Med. 1999;34[6]:409; http://bit.ly/2MvbbS9.) The authors enrolled 838 patients, 413 in the restrictive group and 420 in the liberal group. Patients in the liberal group successfully had their hemoglobin maintained at a higher level than the restrictive group. The average daily hemoglobin concentrations were 8.5±0.7 g/dL in the restrictive group and 10.7±0.7 g/dL in the liberal one. Clinicians were required to transfuse significantly larger quantities of PRBCs: 2.6±4.1 PRBCs per patient in the restrictive group v. 5.6±5.3 in the liberal group to achieve this higher hemoglobin value.

Thirty-day mortality was 18.7 percent in the restrictive group v. 23.3 percent in the liberal group (p=0.11). In-hospital mortality was 22.2 percent v. 28.1 percent in the restrictive and liberal groups, respectively (p=0.05). ICU mortality and 60-day mortality trended toward the restrictive group. Cardiac events (MI, pulmonary edema) were also more frequent in the liberal group (13.2% v. 21.1%).

The results of the TRICC trial have been validated in many pediatric and adult populations. (N Engl J Med. 2007;356[16]:1609, http://bit.ly/31Tk7UN; N Engl J Med. 2013;368[1]:11, http://bit.ly/2Npa2ek; N Engl J Med. 2017;377[22]:2133, http://bit.ly/2ZkTzKu.) It is clear an empirically restrictive strategy is superior to an empirically liberal one, but this trial demonstrated 7 g/dL was preferable to 10 g/dL, not that 7 g/dL was better than 6 g/dL and 5 g/dL and not whether empiric transfusion strategies based on hemoglobin levels were superior to transfusion triggers based on signs indicating the anemia was leading to physiological distress. These questions have been relegated to the musings of the rebellious mind, but the TRACT trial provides clinical data suggesting a single threshold may not be ideal. (N Engl J Med. 2019;381[5]:407; http://bit.ly/2KT2aPi.)

Primary Outcome
Maitland, et al., enrolled children 2 months to 12 years old with uncomplicated severe anemia in a factorial, open-label, randomized, controlled trial. The patients were randomized to immediate transfusion or a control group in which a transfusion was deferred unless the hemoglobin dropped below 4 g/dL or clinical signs of severe anemia developed (prostration or respiratory distress). Patients randomized to immediate transfusion received 20 mL/kg or 30 mL/kg of whole-blood equivalent determined by a second randomization. (Those results are in N Engl J Med. 2019;381[5]:420; http://bit.ly/2Zj26NW.) If a second transfusion was indicated, it was done at the same volume as the first. Patients randomized to the control group who met the threshold for transfusion were transfused 20 mL/kg of whole-blood equivalents.

The Maitland group enrolled 1565 children, 778 to immediate transfusion (390 in the 20 mL group, 388 in the 30 mL) and 787 as controls. All patients in the immediate transfusion group received at least one transfusion, but only 386 (49.0%) in the control group did. The mean total volume of whole-blood equivalent transfused per child during initial hospitalization was 314±228 mL v. 142±224 mL in the immediate-transfusion and control groups, respectively.

The more aggressive transfusion strategy resulted in fewer patients experiencing a severe anemia (hemoglobin<4g/dL; 1.4% v. 39.3%) and more children experiencing an early hemoglobin recovery (>9 g/dL; 51.3% v. 5.5%). But no difference in primary outcome, 28-day mortality, was seen: 0.9 percent in the immediate group v. 1.7 percent in the control group. Nor did they identify differences in mortality at three or six months or in complications from severe anemia or readmission to the hospital during the subsequent six months. In fact, the difference in hemoglobin levels between the two groups at 28 days was minimal, only 0.6 g/dL higher in the immediate-transfusion group.

