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35 Years of Burnout

Published March 4, 2016 Opinions 2 Comments

One of the most prominent definitions describes burnout “as a syndrome of emotional exhaustion, depersonalization, and reduced personal accomplishment that can occur among individuals who work with people in some capacity“. (Maslach, Jackson & Leiter, 1996)

In 1974, the year I started medical school back in Sweden, the German-born American psychologist Herbert Freudenberger published a journal article titled “Staff burn-out”. In it, he wrote about the physical and emotional symptoms of burnout, and he described how cognition, judgment and emotions are affected.

In 1980, while I was working in Sweden’s socialized health care system, Freudenberger wrote his book “Burn Out: The High Cost of High Achievement. What it is and how to survive it”.

In 1981, the year I landed on these shores, Christine Maslach published “The measurement of experienced burnout”, with the Maslach Burnout Inventory, which seems to be the standard tool for quantifying this condition, which was first associated with high stress positions in the service sector. It was seen as related to serving the needs of very needy or complex clients with limited resources at one’s disposal.

Early literature on burnout among physicians focused on physicians in pediatric intensive care units, and later on emergency physicians. Today, burnout is discussed in every specialty. It is described as an epidemic that is threatening the continued contribution to our health care system by half of all practicing physicians.

I never heard much about burnout as a resident, young family doctor or even in my early middle age. Now, there is even an ICD-10 diagnostic code for burnout – Z73.0!

The other day, I listened to a podcast by Richard Swenson, MD. He makes the argument that burnout is linked to having too little margin in life. As I listened and tried to imagine which doctors I knew who may have risked burnout from lack of margin, I could only think of a half dozen private practice doctors I knew when I was a resident. The margin theory seems to me to apply mostly to Marcus Welby’s generation of physicians, who did what they loved to do, and although they were in nearly full control of their day, they allowed their professional sense of duty to infringe on their margins, in Swenson’s words, to stretch their physical and perhaps sometimes also their emotional energy to or even beyond their limit.

I believe today’s epidemic of physician burnout is often unrelated to our margins, but in many cases the result of not being in quite the right position or career situation:

I have written before about the “counterintuitive concept of burnout skills” – the “talents” we possess that often draw us into vicious cycles of self-sacrificing heroics to overcome the unfixable limitations of our individual jobs or of the healthcare systems we work within.

In that context, the antidote to burnout is developing and using the talents that bring us the greatest personal satisfaction. When we use those talents, we become energized, and our work becomes fulfilling and rewarding.

In medicine, that switch to what energizes us might be focusing more on mentoring or education, developing a niche of deeper knowledge and greater expertise in an area that we can feel passionate about, or perhaps serving a special needs population of patients, like deaf, immigrant or mentally challenged patients.

But, sadly, burnout in medicine today is increasingly caused by the relentless shift in the demands of physicians’ time, attention and and energy away from serving patients to also, and with no extra time alotted, fulfilling an increasing number of official mandates.

This dichotomy between what we trained for, treating the sick, and what we never imagined doing, inputting data for only remotely patient-centered purposes, is making physicians feel powerless, and that is the driver of today’s epidemic of burnout.

This burnout is different from the other two kinds in that it is unrelated to individual choices or character traits. It is not a “condition” among physicians as much as it is a consequence of the “working conditions” in today’s American health care. It is a direct consequence of what I call the de-professionalization of medicine.

With every passing year, it drives employed physicians in greater and greater numbers toward a desire to quit medicine altogether. Short of becoming self-employed entrepreneurs in their mid- or late career, they see no escape from the shift in emphasis away from patient-focused and to toward data-driven care. All practices, except cash-only ones, must devote increasing resources to collecting data and documenting compliance with mechanistic actions that often seem irrelevant to patients, who all have their own priorities for their fifteen minutes with their doctor.

The solution to, or cure of, physician burnout is obvious and easy, but not on anyone’s political agenda.

A Really Bad Bruise

Published February 26, 2016 Progress Notes 2 Comments

Theodore Black woke up two weeks ago with a massive bruise from the left side of his chest to his lower abdomen. He ended up admitted to the intensive care unit and wasn’t discharged from the hospital until today.

“Cough and rash”, was his chief complaint in my clinic schedule that morning. I had an emergency room report from Lakeside Hospital, near where he had spent a week at a conference. Two days before I saw him, he had gone to Lakeside’s ER with a nasty cough and pain across his lower chest and upper abdomen, radiating all the way around his mid-back like a vice. They got a normal chest X-ray, and a normal complete blood count and chemistry profile, so they sent him out with prescriptions for pain pills and some cough medicine.

“I’ve still got this really bad cough, and the pain hasn’t let up”, he started, “and when I woke up this morning, I had this rash…”

He lifted his shirt and exposed a massive bruise running along the left side of his body from the level of his nipple to his hip.

My mind raced into action as I listened to his heart and lungs, palpated his lymph nodes, examined his abdomen by inspection, auscultation, palpation and percussion. His breath sounds were slightly diminished at the base of his left lung, the bruised area was dense and extremely tender. His abdomen wasn’t very tender, except under the bruise, but he had some flank dullness on the right. He hurt too much on the left side to let me percuss him there, and he was unable to roll over on his left side to allow me to check if the right-sided dullness to percussion shifted with a chance in position.

His blood pressure was a little lower than usual, but his pulse was low – which was to be expected with the beta blocker he takes for his blood pressure.

I couldn’t remember the eponym for what he had, but I knew he had massive internal bleeding somewhere. In the back of my mind I thought I remembered retroperitoneal bleeding from coagulopathy or cancer, necrotizing pancreatitis or possibly intraabdominal bleeding.

I ordered a fingerstick prothrombin time, which came back normal at 1.0 and a CBC and a chemistry profile which I knew would be ready in just a few minutes with our new chemisty analyzer. I told him I’d be back as soon as the labs were done.

Back in the office I googled “flank ecchymoses” and saw the eponym I had forgotten, Grey Turner’s Sign. Everything I remembered or just instinctively knew about it matched the monograph I found.

His CBC came back first, and his hematocrit had dropped from 40 at Lakeside to 27 – definitely a massive bleeding. I went back in his room and told him that I not only wanted him to go to the hospital but that I didn’t want him going all the way there in a private car, but in the ambulance. Just as Autumn was calling the emergency dispatch number, Ted’s chemistries came back, with the lowest sodium level I have ever seen, 116 mg/deciliter. It had been 140 two days earlier.

I have seldom seen symptomatic hyponatremia, and the correlation between sodium levels in the brain and in peripheral blood isn’t very predictable, but the literature suggests that people with sodium levels as low as Ted’s are likely to be obtunded or having seizures. He seemed quite normal in that regard. Still, it made me feel good about my decision to recommend that he should go to the hospital via ambulance.

Ted had a chest CT angiogram, showing a modest amount of blood in his left chest cavity, but there was no bleeding or any other abnormality in his abdomen or pelvis on those scans. His pancreas and kidneys looked just fine.

They slowly corrected his sodium deficiency and watched him carefully, but he didn’t lose any more blood and he had no seizures or any other neurological symptoms.

In the end, after his long and likely very expensive hospital stay, he was discharged for the second time on pain pills and strong cough medicine.

The final diagnosis was “Hyponatremia secondary to volume loss from left hemothorax and extensive ecchymoses from severe cough”.

I had expected to hear bad news any day from the hospital, but my first and possibly only sighting of Grey Turner’s Sign turned out to be very benign. My colleagues were aware of my initial observations and this afternoon I walked around and told them how things had turned out.

“I’m sure someone will write that case up and publish it”, Dr. Brown said, probably referring to one of the major medical journals.

“Definitely”, I answered. I never did get around to telling Dr. Brown that I am writing this blog.

So, if The New England Journal of Medicine runs a piece on hyponatremia due to severe internal hemorrhage from coughing, you read it here first.

Inside and Out

Published January 31, 2016 Progress Notes Leave a Comment

77 year old Edward Tripp had been to the emergency room with chest pain last Friday night. It was relentless, aching, and involved the upper part of his left chest.

He had no cough, fever or shortness of breath. He was not sweaty or nauseous, and his blood work, EKG and chest X-ray were normal. He was distinctly tender over the part of his rib cage where bone and cartilage join each other a few inches from his breastbone. He had indeed done some heavy work with his arms in the days before, so the doctor made the assessment that his pain was caused by this apparent costochondritis.

Ed received a shot of pain medication at the hospital and was sent home with a prescription for hydrocodone. As the weekend went by, he started to feel worse and worse.

When I saw him Monday morning, he looked pale. He was short of breath and lightheaded. He had no appetite, and he had been sweating with the slightest exertion.