Once again, Maitland, et al., have challenged what we thought we knew about medicine. The authors generated data that can be applied instantly by many practicing around the world. We are uncertain how these results apply to patients outside the population studied, which brings us back to external validity: Can a highly restrictive transfusion strategy be employed in patients outside the trial hospitals in Uganda and Malawi? Is Maitland's population unique, preventing these results from being applied to a broader population of anemic children or even adults? Like the FEAST trial, 62.9 percent had malaria and 21.7 percent had sickle cell disease. Should this limit the trial's generalizability? These concerns remain unanswered without further study, but almost every study examining transfusion strategies in various patients have found restrictive strategies preferable to liberal ones.

External Validity
Can we apply the results to a population with access to ICU care? The authors' major concern was whether allowing hemoglobin levels to fall so low without intensive monitoring was safe, which was why a strict hemoglobin monitoring strategy was incorporated into the methodology. Frequent blood draws are well within the capabilities of any modern ICU, so can we apply the results of this trial to those without the capability to monitor hemoglobin levels regularly?

Finally, can these results be applied to adults with critical anemia? Current pediatric transfusion guidelines appear fairly similar to adult ones (Pediatr Crit Care Med. 2018;19[Suppl 1]:S98), recommending a transfusion trigger of 7 g/dL. The TRIPICU trial in a sense validated the TRICC trial findings in children, demonstrating that a transfusion trigger of 7 g/dL was superior to one of 9.5 g/dL. (N Engl J Med. 2007;356[16]:1609; http://bit.ly/31Tk7UN.) But like the TRICC trial, the authors only asked a dichotomous question and did not examine whether a lower transfusion threshold was preferred to either level.

A greater medical truth hides in the pages of this document. Transfusion of red blood cells can likely occur at a much lower threshold than what we generally employ, and the level at which anemia becomes detrimental probably varies from patient to patient. It is doubtful these results, like FEAST, will be broadly applied. Instead, we are stuck in an endless cycle of dismissal and denial. A trial like this could not have been done outside of this population, but we are unable to apply the results generally because of that population. It is unclear whether the TRACT trial results are generalizable to blood transfusion strategies outside this cohort.

The results should make us question the absurd dichotomy in which we currently exist, where a patient with a 7.1 g/dL hemoglobin is fine and a patient at 6.9 g/dL is in urgent need of red blood cells, with no consideration of the clinical context surrounding these abstract data points.

Dr. Spiegel is an assistant professor of emergency medicine and critical care at Washington Hospital Center in Washington, D.C. Visit his blog at http://emnerd.com, follow him on Twitter @emnerd_, and read his past articles at http://bit.ly/EMN-MythsinEM.


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Wednesday, August 28, 2019

The Unchecked Growth of EM Programs
(and No Sign of Stopping)

BY THOMAS COOK, MD

Should emergency medicine graduates be concerned about a future with too much competition for high-paying jobs? The number of first-year EM positions has increased by almost 37 percent since 2015, according to the 2019 report by the National Resident Matching Program. (http://bit.ly/2XHyheb.) Even if the number of residency positions doesn't increase in the future, there will be more than 7400 EM residents in 2022, and a third of them will graduate that year. This creates a lot of anxiety for EM residents banking on the ability to receive annual incomes typically in excess of $300,000.

Is there any organization not directly providing emergency clinical services that is monitoring this? Is someone asking the right questions and developing a strategy to avoid the overproduction of EPs? After a little investigation, I am pretty sure the answer is no.

The Accreditation Council for Graduate Medical Education (ACGME) has been the umbrella organization that oversees graduate medical education in the United States since 1980. Their mission is summarized in this statement on their website: "The ACGME is a private, 501(c)(3), not-for-profit organization that sets standards for US graduate medical education (residency and fellowship) programs and the institutions that sponsor them, and renders accreditation decisions based on compliance with these standards." (http://bit.ly/2LWjhlo.)

What they don't do is determine how many programs there should be based on the employment marketplace for any given specialty. I called the residency review committee for emergency medicine to confirm this, and was informed that any attempt by the ACGME to limit the number of programs could be interpreted as restriction of trade. Even if they wanted to, the ACGME could not limit the overall number of residents or programs available to medical school graduates.

The ACGME website has a very, very long list of all accredited emergency medicine programs. There are now 239 programs, an incredibly high number.

The ACGME-AOA Merger
I entered each program into a spreadsheet along with the year the program was first accredited. Most of the older programs are listed on the ACGME site as beginning in 1982 because the ACGME only came into existence in 1980. My program started in 1978, according to the ACGME, but it was not accredited until 1982. There were 49 emergency medicine accredited programs that year. After 1982, the annual rate of program accreditation was pretty consistent until 2015. Then something incredible happened.

At least 20 new programs were accredited each year from 2016 to 2018. The data for 2019 are not complete yet, but program accreditation seems to be at a similar pace. A total of 75 programs were accredited by the ACGME for the first time from January 2016 to June 2019. Of course, this information generates a lot of questions. What is driving this? Will it continue, or is this a short-lived phenomenon? Will the rate of new program accreditations stabilize?

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A closer look at the data revealed that the biggest contributor to the rapid increase in the number of programs since 2015 is the merger between the ACGME and American Osteopathic Association, which will establish a single residency accreditation organization in the United States by 2020. The AOA will no longer accredit osteopathic residency programs for training, and all previously AOA-accredited residencies and new osteopathic programs are required to apply for accreditation from the ACGME.

Forty-one of the 75 programs accredited by the ACGME since 2016 were either established osteopathic programs applying for first-time ACGME accreditation or new osteopathic programs. Fifty-five percent of the increase in newly accredited programs since 2016 can be attributed to this merger. But if we factor out the osteopath surge created by the merger, there were more new allopathic programs accredited by the ACGME compared with similar periods over the past 37 years.

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The ACGME-AOA merger is not the sole reason for the dramatic increase in residency positions, nor does it answer the pivotal question of whether there are too many graduates for too few jobs. There are other factors at play, and this is where we will pick up the conversation next month by looking at the influence of contract management groups on the increased production of emergency physicians.

Dr. Cook is the program director of the emergency medicine residency at Palmetto Health Richland in Columbia, SC. He is also the founder of 3rd Rock Ultrasound (http://emergencyultrasound.com). Friend him at www.facebook.com/3rdRockUltrasound, follow him on Twitter @3rdRockUS, and read his past columns at http://bit.ly/EMN-Match.


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Wednesday, August 21, 2019

Is Contrast-Induced Acute Kidney Injury a Myth?

BY JAMES R. ROBERTS, MD

When iodinated contrast was first introduced, many patients with pre-existing kidney disease experienced acute injury, but the evolution of safer agents has resulted in a much lower incidence of acute kidney injury. The risk of this injury due to contrast, in fact, may be overstated. Even its existence has been questioned. Today, contrast is not required as often as it was in the past because of high-resolution CT scanners, but it is often recommended by radiologists for many studies.

Contrast-Associated Kidney Injury
Mehran R, Dangas GD, Weisbord SD
N Engl J Med.
2019;380(22):2146

This review summarizes the known pathophysiology of contrast-associated kidney injury, the diagnostic criteria, and risk stratification, and it discusses the controversies about the actual incidence of this condition. It also investigates interventions that have been studied to prevent contrast-associated kidney injury.

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A CT scan of the head with (right) and without (left) IV contrast. The role of IV contrast causing acute or permanent renal injury has been questioned recently. Contrast material can be toxic to a previously injured kidney, but final adverse consequences of using IV dye have likely been overstated. Some have questioned whether contrast-induced renal injury even exists. Plasma creatinine levels are often elevated after IV contrast administration, but its significance is unclear. Attempts to limit nephropathy have not yielded a definite, useful intervention, but most suggest pre- and post-IV saline as potentially helpful, and even this is difficult to prove.