His blood pressure was low, even for him, a tall, sinewy vegetarian, and his pulse was 115. He did not have a fever, and his oxygen saturation was normal. On exam, there was no heart murmur and his lungs were clear, but his breath sounds seemed a little weaker on the left. His abdomen was diffusely tender, and he was still quite tender over each rib in the upper part of his left rib cage.

His EKG had some very nonspecific changes, which could conceivably go along with impaired blood flow to his left ventricle. Putting all this together, I recommended that we send him back to the hospital for reevaluation. I wondered about angina, a blood clot in his lungs or internal bleeding in his abdomen. His chest wall strain was clearly not the only thing going on.

At the hospital, they did another chest X-ray, which showed some minimal haziness in the left lung. His cardiac enzymes were normal, but he had an elevated D-dimer, so there was a possibility that he had a blood clot in his lung.

His CT angiogram ruled out a clot, but he had a dense infiltrate, by all indications a pneumonia, in his left upper lung, exactly underneath his sore ribs.

When the first chest X-ray was re-read with the second one and the CT as comparisons, the pneumonia was faintly visible.

We all tend to look for one diagnosis that explains everything that is going on with the patient, and we often tend to latch on to the first positive finding we make. But medicine is often more complicated than that, and sometimes we see diseases in early stages, when findings are too subtle to make a diagnosis.

I have come to feel a certain discomfort deep in my gut when an older patient has pain in or even near the chest that appears to have an orthopedic cause.

That feeling dates back to my first job, just out of residency, when an 80 year old woman with shoulder pain I had evaluated came back to the emergency room two hours later with an obvious myocardial infarction on her EKG.

Being the first one to evaluate a patient, you don’t have the advantage of elapsed time that the second examiner has. Such is primary and emergency care.

An Outsider’s View of Cardiology

Published January 24, 2016 Reflections 2 Comments

When I started my first internship, back in Sweden in 1979, I worked under a fifty-something cardiologist who spoke slowly with a southern drawl – yes, there is a southern drawl there, too, slightly reminiscent of Danish, spoken not far from where my supervisor grew up.

He epitomized the the old school of cardiology, before it became a procedural specialty. He diagnosed heart murmurs by auscultation with his stethoscope, and he even claimed he could hear faint cardiac rubs or pulmonary râles in patients who were having a heart attack. He seemed to share the temperament of neurologists – slow and methodical master diagnosticians with, very much then and to a degree also today, limited or no treatment for a substantial portion of the diseases they diagnose.

In 1979, color Doppler echocardiography was not yet invented, and coronary angiography was not available where I worked. Cardiology was a purely cognitive specialty. The most important condition cardiologists treated, angina pectoris, was diagnosed on the basis of history, physical exam and at most a stress EKG.

Over just two decades, cardiology became a procedural specialty, and the diagnosis and management of angina became high tech with nuclear imaging, coronary angiography, cardiac stenting and bypass surgery. The view of angina became focused on stentable, “critical” lesions.

But people still died from heart attacks, even with only minor blockages on angiography and normal nuclear stress tests. And patients with classic angina symptoms were told they had non-cardiac chest pain if their stress EKG was abnormal but their nuclear scan was normal, or if the EKG and scan were abnormal, but the angiogram showed no critical stenosis. For over 100 years, the term “pseudoangina” was used to characterize this syndrome.

Every few years I would ask whichever consulting cardiologist seemed the most approachable, and every time I would get essentially the same answer: Angiogram trumps MIBI, MIBI trumps EKG, EKG trumps clinical history, kind of like the old rock-paper-scissors game.

Ironically, in 1973, the year before I started medical school, Harvey Kemp coined the term “Cardiac Syndrome X” for effort angina with normal coronary arteries. We now have some understanding of the mechanisms behind this condition, and this has led to some techniques for proving and studying it, but the diagnosis is largely clinical. We essentially don’t do coronary angiography with injection of adenosine or acetylcholine, measurements of coronary flow reserve, single photon emission computed tomography, positron emission testing or stress cardiac magnetic resonance imaging, at least not at Cityside Hospital. One thing we have learned is that this condition does progress relentlessly in 20-30% of cases and causes heart attacks and death in some patients, even though this was initially thought to be very rare.

The most dramatic development in cardiology in the last twenty years is probably our understanding that rupture of non-critical cholesterol plaque, small enough to go undetected during routine EKG or nuclear stress testing, accounts for somewhere around 85% of all heart attacks.

So much for all the angiograms, elective stents and bypasses cardiologists have been doing. In acute coronary syndrome, which is unstable angina or a heart attack without classic EKG changes of a completed heart attack, there is still an important role for urgent cardiac catheterization, but its role in stable angina or asymptomatic coronary stenosis is debatable at best.