The exact mechanism by which contrast causes kidney injury is somewhat obscure. Direct and indirect effects and hemodynamic perturbations have been implicated. Contrast agents are directly toxic to epithelial cells, and exposure may cause the outright death of these cells. Indirect injury is related to intrarenal vasoactive activities adversely affected by contrast. The adverse hemodynamic effects of contrast, primarily renal vasoconstriction, are particularly problematic for the renal medulla, a portion of the kidney that is susceptible to injury from decreased blood flow.

Declining kidney function after contrast administration, referred to as contrast-induced nephropathy, has been historically defined as an increase in plasma creatinine of at least 0.5 mg/dL or a 25 percent increase from baseline within two to five days. Other criteria define contrast-induced acute kidney injury as an increase in plasma creatinine by a factor of 1.5 x baseline within seven days of exposure. Plasma creatinine levels, although commonly used, have relatively poor sensitivity to kidney dysfunction.

The strongest independent risk factor for contrast-associated acute kidney injury is preexisting chronic kidney disease. Lower levels of kidney function are associated with higher degrees of risk. Diabetes was once thought to be an independent risk factor, but it is not considered to be associated with kidney injury except for an increased susceptibility in diabetics with underlying chronic kidney disease. Contrast-associated kidney dysfunction has been markedly reduced by the introduction of low-osmolarity contrast agents, and they are now used in all studies. Using a high volume of contrast and repeat administration within 72 hours, however, have been associated with increased risk. Angiography and angioplasty, such as cardiac angioplasty in patients with ST-segment elevation myocardial infarction, are also associated with an increased incidence of deteriorating kidney function from contrast.

There is a lot of uncertainty about the causal relationship between contrast-associated acute kidney injury and adverse clinical outcomes, morbidity, and mortality. Many studies, however, have demonstrated an overall increased mortality associated with contrast-induced acute renal injury and an accelerated progression of underlying chronic kidney disease. The existence of contrast-induced acute kidney dysfunction was questioned in a meta-analysis of 25,950 patients that showed similar risks for acute kidney injury and death in those undergoing procedures with and without iodinated contrast. (Radiology. 2013;267[1]:119; http://bit.ly/2LiSY9P.)

Curiously, another meta-analysis demonstrated a significantly lower risk of acute kidney injury in patients with acute ischemic stroke who underwent CT with and without contrast. (Stroke. 2017;48[7]:1862; http://bit.ly/2XJHygZ.) Importantly, a number of analyses have concluded that using contrast does not appear to be associated with an increased risk of acute kidney injury. These authors questioned the clinical importance of contrast-induced renal dysfunction, and stated that current data are insufficient to declare that contrast agents are not nephrotoxic and that severe acute kidney injury characterized by substantial decrements in kidney function and the need for renal replacement therapy appear to be infrequent after intravascular contrast administration.

Though the question of the existence of contrast-induced kidney injury has not been settled, a number of interventions to prevent it or decrease creatinine elevations have been investigated. Intravascular volume expansion has been touted to have a protective renal effect, but randomized clinical trials are relatively sparse. A number of small studies have demonstrated a markedly lower incidence of contrast-induced acute kidney injury by using saline before administering the dye.

Guidelines from the American College of Radiology and the European Society of Cardiology recommend intravenous isotonic saline for a number of hours before and after administering contrast. The saline volume is relatively small, from 100 mL per hour for six to 12 hours before and 12 hours after angiography to 1.5 mL per kg per hour for 12 hours before and after contrast exposure. The commonly quoted AMACING study did not demonstrate any benefit of preprocedural intravenous saline in preventing acute kidney injury. (Lancet. 2017;389[10076]:1312.) This study had some methodological flaws, however, making it premature to conclude that IV fluids are not effective or unnecessary before administering contrast. Other studies found that adding sodium bicarbonate to normal saline has no benefit in preventing contrast-associated acute kidney injury.

Pretreatment with acetylcysteine was once believed beneficial, but has shown no value. No data support discontinuing a variety of medications (diuretics, ACE inhibitors, and NSAIDs) before dye administration. Even stopping metformin, a previous standard, has not been supported by evidenced-base studies. It should be noted that metformin is associated with lactic acidosis, not acute renal injury.

These authors conclude that the definition of contrast-induced renal injury and the studies showing an association with serious adverse outcomes are unclear. Despite previous dogma, the current thinking is that additional study is needed to address the controversy over the true toxic effects of contrast and to determine whether there is any justification for limiting its use in patients at elevated risk.

Comment: This subject is confusing and the evidence somewhat contradictory, and concepts have changed significantly over the past few years. Recent data have questioned previous views that acute kidney injury is significant in patients given contrast. Clinical relevance of small increases in creatinine have also been questioned. The viscosity and osmolarity of iodinated contrast do show some renal toxicity, but there has been a marked change in our understanding of any true detrimental effect of contrast in patients undergoing CT scans. Emergency physicians do not order dye for angiographic procedures, which are probably most likely to be associated with contrast-induced nephropathy.

The most effective preventive regimen for patients at high risk appears to be intravenous sodium chloride administration, but even the actual benefit of hydration has not been determined. A prolonged infusion of saline before and after a procedure is not possible in the ED, but it seems reasonable to give generous IV saline before contrast in dehydrated patients. I always give one liter of saline for any dye study—500-600 mL before and 400-500 mL after.

Recent studies have caused clinicians to question whether there is actually a condition such as contrast-induced nephropathy. Contrast is necessary to obtain or assess diagnostic accuracy in some radiographic procedures. Omitting contrast when it is indicated or giving it when it is not can lead to diagnostic and treatment errors. It is generally agreed that patients with a GFR greater than 30 mL/min can be safely administered contrast material.

It should be noted that allergic-like (hypersensitivity) reactions and other physiological reactions to contrast do exist. Importantly, allergic-type reactions are idiosyncratic and don't seem to be related to dose or type of contrast. The risk for immediate hypersensitivity reactions to contrast is increased in patients with allergies or asthma, but there is no relationship between dye reactions and allergy to shellfish or topical iodine solutions. It has long been a misconception that patients can have an iodine allergy and not be given contrast safely. Shellfish allergies are not due to iodine but to muscle protein. Iodine sensitivity does not actually exist.

Dr. Roberts is a professor of emergency medicine and toxicology at the Drexel University College of Medicine in Philadelphia. Read the Procedural Pause, a blog by Dr. Roberts and his daughter, Martha Roberts, ACNP, PNP, at http://bit.ly/EMN-ProceduralPause, and read his past columns at http://bit.ly/EMN-InFocus.

P.S. If you liked this post, we think you'd enjoy the EMN enews, which delivers breaking news and online exclusives right to your inbox.

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Wednesday, August 14, 2019

Overcoming Depression is a Journey,
Not Just Flipping a Light Switch

BY SANDRA SCOTT SIMONS, MD

I had days when I hurt enough to think, "I understand why doctors kill themselves." I was in the depths of depression.

Plenty of doctors reach that point, shown by the alarming rate of physician suicide, but we don't talk about it. Our silence isn't helping us or anyone else. Let's do better in honor of National Physician Suicide Awareness (NPSA) Day on Sept. 17.

For every person who dies by suicide, 280 people decide not to go through with it, yet we don't hear their stories of survival. (Active Minds. http://bit.ly/2NWPzja.) We should balance the tragic stories of physician suicide with encouraging ones of the 280 others who have found ways to cope. Not sharing journeys like mine maintains the taboo that is the enemy of hope and healing. The best thing we can do for NPSA Day is to defy labels and stigmas and talk candidly about our mental health.

For starters, let's be honest about feeling overwhelmed. The moral injury physicians experience will always find chinks in our armor and creep into our psyche. I didn't fully grasp how toxic medicine was to my psyche until two years ago when I had five months off between jobs. When I went back to work, the contrast between my states of mental health was sobering.