So, now cardiologists are having to reconcile that their angiograms are a most imperfect predictor of disability and death, their stents don’t save lives except in acute coronary syndrome, and more and more of their patients will be plodding along with medical management of coronary disease that doesn’t show up on angiograms. They may find themselves tinkering with medical management of an incompletely understood syndrome, choosing drugs and dosages based on -gasp- patients’ subjective histories and clinical experience.

The pendulum is swinging back; a circle seems to be completed. Will cardiologists become slow and methodical internists again?

Cave: The Patient Who Suggests a Diagnosis Before Telling You His Symptoms

Published January 21, 2016 Cave! 2 Comments

Sir William Osler wasn’t exactly wrong when he said “Listen to your patient, he is telling you the diagnosis”, but he didn’t mean it literally. His patients did not offer up esoteric and complete medical diagnoses on a silver platter. They left him clues in plain language that he listened carefully to in order to make the correct diagnosis.

His words were penned in an era when medical information was scarce among non-medical people. There was no Dr. Google, Dr. Oz or Dr. House to educate the public about diseases or medical terminology a century ago.

In a way, I think doctors today have to do more filtering of what our patients say in order to get the medical history straight.

For example, Mrs. LaVerdiere made an appointment for nausea some time ago. As soon as I walked into the exam room, she started telling me about how she must have eaten a spoiled crabmeat sandwich on her trip to a coastal fishing village the weekend before. Her conversation was full of theories as to why she was feeling unwell and her husband wasn’t. I finally got her to describe in great detail exactly what she felt, and the gnawing pain that radiated to her back did not fit with a simple case of food poisoning. Her CT scan showed the smallest pancreatic cancer ever diagnosed at Cityside Hospital and she underwent a Whipple procedure as easily as any routine minor surgery.

Mrs. Waller describes ordinary bodily sensations in the most dramatic terms and throws terminology around that rocks me out of my country doctor habitual way of plain-talking. She has, over the years, described ordinary itches as “you know how it feels when you’ve been bitten by a thousand fire ants”, headaches as “I felt like I was about to pop a Berry aneurysm”, and indigestion as “pyloric stricture”. I have the distinct impression she is always trying to make my job easier by describing things in more or less medical terms, in case I forgot to speak English.

During my tenure in medicine, the tendency for patients to offer explanations and theories instead of just describing what they feel has increased dramatically since the creation of the Internet. But I have also come to realize that there have always been people who are simply not able to recognize and describe what they are feeling, particularly emotions. They therefore tend to describe the bodily sensations that their unrecognized emotions produce, or, even harder to decipher, they are only capable of reporting other people’s observations of their own appearance or behavior.

Most of us recognize that anxiety or other strong emotions can cause heart palpitations or abdominal pain, hence our use of expressions like ”gut-wrenching”, but some of us are only aware of the bodily sensation and are clueless about their own emotions that trigger them. They are also usually skeptical about any suggestion of such a connection.

Hedda Brown is one of those people I have always struggled to diagnose, no matter what ailed her. Only a few years ago did I learn the word for her condition – alexithymia, inability to recognize emotions. She would answer questions like “tell me more about in what way you don’t feel well” with stories like this:

“I knew I wasn’t feeling right yesterday morning. I didn’t want breakfast. Harry, my husband, took one look at me and said I looked peaked and told me I looked like I was about to vomit. My daughter also noticed something about me. She said I looked like I was dehydrated. She acted real nice all of a sudden, instead of her usual way of ignoring me, she offered to make me a cup of tea or make me an omelet, but I just didn’t want any.”

No matter how much time I give Hedda to tell her story, I get very little to work on. So I usually try some direct questions, like “did you have chills” or “did your belly hurt”, but even that kind of inquiry usually results in answers about other people’s observations or theories.

I have finally come to realize that Hedda carries with her more than a lifetime’s worth of grief, which now and then erupts as a sensation she has no words for. Because she is so unaware of her emotions, the most I could ever expect from her is a general bodily sensation, like “a pain here” or “not hungry”. In the beginning, she underwent a fair number of tests, but as she has started to trust me more, we have had a few conversations along the lines of “maybe your body is trying to tell you something”. It is a slow process.

Thinking about Sir William’s famous quote, perhaps it could be adapted for the Internet age this way:

“Listen to your patient’s story; he is telling you the diagnosis.”

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