Frazzled and Depleted
I love my new job, but being in the trenches of the ED erodes my capacity to deal with mishaps that I might otherwise take in stride, like surprise last-minute homework projects, overflowing toilets, malfunctioning Xboxes, and the impossible task of getting two kids to two simultaneous practices on opposite sides of town. Many days I feel frazzled and depleted, as most physicians do given the increasingly lofty demands of the job. It has a name—caregiver fatigue, and it has as much to do with the profession as anything innate in me. Physicians should acknowledge it and seek help without shame.

Let's also be frank about the hellacious effect of shift work. Honestly, after 13 years of full-time nights, it's no wonder I'm in therapy. The sleep deprivation, the opposite schedule from family and friends, and the need to be on when our circadian rhythm has other ideas are underrated threats to our wellness. Even though my life circumstances had improved after five months off, my happiness plummeted as soon as I resumed my Sunday-Monday-Tuesday night shifts.

I'd worked that schedule for six years, but it wasn't until I experienced the same level of misery at a great new job that I finally realized that no amount of self-kindness or reframing could make up for that schedule's physical and mental repercussions. Rather than shutting up and powering through as our antiquated culture of bravado encourages, I asked for a schedule change. With the help of an understanding medical director and some custody schedule adjustments, I achieved a scheduling coup of working just two nights a week. Fewer hours mean less money and a part-time status without benefits, but my sanity is worth it. If we don't speak up and address threats to our own wellness, no one else will.

Steps Backward
Let's also talk unabashedly about antidepressants. I've been taking one daily for eight years, and it is life-changing. It was wondrous how crusty old gomers almost immediately became cute little old men again. It's also striking how differently I feel when I forget to take it. Years ago, I remember inexplicably bursting into tears while doing the dishes and hearing U2's "Stuck in a Moment" on the radio; I couldn't figure out why, but then it dawned on me: I hadn't taken my Wellbutrin in two days. Since I was in a better place, I thought I could wean myself off the Wellbutrin. Nope. Pull yourself up is no longer an acceptable approach to mental health. None of us should have to worry about judgment or stigma from starting or continuing medications that help us.

Finally, let's talk about psychotherapy like the valuable resource it is, not like a four-letter word. Too many scoff at therapy or delay even considering it until they're in crisis. It shouldn't take a catastrophe to talk to a therapist. Like diet and exercise, mental health maintenance is an integral part of wellness. If more of us speak candidly about seeing therapists the same way we talk about the race we're training for or the latest diet we're trying, we could fight stigma and encourage others. Therapy is a safe space to talk through whatever troubles me. Sometimes I need someone objective to help me get out of my head, put my stressors in perspective, and see healthier options for dealing with them. Going to therapy means I'm strong, not weak. Psychotherapy every few weeks is a way I push back and take a stand for my own mental health.

Even with antidepressants and therapy, overcoming the darkness of depression is a journey, not just flipping a light switch. We don't hear about the bad days and steps backward on that journey because people don't talk about their personal battles. I remember eating half a dozen cupcakes in a moment of sadness or frustration and then beating myself up, self-critically blind to all the steps forward I'd made and only seeing my sugary screw-up. I wasn't giving myself credit for the small breakthrough of not eating a dozen cupcakes, which I'd been known to do. No one talks about these seemingly inconsequential steps, but taking them day after day is what eventually gets us to a better place. We need to be real about all our steps and stumbles so we can create a realistic map of the journey through depression for everyone struggling.

If you've stumbled or even had a full-on face plant, I urge you to share as a way of debunking the myth that good physicians are happy and perfect all the time. Reach out, seek help, call a therapist. Let's be real about our mental health struggles on NPSA Day and every day.

Dr. Simons is an emergency physician in Richmond, VA, and a mother of two. Follow her on Twitter @ERGoddessMD, and read her past columns at http://bit.ly/EMN-ERGoddess.


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